| ACINIC CELL CARCINOMA / ACINAR CELL CARCINOMA / ACINIC CELL ADENOCARCINOMA: SPECIFIC CHARACTERISTICS | Other Cancer(s) with possible similarities, or sharing these properties | Article Title or Source | Author(s), Journal Title, Book or Database | Publi- cation or conver- sation DATE | NOTES | |||
| Note: This document is currently arranged in reverse chronological order, not by subject matter. | Note: This document is currently arranged in reverse chronological order. | Note: This document is currently arranged in reverse chronological order. | ||||||
| Immunohistochemistry tests
performed 10/2002 on Edgar Stroke's tissue from 6/8/99 needle biopsy. Tissue
was tested for EGFR and P53. P53 was negative. But EGFR produced a result
of “Positive Focally”. Verbal description by pathologist was;
“10% of tissue was positive in a specific area. It was on the edge,
so I’m not sure how reliable that is. Oncologist needs to decide.” |
Other epithelial cancers have shown positivity for EGFR. | Surgical Pathology Report | UCLA Pathologist: Scott D. Nelson, M.D. | Current as of 10/2/2002 | A result of positivity for EGFR could make an ACC patient eligible for treatment with IRESSA, a promising new cancer drug. EGFR stands for Epidermal Growth Factor Receptor. | |||
| PANCREATIC CANCER VERSION: The following
rare non-endocrine tumors are listed alphabetically: Acinar Cell Carcinomas
- These rare cancerous tumors may produce excess amounts of the digestive enzymes normally produced by the pancreas. This increase in enzymes causes distinct symptoms in 20% of acninar cell carcinoma cases. Symptoms may include unusual skin rashes, joint pain and an increased level of eosinophils, a type of white blood cell. Microscopically, these tumors have a characteristic grainy appearance. Special tests, including electron microscopy, can often be used to diagnose this type of tumor. |
Pancreas Cancer Web Johns Hopkins Medical Institutions Dept. of Pathology |
Current as of 7/15/2002 | URL: http://pathology2.jhu.edu/pancreas/QUESTION/TYPTABLE.HTM | |||||
| INCIDENCE: 3rd most common epithelial
malignancy of the salivary gland. 17% of all primary salivary gland malignancies 6% of salivary gland neoplasms SYNCHRONOUS OR METACHRONOUS: 3% of cases are bilateral. |
Acinic Cell Carcinoma | The Doctor's Doctor website page on Acinic Cell Carcinoma | Current as of 6/2002 | URL: http://www.thedoctorsdoctor.com/diseases/aciniccell_ca.htm | ||||
| AGE RANGE-MEDIAN:Mean age is 44 years 12% of patients < 20 years SEX (M:F): 2:3 GEOGRAPHY: No racial predilection. |
Acinic Cell Carcinoma | The Doctor's Doctor website page on Acinic Cell Carcinoma | Current as of 6/2002 | URL: http://www.thedoctorsdoctor.com/diseases/aciniccell_ca.htm | ||||
| GROSS APPEARANCE/CLINICAL VARIANTS:
Single well circumscribed tumors 1-3 cm Lobular tan to reddish surface Solid to cystic |
Acinic Cell Carcinoma | The Doctor's Doctor website page on Acinic Cell Carcinoma | Current as of 6/2002 | URL: http://www.thedoctorsdoctor.com/diseases/aciniccell_ca.htm | ||||
| GENERAL: Sheets of polygonal cells with
granular, lightly basophilic cytoplasm and uniform nuclei resembling serous
acinar cells. May be separated by thin fibrovascular septa. Vacuolated cells characteristic. Clear cells may be abundant. Usually infiltrate surrounding tissue. |
Acinic Cell Carcinoma | The Doctor's Doctor website page on Acinic Cell Carcinoma | Current as of 6/2002 | URL: http://www.thedoctorsdoctor.com/diseases/aciniccell_ca.htm | ||||
| FOLLICULAR: Multiple cystic lumens filled
with eosinophilic proteinaceous material, resembling thyroid follicles.
PAPILLOCYSTIC: In rare cases, the tumor may dedifferentiate resulting in
areas of poorly differentiated or undifferentiated carcinoma. Hemorrhage
more common with this type. MICROCYSTIC:
SOLID ACINAR:
SPECIAL STAINS: Granules PAS positive,
diastase resistant. IMMUNOPEROXIDASE: Cytokeratin, transferrin, CD15,
CEA Some positive for S100 and GFAP. ELECTRON MICROSCOPY (EM): Multiple round electron dense secretory granules. |
Acinic Cell Carcinoma | The Doctor's Doctor website page on Acinic Cell Carcinoma | Current as of 6/2002 | URL: http://www.thedoctorsdoctor.com/diseases/aciniccell_ca.htm | ||||
| Most Acinic Cell Carcinomas are LOW GRADE and are associated with less aggressive growth and good survival rates (70% at 10 years). High grade variants have also been described (papillocystic carcinoma) or carcinomas with undifferentiated cells in a medullary pattern. The high grade variants are very uncommon and associated with much poorer survival. | OncoLink - Univ. of Penn. Cancer Center Website | Last reviewed: 11-1-2001 | ||||||
| Acinic Cell Carcinomas are often ENCAPSULATED, and may mistakenly believed to be benign. However, on microscopic analysis there may be extensions of tumour cells into surrounding tissue and metastases may occur over time. | OncoLink - Univ. of Penn. Cancer Center Website | Last reviewed: 11-1-2001 | ||||||
| Edgar's tumor tissue (from 11/99 surgery) was tested for C-Kit overexpression (CD117). It came up negative. Official results were: Slide Block Description: (1) Unstained Slide, pathology report dated 11/22/99. Clinical diagnosis: metastastic adenocarcinoma. Results: Paraffin Immunohistochemistry: CD117 - NEGATIVE. | 4/27/01 | This was for potential consideration for effectiveness of drug STI-571 / Gleevec. | ||||||
| OBJECTIVE: CD34-positive dendritic
interstitial cells may be associated with the regulation of tumor growth.
This association has been studied in various human neoplasms, especially skin
tumors. In this study, we evaluated the distribution of dendritic interstitial
cells and myofibroblastic cells at the tumor periphery of various benign and
malignant salivary gland neoplasms. METHODS: Forty-nine cases of salivary
gland tumors were selected: 16 pleomorphic adenomas, 12 Warthin tumors, 8
polymorphous low-grade tumors, 5 adenoid cystic carcinomas, 6 acinic cell carcinomas, and 2 mucoepidermoid carcinomas. Immunohistochemical analysis was performed by using antibodies for CD34 (dendritic cells) and alpha-smooth muscle actin (myofibroblast) on formalin-fixed, paraffin-embedded archival tissue. Staining intensity was graded as marked (3+), moderate (2+), weak (1+), and absent (0). (more) |
Dendritic interstitial and myofibroblastic cells at the border of salivary gland tumors. | Soma L, LiVolsi VA, Baloch ZW TITLE:Dendritic interstitial and myofibroblastic cells at the border of salivary gland tumors. Arch Pathol Lab Med; 125(2):232-6 2001 UI: 21092141 |
2001 | |||||
| (cont'd) RESULTS: Staining intensity for CD34 was 3+ in 24 (86%) of 28 benign tumors (pleomorphic adenomas and Warthin tumors) and 6 (29%) of 21 malignant tumors (polymorphous low-grade tumors, acinic cell carcinomas, adenoid cystic carcinomas, and mucoepidermoid carcinomas) and 2+ in 4 (19%) of 21 malignant tumors. CONCLUSION: We conclude that the dendritic interstitial cells and myofibroblastic cells may be associated with the regulation of tumor growth in salivary gland tumors. | polymorphous low-grade tumors, adenoid cystic carcinomas, and mucoepidermoid carcinomas | Dendritic interstitial and myofibroblastic cells at the border of salivary gland tumors. | Soma L, LiVolsi VA, Baloch ZW TITLE:Dendritic interstitial and myofibroblastic cells at the border of salivary gland tumors. Arch Pathol Lab Med; 125(2):232-6 2001 UI: 21092141 |
2001 | ||||
| Genetic alterations of oncogene MDM2 promote malignant transformation of several human tumors. METHODS AND RESULTS: Benign and malignant tumors of the salivary gland (6 pleomorphic adenomas, 3 Warthin's tumors, 1 adenocarcinoma, 1 basal cell adenocarcinoma, 1 mucoepidermoid carcinoma, 3 acinic cell carcinomas, 2 adenoid cystic carcinoma, 1 squamous cell carcinoma) were analyzed by fluorescence-based PCR techniques and immunochemistry for MDM2 gene amplification, MDM2 gene expression, MDM2 gene mutation, MDM2 RNA splicing and MDM2 accumulation. Data show that all samples contained nonamplified MDM2 genes with nonmutant zinc finger regions. However, in two benign and two malignant samples, novel MDM2 mRNA splicing variant types 1 and 2 were detected. Furthermore, three malignant tumors revealed significant nuclear MDM2 accumulation. Correlation between levels of MDM2 mRNA and MDM2 protein could not be detected in the specimens. (cont'd below) | Genetic analysis of the human oncoprotein MDM2 in
benign and malignant tumors of the salivary gland. |
Schlott T; Nagel H; Laskawi R; Eiffert H; Droese M
Pathobiology 2001;69(2):67-76 Department of Cytopathology, Georg August University, Gottingen, Germany. tschlott@med.uni-goettingen.de |
2001 | Check full text for more details. | ||||
| (Cont'd) CONCLUSION: The present study suggests that MDM2 gene mutation and gene amplification do not contribute to MDM2 accumulation detected in malignant tumors of the salivary gland. However, the role of novel MDM2 splicing variants in MDM2 expression and malignant transformation must be elucidated further. | Genetic analysis of the human oncoprotein MDM2 in
benign and malignant tumors of the salivary gland. |
Schlott T; Nagel H; Laskawi R; Eiffert H; Droese M
Pathobiology 2001;69(2):67-76 Department of Cytopathology, Georg August University, Gottingen, Germany. tschlott@med.uni-goettingen.de |
2001 | Check full text for more details. | ||||
| The clinicopathological features of six cases of breast carcinomas showing features of acinic cell differentiation, which are similar to those seen in homologous tumors of salivary glands, are presented. The patients, all women, were 35-80 years of age. One case recurred after 4 years, and in two cases axillary lymph node metastases were found at the time of surgery. Histologically the tumors showed a microglandular pattern merging with solid areas. Cytologically, immunohistochemically, and ultrastructurally the tumors were very similar to cases of acinic cell carcinoma of the parotid gland. The differential diagnostic criteria with microglandular adenosis and carcinomas showing granular cytoplasm are discussed. It seems that acinic cell carcinomas of the breast have to be added to the long list of tumors that affect the salivary glands and can also arise in the breast. | Breast Cancers | Acinic cell carcinoma of the breast: an immunohistochemical and ultrastructural study. - |
Virchows Arch; 437(1):74-81 2000 UI: 20417373 - Damiani S, Pasquinelli G, Lamovec J, Peterse JL, Eusebi V | 2000 | ||||
| Edgar's tumor tissue (from 11/99 surgery) was tested for carcinoembryonic antigen (CEA) expression. It came up negative. | 8/23/00 | |||||||
| Galectins are a family of non-integrin beta-galactosidase-binding lectins. Altered expression of galectins has been associated with neoplastic transformation and progression in several human tumors. In this study, we examined the distribution patterns of galectin-1 and galectin-3 in normal (n=45), benign (n=16), and malignant (n=49) salivary gland specimens using immunohistochemistry to determine their diagnostic and/or biological implications in salivary gland tumorigenesis. In malignant tumors, most of the polymorphous low-grade adenocarcinomas and carcinoma ex-pleomorphic adenomas expressed both galectins, whereas adenoid cystic and acinic cell carcinomas showed dramatically reduced galectin-3 expression and heterogeneous galactin-1 staining. Our data demonstrated altered localization and expression of galectin-3, and to lesser extent, galectin-1 in salivary gland carcinomas. These findings may assist in the differential diagnosis of some salivary gland malignancies, especially when using small and limited fine-needle aspiration materials. | adenoid cystic | Differential expression of galectin-1 and galectin-3 in benign and malignant salivary gland neoplasms | Int J Oncol 2000 Aug;17(2):271-6 - Xu XC, Sola Gallego JJ, Lotan R, El-Naggar AK | Aug-00 | ||||
| OBJECTIVE: To assess the prevalence of activating mutations in K-ras and H-ras genes in salivary gland tumors with ductal or acinar differentiation and to evaluate their potential correlation with clinical parameters. PATIENTS: Twenty-four patients with salivary gland carcinoma were surgically treated. Nine had adenocarcinoma, 1 had adenosquamous carcinoma, 11 had mucoepidermoid carcinoma, and 3 had acinic cell carcinoma. CONCLUSION: Our data suggest that K-ras gene alteration is probably not an important factor in the oncogenesis of human salivary gland tumors. However, mutational activation of the H-ras gene appears to play a role in the development and/or progression of salivary gland mucoepidermoid carcinomas. | Other salivary gland cancers | ras gene mutations in salivary gland tumors | Arch Pathol Lab Med 2000 Jun;124(6):836-9 - Yoo J, Robinson RA | Jun-00 | ||||
| The expression and mutation patterns of p53 were studied in a series of 68 benign pleomorphic adenomas and 237 malignant salivary gland tumors. p53 overexpression (nuclear staining exceeding 10%) was detected in 20% of the malignant salivary gland tumors, with the highest prevalence observed in polymorphous low grade adenocarcinoma, squamous cell carcinoma, and carcinoma ex pleomorphic adenoma and the lowest in adenoid cystic carcinoma and acinic cell carcinoma. Our findings indicate that p53 may be a useful marker to help discriminate between benign and malignant salivary gland tumors. | adenoid cystic carcinoma | Expression and mutation patterns of p53 in benign and malignant salivary gland tumors. | Int J Oncol 2000 Mar;16(3):477-83 - Nordkvist A, Roijer E, Bang G, Gustafsson H, Behrendt M, Ryd W, Thoresen S, Donath K, Stenman G | Mar-00 | ||||
| Report on Edgar's Chemistry: End of April/beginning of May 2000: Edgar's urine was tested for growth factors which could make me a more likely candidate for certain angiogenesis inhibitors (alpha-interferon for example). Edgar's Basic Fibroblast Growth Factor (fGf) was 2690 picograms/liter. Normal levels are less than 4000 (so I was normal). For Vascular Endothelial Growth Factor (veGF), Edgar's levels were 312 picograms/millileter. Normal levels are less than 300, so this was slightlyhigh. | Person who recommended testing, and performed tests at her lab was: Susan Connors (in Judah Folkman's research group) - Children's Hospital, Boston. | May-00 | ||||||
| Acinic Cell Carcinoma - Characteristics: Description of slide on website: Sheets of large, polygonal cells with granular, basophilic cytoplasm and eccentric nuclei, reminiscent of serous acinar cells. Striated ducts and the normal lobular architecture are absent. Vacuolated cells and intercalated duct cells are often seen. So are clear cells; these do not contain glycogen. Note that many tumors have a mixture of cell types and architectural patterns. All acinic cell carcinomas, however, have at least a focal component of serous acinar differentiation. |
Medscape (www.Medscape.com) - Pathology Case Challenge
<http://oncology.medscape.com/Medscape/features/PathCases/ |
Amir Rahemtulla, MD, MA - clinical pathology instructor at Harvard Medical School. | 4/21/00 | |||||
| Acinic Cell Carcinoma - Characteristics:
- The most common malignant epithelial tumor
to occur bilaterally (although 97% of acinic cell carcinomas are
unilateral). - Acinic cell carcinoma is the third most common malignant epithelial tumor of the salivary glands. - It is the third most common epithelial tumor of the salivary gland in children (after pleomorphic adenoma and mucoepidermoid carcinoma). - Most occur in the parotid gland. - The papillary-cystic variant reportedly has a worse prognosis. - The tumor is positive for alpha 1 antitrypsin, alpha 1 antichymotrypsin, PAS with diastase and, sometimes, amylase. Though not typically present, some mucicarmine staining in an otherwise diagnostic case is still compatible with acinic cell carcinoma. |
Medscape (www.Medscape.com) - Pathology Case Challenge
<http://oncology.medscape.com/Medscape/features/PathCases/ 2000/04.00/med0420.14/med0420.14.default.html> |
Amir Rahemtulla, MD, MA - clinical pathology instructor at Harvard Medical School. | 4/21/00 | |||||
| Surgical Pathology of Edgar's Sacral
Tumor, 11/18/99: Histologic sections reveal a metastatic adenocarcinoma
comprising sheets of acinic type cells with abundant eosinophilic and
granular cytoplasm and numerous variable sized intracytoplasmic vacuoles.
The tumor cells are arranged around fibrovascular cores forming papillary
pattern. |
City of Hope Pathologist: Peiguo Chu | 11/20/99 | ||||||
| Other Characteristics of Edgar's pelvic
tumor, noted during 11/18/99 surgery: Color: Very vascular purplish tumor
(noted in left sacral ala). Other areas (more midline, pushing cauda equina
posteriorly) were more yellowish. Texture: Very soft and liquid. Blood Supply: Very vascular. Good blood supply (to tumor). On capillary level, seemed average. |
Surgeons: Adam Mamelak, Maria Li, Gary Moscarello. | 11/18/99 | ||||||
| Bone morphogenetic protein (BMP-6, also known as vegetal-pale-gene-related and decaplentaplegic-vegetal-related) is a member of the transforming growth factor-beta superfamily of multifunctional signaling molecules. BMP-6 appears to play various biological roles in developing tissues, including regulation of epithelial differentiation. To study the possible involvement of BMP-6 in normal and neoplastic human salivary glands, we compared its mRNA and protein expression in 4 fetal and 15 adult salivary glands and in 22 benign and 32 malignant salivary gland tumors. In situ hybridization and Northern blot analysis indicated that BMP-6 transcripts are expressed at low levels in acinar cells of adult submandibular glands but not in ductal or stromal cells. BMP-6 was immunolocated specifically in serous acini of parotid and submandibular glands. None was found in primitive fetal acini or any other types of cell in adult salivary glands, including mucous acini and epithelial cells of intercalated, striated, and excretory ducts. (more) | Bone morphogenetic protein-6 is a marker of serous acinar cell differentiation in normal and neoplastic human salivary gland. | Cancer Res 1999 Nov 15;59(22):5815-21 - Heikinheimo AK, Laine MA, Ritvos OV, Voutilainen RJ, Hogan BL, Leivo IV - Institute of Dentistry, University of Turku, Finland. heikinhe@netlife.fi | Nov-99 | POSSIBLY VERY IMPORTANT | ||||
| (continued): All 16 cases of acinic cell carcinoma consistently exhibited cytoplasmic BMP-6 staining in the acinar tumor cells. Other cell types in these tumors, including intercalated duct-like cells, clear, vacuolated cells, and nonspecific glandular cells, exhibited no cytoplasmic BMP-6 staining. Other benign and malignant salivary gland tumors lacked BMP-6 immunoreactivity, except in areas of squamous differentiation. The results indicate that in salivary glands, BMP-6 expression is uniquely associated with acinar cell differentiation and suggest that BMP-6 may play a role in salivary gland function. More importantly, our experience of differential diagnostic problems related to salivary gland tumors suggests that the demonstration of consistent and specific BMP-6 immunoreactivity in acinic cell carcinoma is likely to be of clinical value. | Bone morphogenetic protein-6 is a marker of serous acinar cell differentiation in normal and neoplastic human salivary gland. | Cancer Res 1999 Nov 15;59(22):5815-21 - Heikinheimo AK, Laine MA, Ritvos OV, Voutilainen RJ, Hogan BL, Leivo IV - Institute of Dentistry, University of Turku, Finland. heikinhe@netlife.fi | 11/15/99 | |||||
| The chromosomal locus 9p21 contains the p16 (INK4a/CDKN2/MTS1) tumor suppressor gene that has been implicated in a variety of tumor types, including carcinomas of the head and neck, esophagus, and pancreas. To determine whether the loss of this gene is involved in salivary gland cancers, 35 carcinomas and paired nonneoplastic specimens were analyzed for loss of heterozygosity (LOH) of polymorphic genetic markers located in the region of interest. Loss of heterozygosity was found in 1 of 10 adenoid cystic carcinomas and 1 of 8 mucoepidermoid carcinomas and was absent in the remaining subtypes, including acinic cell carcinoma. These results suggest that inactivation of p16 is important in the development or progression of at least some salivary duct carcinomas, but we found no evidence that its alteration plays a role in the other subtypes examined. | mucoepidermoid carcinoma, salivary duct carcinoma, adenoid cystic carcinoma, and polymorphous low-grade adenocarcinoma. | Analysis of chromosome 9p21 deletion and p16 gene mutation in salivary gland carcinomas. | Hum Pathol 1999 Oct;30(10):1242-6 - Cerilli LA, Swartzbaugh JR, Saadut R, Marshall CE, Rumpel CA, Moskaluk CA, Frierson HF Jr | 10/30/99 | ||||
| Acinic Cell (Adeno)carcinoma -
DEFINITION: A neoplastic growth of epithelial cells showing serous acinar differentiation GROSS FEATURES: - Single, well circumscribed to multinodular and ill-defined - Firm to cystic - 0.5-13 cm - Lobular, red to tan cut surface |
FRONTIERS IN BIOSCIENCE; LECTURE SERIES: SALIVARY GLAND TUMORS; CLINICAL AND PATHOLOGICAL FEATURES Dept of Pathology, Moffitt Cancer Center and University of South Florida, 12902 Magnolia Drive, Tampa, FL 33612 |
S Tabibzadeh | As of 9/19/99 | WEBSITE: http://www.bioscience.org/lecture/tabibza/list.htm | ||||
| Acinic Cell Carcinoma - CLINICAL FEATURES: - Occurs most commonly in parotid gland - Occurs unilaterally. May occur bilaterally. - Occurs more frequently in women than men (3:2) - Occurs in young and old individuals - Slowly growing, mobile or fixed mass of various durations. - Asympotatic - Pain or tenderness - Facial muscle weakness |
FRONTIERS IN BIOSCIENCE; LECTURE SERIES: SALIVARY GLAND TUMORS; CLINICAL AND PATHOLOGICAL FEATURES Dept of Pathology, Moffitt Cancer Center and University of South Florida, 12902 Magnolia Drive, Tampa, FL 33612 |
S Tabibzadeh | As of 9/19/99 | WEBSITE: http://www.bioscience.org/lecture/tabibza/list.htm | ||||
| Acinic Cell Carcinoma: ULTRASTRUCTUAL FEATURES: Main epithelial cells, Multiple round, membrane bound, electron dense cytoplasmic granules, Vacuoles, Lumina, Apical junctional complexes, Few microvilli, Clear cells, Dilated ER, Lipid inclusions, Intracytoplasmic pseudolumina, Myoepithelial cells, Elongated, Microfilaments, Dense bodies. | FRONTIERS IN BIOSCIENCE; LECTURE SERIES: SALIVARY GLAND TUMORS; CLINICAL AND PATHOLOGICAL FEATURES Dept of Pathology, Moffitt Cancer Center and University of South Florida, 12902 Magnolia Drive, Tampa, FL 33612 |
S Tabibzadeh | As of 9/19/99 | WEBSITE: http://www.bioscience.org/lecture/tabibza/list.htm | ||||
| Acinic Cell Carcinoma MICROSCOPIC FEATURES: Patterns Sheets Cysts, some with papillary growth Microcystic Acini Ducts Glands Follicles (similar to thyroid) Epithelium Large polygonal Lightly basophilic cytoplasm Uniform to variable eccentic nuclei (more) |
FRONTIERS IN BIOSCIENCE; LECTURE SERIES: SALIVARY GLAND TUMORS; CLINICAL AND PATHOLOGICAL FEATURES Dept of Pathology, Moffitt Cancer Center and University of South Florida, 12902 Magnolia Drive, Tampa, FL 33612 |
S Tabibzadeh | As of 9/19/99 | WEBSITE: http://www.bioscience.org/lecture/tabibza/list.htm | ||||
| Acinic Cell Carcinoma MICROSCOPIC FEATURES: Acinar epithelium Large polygonal Lightly basophilic cytoplasm (blue dot tumors) Protuberance of luminal membrane producing a tombstone appearance Uniform to variable eccentic nuclei Cytoplasmic granules (PAS positive-diastase resistant; mucicarcmine positive) Hemosiderin Duct epithelium Eosinophilic cytoplasm Variable cell size Central lumen of various size (more) |
FRONTIERS IN BIOSCIENCE; LECTURE SERIES: SALIVARY GLAND TUMORS; CLINICAL AND PATHOLOGICAL FEATURES Dept of Pathology, Moffitt Cancer Center and University of South Florida, 12902 Magnolia Drive, Tampa, FL 33612 |
S Tabibzadeh | As of 9/19/99 | WEBSITE: http://www.bioscience.org/lecture/tabibza/list.htm | ||||
| Acinic Cell Carcinoma MICROSCOPIC FEATURES: Stroma Delicate fibrovascular tissue Collagenous tissue Lymphoid infiltration (in some cases) Hemorrhage Hemosiderin Psammoma bodies Vacuolated cells Eosinophilic to amphophilic cytoplasm Clear vacuoles PAS and mucicarmine negative Clear cells Lack of glycogen Glandular cells Round to polgonal Eosinophilic to amphophilic cytoplasm Lack of cytoplasmic granules or PAS positivity Nuclear pleomorphism |
FRONTIERS IN BIOSCIENCE; LECTURE SERIES: SALIVARY GLAND TUMORS; CLINICAL AND PATHOLOGICAL FEATURES Dept of Pathology, Moffitt Cancer Center and University of South Florida, 12902 Magnolia Drive, Tampa, FL 33612 |
S Tabibzadeh | As of 9/19/99 | WEBSITE: http://www.bioscience.org/lecture/tabibza/list.htm | ||||
| Acinic Cell Carcinoma IMMUNOHISTOCHEMICAL FEATURES: Cytokeratin(present) CEA (present) alpha 1 antitrypsin (present) alpha 1 antichymotrypsin (present) Leu-M1 (present) Amylase (present) Transferrin (present) Lactoferrin (present) Vasocactive intestinal polypeptide (present) S-100 (some) GFAP (some) |
FRONTIERS IN BIOSCIENCE; LECTURE SERIES: SALIVARY GLAND TUMORS; CLINICAL AND PATHOLOGICAL FEATURES Dept of Pathology, Moffitt Cancer Center and University of South Florida, 12902 Magnolia Drive, Tampa, FL 33612 |
S Tabibzadeh | As of 9/19/99 | WEBSITE: http://www.bioscience.org/lecture/tabibza/list.htm | ||||
| Acinic Cell Carcinoma DIFFERENTIAL DIAGNOSIS: Papillary-cystic and follicular type Cystadenocarcinoma (lack of microcycstic and vacuolated cells) Mucoepidermoid carcinoma (presence of mucous cells) Metastatic thyroid carcinoma (presence of thyroglobulin) Polmorphous low-grade adencarcinoma (perineural invasion, homogeneous cell population, single cell infiltration at the periphery) Clear cell type Clear cell carcinoma (lack of glycogen, lack of serous differentiation) Epithelial-myoepithelial carcinoma (lack of glycogen) Squamous cell carcinoma (lack of glycogen) Metastatic renal cell carcinoma (lack of glycogen) |
FRONTIERS IN BIOSCIENCE; LECTURE SERIES: SALIVARY GLAND TUMORS; CLINICAL AND PATHOLOGICAL FEATURES Dept of Pathology, Moffitt Cancer Center and University of South Florida, 12902 Magnolia Drive, Tampa, FL 33612 |
S Tabibzadeh | As of 9/19/99 | WEBSITE: http://www.bioscience.org/lecture/tabibza/list.htm | ||||
| We report a rare case of acinic cell carcinoma of the palate in a 63-year-old Japanese woman. Clinical examination demonstrated a firm, mobile mass without regional lymph-adenopathy. Histopathologically, the tumor was composed of large, polyhedral or round cells with basophilic granular cytoplasm (serous acinar-like cells) and reticular or clear cytoplasmic cells. These tumor cells were positive for the periodic acid-Schiff reaction, but negative for alcian blue. The tumor nests were separated by thin vascular tissue and incompletely encapsulated. Immunohistochemically, the tumor cells exhibited positive reactivity for alpha-amylase, lactoferrin, secretory component, S100 protein, and epithelial membrane antigen, but were negative for actin, glial fibrillary acidic protein, keratin, and carcinoembryonic antigen. These results suggest that this tumor is well differentiated into serous acinar cells and that the reticular and clear cytoplasmic cells are a modified form of these cells. | Acinic cell carcinoma of the palate: case report and immunohistochemical observation. | Arch Otolaryngol Head Neck Surg 1999 Sep;125(9):1025-8 - Utsunomiya T, Yamamoto H, Kuyama K, Itami M, Asanuma K - Department of Pathology, Nihon University School of Dentistry at Matsudo, Chiba, Japan. | Sep-99 | |||||
| Immunohistochemistry Report on Edgar's Biopsy Tissue of 6/8/99: Tests for Her2Neu overexpression, Estrogen Receptors and Progesterone Receptors ALL CAME BACK NEGATIVE. | It HAS been reported that some salivary gland cancers (and some Acinic Cells) have been positive for these tests. | UCLA Pathologist: Scott D. Nelson M.D. & Andrea Chang M.D. - Resident | 7/27/99 | According to Scott Nelson, results are completely reliable. | ||||
| Conversation with authority: In salivary gland cancers (mucoepidermoid carcinomas) he studied (together with MD Anderson), Her2Neu was overexpressed in 20-30% of cases. They found that when Her2neu gene is amplified/ overexpressed, cancers are more aggressive and prone to higher rate of metastatic disease (and higher death rate). | mucoepidermoid carcinomas | Pathologist: Mike Press - USC, Norris Cancer Center | 7/12/99 | |||||
| Conversation with authority: There are similarities between salivary glands and mammary glands | Mammary glands /breasts. | Pathologist: Mike Press - USC, Norris Cancer Center | 7/12/99 | |||||
| Conversation with authority: My case: Unusual; torpid but persistent pattern of growth. Slow growth / slow "turnover". Very long G1 Phase of growth. | Most Breast Cancers have similar characteristics. See Waterhouse. (also adenocarcinomas) | Oral Pathologist: J. Sciubba - LI Jewish (soon Johns Hopkins) | 7/7/99 | |||||
| Cytogenetics Report of Edgar's Biopsy -
Metastatic Site, Pelvic Recurrence, Needle Biopsy 6/8/99:
ANALYSIS: Metaphases counted: 15 Colonies Counted: Metaphases analyzed: 15 Banding Technique: GPG Metaphases karotyped: 3 Banding Resolution: 450 RESULTS: KARYOTYPE: 46, XY, der(1) add (1p), -3, del(4) q(12), del(6) (q21), del(10q), der(11) add(11p), der (12q), der(18q) [cp15] INTERPRETATION: Highly abnormal * male chromosome analysis with several unusual abnormalities, suggestive of an aggressive phase. The most relevant of these abnormalities are deletion 4q and 6q, both consistent with tumors of the salivary glands. |
UCLA Pathologists: Wayne W. Grody, M.D. P. Nagesh Rao, Ph.D. | 7/2/99 | ||||||
| * Conversation with authority: Re: Edgar's Cytogenetics Report - The cells are highly abnormal as compared with normal cells. But it is NOT atypical for salivary gland cancer. Don't put TOO much weight on "aggressive" part. However, it COULD be, if Edgar's experience backs that up. | There ARE similarities with Breast CancersŠin the normal biology;glandular structure. But he doesn't know much about. It's not his area. | UCLA Pathologist: Scott D. Nelson, M.D. - Wrote Edgar's Pathology Report 6/99, and ordered cytogenetics study. | 7/15/99 | |||||
| P53 protein and vascular endothelial
growth factor (VEGF) expression, and mean intratumoral microvessel density
(IMVD) were studied by immunohistochemistry in 31 salivary gland carcinomas, consisting of 11 adenoid cystic carcinomas (AdCCs), 10
mucoepidermoid carcinomas (MECs), 7 acinic cell
carcinomas (AcCCs), and 3 squamous cell carcinomas
(SCCs). Cases with p53 protein in more than 20% of
tumor cells were detected in one AdCC, four MECs, one AcCC, and two SCCs.
Both frequency of p53 and VEGF expression, and mean IMVD, were higher in the
MECs and SCCs than in the AdCCs and AcCCs. Similarly, both VEGF expression
and mean IMVD were significantly higher (P<0.05) in the eight p53-positive
tumors than in the 23 negative tumors. Six cases with survival periods less
than 5 years showed significantly higher frequency of p53 and VEGF expression
and of mean IMVD than those with longer survival periods. These results
indicate that p53 expression might partly correlate with VEGF expression and
mean IMVD, and be a factor in the survival of patients with salivary gland
carcinomas. |
Adenoid cystic carcinomas showed similar traits (lower frequency of P53 protein, VEGF expression, and mean IMVD). | Expression of p53 oncoprotein increases intratumoral
microvessel formation in human salivary gland carcinomas. |
Doi R, Kuratate I, Okamoto E, Ryoke K, Ito H - First
Department of Pathology, Faculty of Medicine, Tottori University, Japan - J
Oral Pathol Med 1999 Jul;28(6):259-63 |
Jul-99 | ||||
| Conversation with authority: Acinic Cell of salivary glands is similar to Acinic Cell Pancreatic Cancer (only one he can think of). But that lesion is almost as rare as salivary gland Acinic Cell. (Probably more literature on Pancreatic version.) Pancreas and Parotid are similar glands. Pancreatic Acinic cell is ALSO SLOW GROWING. Many salivary gland cancers DO have Estrogen Receptors or Progestin Receptors. Radiation Therapy in general will control, but never cure. Radiation AND Chemotherapy generally prefer something LESS DIFFERENTIATED for successful treatment. Acinic Cell is rather "torpid" (sluggish). | Pancreatic Acinic Cell Type, not ductal. They have similar type of gland. | John Batsakis - ex. MD Anderson, now retired (major authority) | 6/30/99 | |||||
| Conversation with authority: Acinic cell falls into larger salivary gland group of Adenocarcinomas. Adenoid Cystic in same family. His experience is that Adenoid Cystic has some response to chemotherapy, and that it will react similarly to ACC as far as treatments. | Acinic cell falls into larger salivary gland group of Adenocarcinomas. Adenoid Cystic in same family. It's a sister disease, but not quite as slow growing. It is also well-differentiated though. Acinic Cell and Adenoid Cystic attack different sections of glands. | George J. Bosl - Chair, Dept. of Medicine, Clinical Oncology/Head and Neck Cancers, Medical Oncology | 6/29/99 | |||||
| Conversation with authority: Acinic Cell is most similar acting to Breast Cancer. You CAN get Acinic Cell in Breast! | Breast Cancers. | Gary Clayman - MD Anderson; rec. by John Batsakis; Head, neck and Oral Surgeon and Researcher. "cutting edge" | 6/29/99 | |||||
| Conversation with authority: Edgar's tumor is VERY WELL DIFFERENTIATED, which means that it closely mimics normal tissue. One interesting note about HIS TUMOR: Lots of times cancers get more poorly differentiated over time and metastases. But Edgar's hasn't changed much. But that's a double edged sword... It's good because it's slow-moving. But it also means things like chemo are LESS EFFECTIVE. LOW GRADE / WELL-DIFFERENTIATED mean same thing. | Will act like other WELL DIFFERENTIATED cancers. Pancreatic is similar, but more aggressive. Pancreas is closest cousin. | UCLA Pathologist: Scott D. Nelson, M.D. - Wrote Edgar's Pathology Report 6/99, and ordered cytogenetics study. | 6/24/99 | |||||
| Transgenic mice overexpressing transforming growth factor-alpha (TGF-alpha) display an expansion of intrapancreatic fibroblasts and a progressive accumulation of extracellular matrix. This massive fibrosis is associated with an increase in pancreatic size and weight. In parallel, tubular complexes appear that are composed of acinar cells with a decreased height. These acinar cell lose zymogen granules and become transitional cells, which subsequently gain duct cell features. In animals older than one year dysplastic lesions develop, which originate from tubular complexes. Occasionally these dysplastic foci transform to papillary and cystic pancreatic carcinoma. These tumors are positive for the duct-specific antigen Duct-1 and carbonic anhydrase activity indicative of ductal differentiation. Tumors overexpress the epidermal growth factor (EGF)-receptor and p53, but lack K-ras mutations. These data suggest an acinar-ductal-carcinoma sequence in TGF-alpha transgenic mice. | Acinar-ductal-carcinoma sequence in transforming
growth factor-alpha transgenic mice. |
Schmid RM, Kloppel G, Adler G, Wagner M - Ann N Y Acad Sci 1999 Jun 30;880:219-30 | 6/30/99 | |||||
| Pathology of Edgar's Biopsy - Metastatic Site, Pelvic Recurrence, Needle Biopsy 6/8/99: Sections show a tumor with a prominent microcystic and focally solid pattern. The tumor cells have abundant granular, basophilic cytoplasm, small round nuclei with prominent nucleoli. Mitotic figures are present. | UCLA Pathologist: Scott D. Nelson, M.D. | 6/10/99 | ||||||
| Conversation with authority: Acinic cell mostly in 2 organ systems: Salivary Gland and Pancreas. Acinic Cell is part of family of adenocarcinomas, which make a glandular structure. There are two types of adenocarcinomas; those with mucous granules, and those with serrous granules. Acinic Cell has SERROUS GRANULES. Acinic Cell is also special because it has LARGE GRANULES... specifically called ZYMOGEN GRANULES. The entire Parotid Gland, when normal, is made up of ACINOUS GRANULES. One day they can become cancerous, leading to "Acinic Cell Carcinoma". In Pancreatic Cancer, the most common type is cancer of duct (ductal). A small # of pancreatic cancers may be Acinic Cell. Acinic Cell is also special because it can look quite similar over long period of time, and at various metastastatic sites. (Many other cancers change over time.) | Pancreatic Cancer - Acinic Cell Type, not ductal. | Sunita Bhuta, UCLA Pathologist | Jun-99 | |||||
| Immunoreactivity of prostate-specific antigen (PSA), a kallikrein-like enzyme present in the seminal plasma, was demonstrated by indirect immunoperoxidase staining using a PSA antiserum in the apical cytoplasm along the luminal border of small-sized duct epithelial cells of the major salivary (parotid and submandibular) gland of both sexes (56/56, 100%). No PSA-like immunoreactivity was seen in large-sized duct epithelial cells and acinar cells. Minor salivary gland ducts were negative. When inflammatory and atrophic changes were observed, ductal expression of PSA-like immunoreactivity was decreased (12/37, 32%) and the site of intracellular localization often became diffusely cytoplasmic. The immunoreactivity was absorbed by human seminal plasma. Immunoreactivities of prostatic acid phosphatase and sex hormone receptors were undetectable in the salivary gland. Twenty-nine (34%) of 86 salivary gland tumors with ductal differentiation were immunoreactive for PSA mainly in the cytoplasm. (more) | No PSA-like immunoreactivity was seen in large-sized duct epithelial cells and acinar cells. | Localization of prostate-specific antigen-like immunoreactivity in human salivary gland and salivary gland tumors. | Tazawa K, Kurihara Y, Kamoshida S, Tsukada K, Tsutsumi Y -Pathol Int 1999 Jun 18;49(6):500-505 | Jun-99 | ||||
| (cont'd): A PSA monoclonal antibody ER-PR8 detected immunoreactivity in the prostate but not in the salivary glands or their tumors. Prostate-specific antigen-like immunoreactivity in small-sized (intercalated) duct epithelial cells of the major salivary gland and their tumors may be due to cross-reactivity of the antiserum with kallikrein-like substances. | No PSA-like immunoreactivity was seen in large-sized duct epithelial cells and acinar cells. | Localization of prostate-specific antigen-like immunoreactivity in human salivary gland and salivary gland tumors. | Tazawa K, Kurihara Y, Kamoshida S, Tsukada K, Tsutsumi Y -Pathol Int 1999 Jun 18;49(6):500-505 | Jun-99 | ||||
| Acinic cell carcinomas arise from pluripotential stem cells found at the acinar-intercalated duct junctions and/or in the intercalated ducts proper of mature salivary glands. Multiple growth patterns are possible, with the most common growth patterns being solid-lobular and acinar-microcystic. In contrast to most other salivary gland tumors, acinic cell carcinomas normally produce large lobules or nests with little intervening stroma. Cytoplasmic basophilic granules and vacuolated cells are characteristic of these tumors; immunohistochemical staining and electron microscopy are normally not necessary for diagnosis. | Pathologic Diagnosis: Acinic cell carcinoma of the deep lobe of the parotid gland involving the right parapharyngeal space. References: Batskis JG, Luna MAA, El-Naggar AK. Histopathologic grading of salivary gland neoplasms, II: acinic cell carcinomas. Ann Otol Rhinol Laryngol. 1990;99:929-933. | Archives of Otolaryngology Head and Neck Surgery:
Vol. 125 No. 6, June 1999 Also online at: http://archotol.ama-assn.org/issues/v125n6/ffull/orp0699-1b.html |
Jun-99 | |||||
| There is no conclusive evidence to
correlate the histopathologic characteristics of acinic cell carcinomas and
overall prognosis. However, larger, poorly circumscribed tumors with both
solid and cystic areas, high degrees of mitotic activity, and atypia with
lymph node involvement are associated with a worse prognosis. Also, Lewis et
al found that the presence of
desmoplastic stromal reaction is associated with a poor outcome. Other
studies have shown a worse prognosis for tumors with a papillary-cystic
pattern. Perzin and LiVolsi found an association between tumor involvement of
the deep lobe of the parotid gland and local recurrence and metastasis. |
Pathologic Diagnosis: Acinic cell carcinoma of the
deep lobe of the parotid gland involving the right parapharyngeal space.
References: Yokoyama M, Nomura Y, Semba T. Acinic cell carcinoma of the
parapharyngeal space: case report. Head Neck. 1993;15:67-69. Perzin KH, LiVolsi VA. Acinic cell carcinomas arising in salivary glands: a clinicopathologic study. Cancer. 1979;44:1434-1457. Lewis JE, Olsen KD, Weiland LH. Acinic cell carcinoma: clinicopathic review. Cancer. 1991;67:172-179. |
Archives of Otolaryngology Head and Neck Surgery:
Vol. 125 No. 6, June 1999 Also online at: http://archotol.ama-assn.org/issues/v125n6/ffull/orp0699-1b.html |
Jun-99 | |||||
| Telomerase activity can be detected in most human cancers. This is consistent with the telomere hypothesis, which predicts upregulation of telomerase expression after a number of mitotic divisions to prevent the progressive and catastrophic loss of telomeres. In this report, telomerase activity was analyzed in 31 human oral malignant tumors, 11 leukoplakias, three pleomorphic adenomas, and 40 samples taken from normal tissues of the oral cavity, using a polymerase chain reaction (PCR)-based telomeric repeat amplification protocol assay. Telomerase activity was detected in most oral cancers [squamous cell carcinoma (SCC), non-Hodgkin's lymphoma, adenoid cystic carcinomas, mucoepidermoid carcinoma, osteosarcoma, acinic cell carcinoma, rhabdomyosarcoma]. None of the normal tissues or pleomorphic adenomas displayed telomerase activity. These results suggest that detection of telomerase activity in oral tissues could be used to differentiate malignant from benign or normal tissues. | squamous cell carcinoma, non-Hodgkin's lymphoma, adenoid cystic carcinomas, mucoepidermoid carcinoma, osteosarcoma, rhabdomyosarcoma | Telomerase activity in oral cancer. | Oral Oncol 1999 May;35(3):283-9 - Miyoshi Y, Tsukinoki K, Imaizumi T, Yamada Y, Ishizaki T, Watanabe Y, Sasakura Y, Lin Y, Hosaka M, Kubota Y | May-99 | ||||
| A dedifferentiated acinic cell carcinoma
(AciCC) of the right parotid gland with lymph node metastases occurred in a
36-year-old woman. The tumour was associated with a bilateral
well-differentiated AciCC. The two components of this tumour had different (high
and low) proliferative activity measured by Mib-1 and different (aneuploid
and diploid) DNA content. Despite the presence of a
high-grade component, TP53 mutations, microsatellite instability (MSI) and/or
loss of heterozygosity (LOH) at the p53 locus were not detected. Although the follow-up of the patient is very short, the
aggressiveness of the tumour is shown by a recurrence in the right parotid
within 4 months and by the rapid development of regional metastases. |
Unilateral aneuploid dedifferentiated acinic cell
carcinoma associated with bilateral-low grade diploid acinic cell carcinoma of the parotid gland. |
Di Palma S, Corletto V, Lavarino C, Birindelli S, Pilotti S - Division of Pathology and Cytopathology, Istituto Nazionale per lo Studio e la Cura dei Tumori, Milano, Italy. dipalma@istitutotumori.mi.i - Virchows Arch 1999 Apr;434(4):361-5 | Apr-99 | |||||
| This study is to investigate some
characteristics of lung tumor associated with exposure to coal combustion
emissions. In Xuan Wei (XW) county, China, lung cancer mortality in females
(99% nonsmokers) is the highest in China and has been associated with exposure
to indoor smoky-coal emissions which contain high concentrations of
carcinogenic PAHs. Expression of the proliferation nuclear
antigen, Ki-67 and accumulation of p53 protein were investigated by
immunohistochemistry in 33 XW nonsmoking female patients with non-small cell
lung cancer. The mean Ki-67 index was 24.9% in acinar adenocarcinoma, 6.87% in papillary adenocarcinoma, 38.6% in solid
adenocarcinoma, 24.1% in adenosquamous carcinoma, 3.23% in squamous carcinoma
and 21.88% in bronchioloalveolar carcinoma. The
above subtypes showed positive in p53 staining in 4/6, 1/2, 2/5, 1/2, 2/2, and 13/16, respectively. Among the subtypes
of adenocarcinomas, bronchioloalveolar carcinoma was most frequently found,
as high as 55% (16/29), which is much higher than published reports. (more below) |
Acinar adenocarcinoma of the LUNG. (also mentioned by other physician sources)... Adenosquamous carcinoma had almost the same Ki-67 index. | Cell proliferation related antigen Ki-67 and p53 protein accumulation in non small-cell lung cancer from nonsmoking females exposed to indoor coal emissions. | [PROC. AMER. ASSOC. CANCER RES. 40, March 1999] Copyright © 1999 by the American Association for Cancer Research - Tian, D., Feng, Z., Li, X. Mumford, J. L. - University of North Carolina, Chapel Hill, NC 27599, Institute of Environmental Health and Engineering, Beijing, China. U.S. Environmental Protection Agency, Research Triangle Park, NC 27711. | Mar-99 | ||||
| (no abstract available) | Acinar adenocarcinoma of the LUNG. (also mentioned by other physician sources) | Cell proliferation related antigen Ki-67 and p53 protein accumulation in non small-cell lung cancer from nonsmoking females exposed to indoor coal emissions. | [PROC. AMER. ASSOC. CANCER RES. 40, March 1999] Copyright © 1999 by the American Association for Cancer Research - Tian D., Feng Z., Li X. Mumford J. L. - University of North Carolina, Chapel Hill, NC 27599, Institute of Environmental Health and Engineering, Beijing, China. U.S. Environmental Protection Agency, Research Triangle Park, NC 27711. | Mar-99 | ||||
| The purpose of this study was to determine the estrogen and progesterone receptor status of a selection of salivary tumours. Using immunohistochemistry, we detected nine oestrogen receptor and six progesterone receptor positive tumours from a sample of 36. One acinic cell carcinoma and two mucoepidermoid carcinomas demonstrated positivity for both receptors. We suggest that there may be role for oestrogen manipulation in the management of some salivary tumours. | mucoepidermoid & maybe more? (need full text) | Immunohistochemical detection of oestrogen and progesterone receptors in salivary tumours. | Clin Otolaryngol 1999 Feb;24(1):52-4 - Jeannon JP, Soames JV, Bell H, Wilson JA | Feb-99 | ||||
| The tumor was considered to be the recurrence 22 years after initial surgery... Although this tumor is of low grade malignancy, complete resection with adequate surgical margins is advisable due to high incidence of this tumor to recur after long periods of time. | Acinic Cell carcinoma of maxillary sinus | Fujii M, Kumanomidou H, Ohno Y, Kanzaki J - Auris Nasus Larynx, 25(4): 451-7 | Dec-98 | |||||
| The purpose of this study was to determine the oestrogen and progesterone receptor status of a selection of salivary tumours. Using immunohistochemistry, we detected nine oestrogen receptor and six progesterone receptor positive tumours from a sample of 36. One acinic cell carcinoma and two mucoepidermoid carcinomas demonstrated positivity for both receptors. We suggest that there may be role for oestrogen manipulation in the management of some salivary tumours. | Mucoepidermoid carcinomas also demonstrated positive estrogen and progesterone receptors. | Immunohistochemical detection of oestrogen and
progesterone receptors in salivary tumours. |
Jeannon JP, Soames JV, Bell H, Wilson JA - Clin Otolaryngol 1999 Feb;24(1):52-4 |
Nov-98 | ||||
| PURPOSE: To investigate the effects of
increasing concentrations of cholecystokinin octapeptide (CCK-8) on a pancreatic acinar adenocarcinoma. METHODS: Growth of the tumour was estimated in vivo on rats bearing a subcutaneous pancreatic carcinoma, and in vitro on primary cultured tumour cells. CCK receptors were characterized by binding assays. RESULTS: CCK-8, administered for 12 successive days, exerted a biphasic action on tumour growth: a dose-dependent stimulation with low doses (0.1 and 0.5 microg/kg) and inhibition with high doses (2 and 4 microg/ kg) as shown by respective increases and decreases in tumor volume, protein, RNA and amylase contents. In cell cultures, [3H]thymidine incorporation was dose-dependently increased with 10-(10) to 10(-8) M CCK-8 and inhibited with 10(-7) M. Both effects were completely suppressed by the CCK-receptor antagonists CR 1409 and L 364,718 (10(-4) M). Binding studies showed the overexpression of two classes of CCK-A receptors of low and high affinity when compared to the normal pancreas which was less sensitive to CCK-8. (more below) |
Effects of cholecystokinin octapeptide on a pancreatic acinar carcinoma in the rat. | Hajri A, Damge C: Pharm Res 1998 Nov;15(11):1767-74 | Nov-98 | |||||
| (cont'd): CONCLUSIONS: CCK-8 exerts a biphasic growth response on the
acinar pancreatic carcinoma, mediated by two classes of CCK-A receptors
overexpressed in the tumour. |
Effects of cholecystokinin octapeptide on a
pancreatic acinar carcinoma in the rat. |
Hajri A, Damge C: Pharm Res 1998 Nov;15(11):1767-74 | Nov-98 | possibly IMPORTANT? | ||||
| Human acinic cell adenocarcinoma cell
(HACC) line was established from the pleural effusion that contain metastatic
tumor cells of acinic cell adeno-carcinoma of papillary and microcystic type
originating from the parotidgland. The HACC cells grew in
an adherent monolayer with a doubling time of 66 h. Implanted tumor of
SCIDmice revealed similar histological findings to that of the primary tumor.
The HACC cells produced mucin and expressed
epithelial markers as well as alpha1-antitrypsin and lysozyme, whereas
salivary peptide P-C was expressed in cultured HACC cells but not in the
primary and implanted HACC cell tumors. S-100 protein was also expressed in
both the primary tumor and HACC cell line. Neither
amplification of common oncogenes nor expression of p53 was observed. The receptor for epidermal growth factor (EGF) was expressed,
indicating EGF and transforming growth factor-alpha (TGF-alpha) enhanced the
growth of the HACC line. Unexpectedly, tumor necrosis factor-a (TNF-alpha)
also enhanced the growth of the HACC line significantly. (more below) |
Characterization of a newly established human acinic
cell adenocarcinoma cell line (HACC) originating from the salivary gland: morphological features and role of various growth factors on the growth of the HACC cell line. |
Fukuda T; Tominaga K; Abe M; Kusakabe T; Yamaki T; Hiraki H; Itoh S; Suzuki T - Pathol Int, 48(10): 791-9 | Oct-98 | |||||
| (cont'd) However, there was no evidence of autocrine growth using these
growth factors. In contrast, TGF-beta1 inhibited the growth of the HACC cell
line through apoptosis. The HACC cell line has features similar to both
acinar and intercalated ductal cells of the salivary gland. Epidermal growth
factor, TGF-alpha and TNF-alpha are potential growth factors for the HACC
cell line. The HACC cell line may be a good model for studying the biological
behavior of salivary gland neoplasms. |
a biphasic growth response on the acinar pancreatic carcinoma, mediated by two classes of CCK-A receptors | Characterization of a newly established human acinic
cell adenocarcinoma cell line (HACC) originating from the salivary gland: morphological features and role of various growth factors on the growth of the HACC cell line. |
Fukuda T; Tominaga K; Abe M; Kusakabe T; Yamaki T; Hiraki H; Itoh S; Suzuki T - Pathol Int, 48(10): 791-9 | Oct-98 | ||||
| ACINIC CELL CARCINOMA - STATISTICS: The National Cancer Institute Data Base (NCDB) identified 1353 cases of acinic cell carcinoma of the head and neck for years 1985 to 1995. (Cells below provide various statistics from this report.) | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACINIC CELL CARCINOMA - OCCURRENCE STATISTICS: The National Cancer Institute Data Base (NCDB) identified 1353 cases of acinic cell carcinoma of the head and neck for years 1985 to 1995. Salivary gland cancers comprise between 0.3% and 0.9% of all cancers in the United States. Acinic cell carcinomas account for approximately 5% to 11% of these salivary gland cancers. The Armed Forces Institute of Pathology (AFIP) Salivary Gland Registry (having the largest series of salivary gland tumors to date) identified acinic cell carcinoma as the third most common epithelial malignancy of the salivary glands (after mucoepidrmoid and adenocarcinoma NOS (not otherwise specified). In AFIP series, acinic cell represented 17% of primary malignant salivary gland neoplasms and 6% of all (including benign) salivary gland neoplasms. Note: Data from the distant past may not be accurate, due to the past practice of classifying poorly differentiated acinic cell carcinomas as "unspecified adenocarcinomas", or "undifferentiated carcinomas". | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACINIC CELL CARCINOMA HISTOLOGY: According to Batsakis et al, acinic cell carcinoma derives from progenitor reserve cells of the terminal tubules and intercalated ducts of salivary tissue. Batsakis et al demonstrated that varieties of acinic cell carcinoma occur within a histomorphologic spectrum defined by the lowest and highest grades. Low grade acinic cell carcinomas are broadly interpreted as those most closely resembling the architecture of a normal salivary lobule. High grade acinic cell carcinomas are poorly differentiated and resemble the early phases of embryonic development of acini. Although a single pattern usually dominates, mixtures of grades may be apparentwithin a single tumor. Solid, solid-lobular, papillary-cystic, follicular, microcystic, tubuloductal, and solid undifferentiated patterns have also been reported. Controversy persists regarding the prognostic value of assigning grade by histological analysis of acinic cell carcinoma. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | Some quoted from Batsakis JG (et al) - The pathology of head and neck tumors; salivary glands, Part 2: Head and Neck Surgery 1978;1: 167-171 | ||||
| ACC HISTOLOGY AND PRIMARY SITE: Although serous-type cells do not necessarily predominate in all cases, acinic cell carcinomas are commonly characterized by cytologic differentiation toward the serous acinar cells. The parotid gland, which is dominated by serous cells, and is the largest of the major salivary glands, is also the most common site of acinic cell carcinoma. Acinic cell carcinomas are distinctly less common in the mixed serous and mucous submandibular and sublingual glands and in the predominantly mucous minor salivary glands. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC Patient Profiles: Most reports have identified that acinic cell carcinoma presents at an earlier age than other salivary gland cancers, and affects women more commonly than men. Income grouping reflected a disproportionately large number of high-income cases (12.3%) relative to low-income cases (8.2%). Cases were predominantly white non-Hispanic (86.0%). ACC was more common in women (58.8%) than in men (42.2%). The median age at diagnosis was approximately 52 years, with 16.2% of cases among patients younger than 30 years. Women comprised a significantly larger proportion of this younger group (64.4%), than in older group (57.7%). | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC Tumor Statistics - SITE: The tumors arose in the parotid gland in 1167 cases (86.3%), and the submandibular gland in 37 cases (2.7%). 26 cases (1.9%) were recorded as arising in the major salivary glands, but without a specific gland identified. Only one case was identified as arising in the sublingual gland. The remaining 122 cases (9.0%) arose in sites other than the major salivary glands, which presumably reflect involvement of the minor salivary glands. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC Extent of Disease: Among cases submitted by hospitals using the 3rd and 4th editions of the AJCC staging manual *: The median tumor size at the time of diagnosis was 2.0 cm. Approx. two thirds (67.4%) were stage I. The remainder were distributed between stage II (14.4%), stage III (11.0%), and stage IV (7.1%). At the time of initial presentation, disease was confined locally for 88% of the patients classified. Regional metastasis was identified in 9.9%, and distant metastasis in 2.1% of patients. Regional metastases, distant metastases and large tumor size were all more common among patients 30 years of age and older. Incidence of regional node involvement and cervical metastases are discussed, but not with an overall accurate rate. A previous study of 42 patients, which ended in 1978, had a median follow-up of 11 years. That review identified an overall regional metastatic rate of 11%, occuring either at presentation or as a recurrence. Distant metastases were identified in 13% of patients. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| * Over the time period covered, classification frequently employed editions of the AJCC staging manual that were outdated, which confounds comparisons of populations across different periods. Advances in imaging technology may also affect these statistics. Additionally, some systems employ three separate grade categories, whereas others employ four. There is also a recognized subjective nature of staging. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC Grade of Disease: * Among those cases with recorded grade, grade I (57.8%) was most common, and grade 4 (4.6%) was least. Higher grade cancers were significantly associated with age 30 years or greater (p=.0024), advanced stage (p=.0002), and the presence of metastatic disease at presentation (p<.0001). This report also identifies a strong correlation between grade and aggressive behavior. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC High Grade Variety: An aggressive subset of acinic cell carcinoma which is characterized by high grade and advanced stage rarely occurs in patients younger than 30 years old. The association between advanced grade and greater extent of disease at presentation clearly identifies this subset of acinic cell carcinomas with aggressive behavior and histologically determined differences. It is noteworthy that, although this higher grade did not appear to compromise the surgeons' capacity to obtain negative surgical margins, treatment with postoperative radiotherapy was used nearly three times more commonly for high grade than low grade varieties. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| Acc High Grade Variety: The association between advanced grade and greater extent of disease at presentation clearly identifies a subset of acinic cell carcinomas with aggressive behavior and histologically determined differences. It is noteworthy that, although this higher grade did not appear to compromise the surgeons' capacity to obtain negative surgical margins, treatment with postoperative radiotherapy was used nearly three times more commonly for high grade than for low-grade acinic cell carcinomas. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC Grade: The association between tumor grade and biologic behaviorhas been well documented for many neoplasms but has remained controversial for acinic cell carcinoma. The assertion is made in the 1972 WHO mongraph that it is not possible to identify the small subset of acinic cell neoplasms that are likely to metastasize based on histologic features alone. Wide acceptance of this concept has resulted in the practice of lumping all acinic cell carcinomas into the same favorable prognostic group as low-grade mucoepidermoid carcinoma and low-grade adenocarcinoma without further segregating acinic cell carcinoma cases according to grade. This broad grouping has not notably affected most analyses, possibly because of the minor contribution made by the addition of the small number of cases of high-grade acinic cell carcinoma. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACINIC CELL CARCINOMA TREATMENT STATISTICS: Single modality treatment with surgery was employed in 64% of cases. Surgery with radiotherapy was employed in 30.1% of cases. Chemotherapy was used as adjuvant therapy along with surgery or radiotherapy in 1.0% of cases. Among patients receiving treatment of known type, surgery (alone or with adjuvant therapy) was employed in 1285 of 1345 cases (95%). Advanced stage and grade were highly associated with the more common use of surgery and radiotherapy. Lower stage and grade were most commonly treated with surgery alone. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACINIC CELL CARCINOMA TREATMENT PROTOCOLS: General guidelines for management of salivary gland cancer support surgical excision as the primary treatment. Supplemental irradiation has been reserved for those case with indicators of poor prognosis. Although better outcome was not statistically demonstrated for combined therapy, surgery with irradiation is the most common management in the United States for cases with regional metastases, high grade and microscopic positive margins. Although it is widely accepted that surgical excision is the preferred treatment for acinic cell carcinoma, debate continues regarding the extent of resection needed, as well as the role for neck dissection and adjuvant radiotherapy. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC Treatment Protocols, contd - Neck Dissection: The practice of elective neck dissection in the treatment of high-grade salivary gland cancers has been widely advocated in the past. Others have suggested that an elective staging supraomohyoid selective neck dissection was useful not only for all high-grade salivary gland cancers, but also for those with primary tumors larger than 4 cm, regardless of grade. The weight of more recent publications appears to support a less aggressive surgical approach to the uninvolved neck. These reports propose that the few occult metastases that exist will be adequately addressed by postoperative radiotherapy. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC Treatment Protocols, contd - Radiation: Some have recommended postoperative radiation for ALL cases of salivary gland cancer except for those tumors staged as T1N0 or T2N0 with low grade histology, which were excised with negative margins. Factors that have been reported as useful in supporting postoperative radiotherapy have been listed as: skin invasion, high grade, facial nerve paralysis, advanced stage (III or IV), and the presence of neck metastases. Salivary gland cancers in general and acinic cell in particular have traditionally been considered radioresistant. Over the past two decades, reports of improved locoregional control through use of postoperative radiotherapy have provoked a wider acceptance of the value of administering radiotherapy after surgery for cases with poor prognosis. Authors Note: This review does not mention Fast Neutron Radiation separately from all other forms of radiotherapy. (more below) | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC Treatment Protocols, contd - Radiation: It is noteworthy that NCDB reveals 5-year disease-specific survival for patients treated with surgery only was 96.8% compared with 88.2% for those receiving combined surgery and radiotherapy. HOWEVER, it is difficult to determine the true efficacy of radiotherapy based on this sampling becasue of the clear selection bias influencing use of postoperative radiotherapy. Despite the lack of data supporting its use for acinic cell carcinoma, in the United States, cases characterized by high grade, positive margins or nodal metastases are most commonly treated with combined surgey and postoperative radiotherapy. ACCIC Authors Note: This review does not mention Fast Neutron Radiation separately from all other radiotherapy. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC Treatment Protocols, contd - Radiation: Salivary gland cancers in general and acinic cell carcinoma in particular have traditionally been considered radioresistant. Over the past two decades, reports of improved locoregional control through the use of postoperative radiotherapy have provoked a wider acceptance of the value of administering radiotherapy after surgery for cases with poor prognosis. It is noteworthy that the NCDB reveals 5-year disease-specific survival for patients treated with surgery only was 96.8%, compared with 88.2% for those receiving combined surgery and radiotherapy. It is difficult to determine the efficacy of radiotherapy based on this sampling because of the clear selection bias influencing postoperative radiotherapy. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC Treatment Protocols, contd - Radiation: In the effort to address this bias, comparative analyses of subsets of patients with poor prognosis were performed to analyze for the impact of postoperative radiotherapy. Unfortunately, the numbers of evaluable cases was too small to offer definitive statements regarding the value of postoperative radiotherapy for cancers characterized by high grade, positive margins, or regional spread of disease at the time of presentation. The relative rarity of acinic cell carcinoma has prevented the execution of a study capable of statistically demonstrating improved survival for patients treated with postoperative radiotherapy. Despite the lack of data supporting its use for acinic cell carcinoma, in the United States, cases characterized by high grade, positive margins, or nodal metastases are most commonly treated with combined surgery and postoperative radiotherapy. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| Treatment Protocols, contd - Surgery: It is clear from reports of salivary gland cancer treated in the remote past that recurrence and survival is compromised when treatment is limited to excision by enucleation. Spiro et al indentified that among 67 cases of acinic cell carcinoma,the best results were observed in patients receving conservative operations. These investigators concluded that outcome was more dependent on the extent of of the tumor than the type of operation performed. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC Recurrence Statistics: Because of limited data, and inaccuracies in record-keeping, this report did not provide overall statistics on recurrence. Some data is provided in report, but it cannot be used to determine an accurate overall percentage. (See "ACC Outcome" section later.) | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC Survival Statistics: Five year survival was 83.3% (observed) and 91.4% (disease specific) in this review. Worse survival was associated with high grade (p<.0001), age greater or equal to 30 years (p+.0055), the presence of metastatic disease (p,.0001) (regional or distant at presentation), and site of cancer in the submandibular gland. In this review, overall survival has been crudely estimated to be about 84%. But survival analyses should be interpreted with the understanding that 10 to 20 years follow-up is needed to identify the full impact of acinic cell carcinoma on extended survival. The indolent behavior of this cancer is underscored by reports that recurrent tumor has been identified up to 30 years after initial treatment. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC Outcome: Acinic cell carcinoma has been identified as the least aggressive of the salivary gland cancers. From a review of multiple reports, the most recent AFIP fascicle addressing salivary gland cancer identifies the overall recurrence rate for acinic cell carcinoma to be 35%. These investigators identified that death from persistent or recurrent disease occurred in 16%. Other reports have identified similar statistics, with the observation that prolonged survival despite persistence of disease is possible. The prolonged survival that may occur despite persistent disease appears to support the practice of managing incurable disease with aggressive treatment as needed for palliation. Disease characteristics reported to indicate a poor prognosis include location of tumor in the deep lobe of the parotid gland and presence of infiltrative margins, presumably because these factors influence completeness of excision. The current results demonstrate that incomplete excision is associated with a lower chance of survival. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| ACC Overview Conclusion: Survival was best for cases characterized by younger age and lower stage. Although better outcome was not statistically demonstrated for cases treated with combined therapy, surgery with radiotherapy is the most common management for cases with regional metastases, grades 3 or 4, and microscopic positive margins. The clear association identified between higher grade and aggressive behavior supports the wider application of a standardized approach to grading acinic cell carcinoma. | National Cancer Data Base Report on Cancer of the Head and Neck: Acinic Cell Carcinoma (1985-1995) | Henry T. Hoffman M.D., Lucy Hynds Karnell PhD, Robert A. Robinson MD, John A. Pinkston M.D., Herman R. Menck, MBA | 8/27/98 (submitted) July 1999 published | |||||
| The paradigm that human malignancies are
monoclonal has been questioned during recent years by the finding of
unrelated, cytogenetically aberrant clones in short-term cultures from
certain tumour types, notably carcinomas of the breast, skin and upper aerodigestive
tract. In order to analyse whether cytogenetically unrelated clones are also
unrelated at the molecular level, we analysed the X-chromosome inactivation
status in cell cultures from a cytogenetically highly polyclonal acinic cell
carcinoma of the parotid gland. By using cell cultures dominated by a single
abnormal clone, obtained through in vitro culturing for 3-5 passages, we
showed that the different clones must indeed have originated from different
cells. |
Cytogenetic and molecular genetic demonstration of polyclonality in an acinic cell carcinoma. |
Author: Jin C; Jin Y; H¨oglund M; Wennerberg J;
Akervall J; Will´en R; Dictor M; Mandahl N; Mitelman F; Mertens F Address: Department of Clinical Genetics, University Hospital, Lund, Sweden. Source: Br J Cancer, 78(3):292-5 1998 Aug |
Aug-98 | |||||
| The monoclonal antibody 44-3A6 detects a
cell-surface protein that has been shown to be a useful marker in
distinguishing adenocarcinomas from other histologic tumor types in a variety
of tissues. The objective of this study was to determine whether 44-3A6 could
be used as a tool in the classification of salivary gland neoplasms. These
complex tumors share overlapping pathologic features but distinct clinical
outcomes. This study used 44-3A6 to immunohistochemically describe the
pattern and frequency of this antigen in salivary gland neoplasms.
Formalin-fixed, paraffin-embedded tissue sections of 22 benign and 26
malignant salivary tumors were evaluated. The patient population consisted of
25 (52.1%) women and 23 (47.9%) men selected from archival pathology files to
reflect a range of salivary gland diseases. Normal surrounding salivary glands were found to have intense focal staining almost exclusively localized to ductal luminal cells. There was little staining of either myoepithelial or acinar cells. (more below) |
Expression of the adenocarcinoma-related antigen recognized by monoclonal antibody 44-3A6 in salivary gland neoplasias. | Bentz BG; Haines GK 3rd; vonSchlegell AS; Elseth KM; Hanson DG; Radosevich JA - Otolaryngol Head Neck Surg, 118(5):603-9 May, 1998 | May-98 | |||||
| (cont'd.) A wide spectrum of expression was found between and within tumor
types, but a trend toward more expression of this antigen with decreasing differentiation was seen. A significant increase in staining was also seen in those tumors with ductal differentiation (n = 41) as opposed to those with predominantly acinar (i.e., acinic cell carcinoma) or myoepithelial (i.e., myoepithelioma; n = 8) differentiation (2.6 vs. 1.3, p< 0.05). No correlation was found between staining intensity and facial paralysis, pain, skin involvement, TNM stage, residual disease, or disease-free or total survival. Therefore this antigen appears to designate a duct luminal phenotype in normal and neoplastic salivary tissues. |
myoepithelial cells | Expression of the adenocarcinoma-related antigen recognized by monoclonal antibody 44-3A6 in salivary gland neoplasias. | Bentz BG; Haines GK 3rd; vonSchlegell AS; Elseth KM; Hanson DG; Radosevich JA - Otolaryngol Head Neck Surg, 118(5):603-9 | May-98 | ||||
| Abstract: We investigated, for the first time, the genetic alterations at certain chromosomal loci in 25 primary parotid acinic cell carcinomas to define the most frequently altered chromosomal regions and their association with pathologic features and DNA content analysis. Our results showed that 21 (84.0%) of the tumors had alteration in at least one of the loci tested. In general, chromosomal regions at chromosomes 4p, 5q, 6p, and 17p were more frequently altered than those on chromosomes 1p and 1q, 4q, 5p, and 6q. Certain markers at 4p15-16, 6p25-qter, and 17p11 regions showed the highest incidence of LOH, suggesting the presence of tumor suppressor genes associated with the oncogenesis of these tumors. LOH was significantly associated only with tumor grade. No apparent correlation between LOH and other clinicopathologic and DNA content characteristics was identified. Our study broadly defined the chromosomal arms and loci that may be targeted for further localization of the minimally deleted regions involved in the tumorigenesis of these tumors. | Genetic alterations in acinic cell carcinoma of the parotid gland determined by microsatellite analysis. | el-Naggar AK; Abdul-Karim FW; Hurr K; Callender D; Luna MA; Batsakis JG - Department of Pathology, University of Texas, M. D. Anderson Cancer Center, Houston 77030, USA. - Cancer Genet Cytogenet, 102(1): 19-24 | Apr-98 | This article focuses on chromosomal abnormalities. | ||||
| Gabapentin (Neurontin®)(1-(aminomethyl) cyclohexaneacetic acid)(GPN), a structurally similar compound to [gamma]-aminobutyric acid was developed as an anticonvulsant. In genotoxicity assays, GPN has been shown to be nongenotoxic in numerous assays. However, in the 104-week rat bioassay a significant number of male rats developed pancreatic acinar cell tumors. At doses of 1000 and 2000 mg/kg, 20 to 50-fold multiples of the human daily dose, 26% and 48% of the male rats developed acinar cell tumors as compared to 14% in controls. The lack of genotoxicity activity suggests that an epigenetic mechanism may be involved in the carcinogenesis. Cell proliferation was assessed using 3H-thymidine incorporation in the azaserine-induced tumor cell line AR42J and in primary cultures of male rat acinar cells. In both cell types, GPN >= 100 µg/ml were cytotoxic. While GPN had no effect on the proliferating AR42J cell line, at >=100 ng/ml increased 3H-thymidine incorporation in the primary cell cultures. (more below) | The effect of Gabapentin on the MAP kinase signal
transduction pathway in pancreatic cells. |
[PROC. AMER. ASSOC. CANCER RES. 39, March 1998]
Copyright © 1998 by the American Association for Cancer Research - S.J. Bulera, T. Festerling, J.L.V. Samoy, and J.C. Theiss. Parke-Davis Pharmaceutical Research Division, Warner-Lambert Company, Ann Arbor, MI 48105, USA. |
Mar-98 | This is from studies for the medication Neurontin (Gabapentin). | ||||
| (cont'd. from above) The induction of the MAP Kinase signal transduction pathway by cholecystokinin (CCK) is an important mediator of acinar cell proliferation. The ability of CCK and GPN to activate MAP Kinase in vitro was compared using 32P-ATP and Myelin Basic Protein as substrates. SDS-PAGE analysis revealed that GPN activated MAP Kinase in a time dependent manner although to a lesser extent than CCK. MAP Kinase activity induced by GPN may be important in pancreatic acinar cell proliferation and tumor formation. | The effect of Gabapentin on the MAP kinase signal
transduction pathway in pancreatic cells. |
[PROC. AMER. ASSOC. CANCER RES. 39, March 1998]
Copyright © 1998 by the American Association for Cancer Research - S.J. Bulera, T. Festerling, J.L.V. Samoy, and J.C. Theiss. Parke-Davis Pharmaceutical Research Division, Warner-Lambert Company, Ann Arbor, MI 48105, USA. |
Mar-98 | This is from studies for the medication Neurontin (Gabapentin). | ||||
| Reduction in the incidence of common cancers often requires successful preventive interventions. Epidemiological studies have consistently reported a risk reduction for several cancers with various protective micronutrients. Vitamins and minerals are possible cancer-protective agents through their antioxidant or pro-oxidant mechanisms. S-adenosylmethionine (SAM), a major methyl donor for a number of macromolecules in cells, is often detected at low levels in cancer cells or in cells induced by certain chemicals. SAM has been reported to have beneficial effects in the treatment of several chronic diseases and protect against a number of toxic agents. Previous studies in our laboratory demonstrated that primary and secondary cultures of pancreatic acinar cells obtained from ddI-treated rats have a significantly lower level of SAM when compared to controls. These cells also demonstrated transformed characteristics such as enhanced growth, and RT-PCR analysis revealed increased expression of the K-ras gene. (more to right) | (cont'd. from left) This study, using HPLC analysis, showed a SAM level of 2.21±0.05 ng/million cells in ddI-treated cells. Folic acid (100µM) increased SAM to 3.14±0.10, low concentrations of ZnCl (.5µM) increased SAM to 3.48±0.03 and vitamin C (100 µg/ml) increased SAM to 4.82±1.30. This study demonstrates that certain micronutrients such as folic acid, vitamin C and low concentrations of zinc enhance the methionine pathway in transformed pancreatic cells. Increased SAM levels may play a role in the anticarcinogenic effects shown by these micronutrients in a number of epidemiological studies. | Micronutrient regulation of S-adenosylmethionine levels in transformed pancreatic cells in vitro. | [PROC. AMER. ASSOC. CANCER RES. 39, March 1998] - B.D. Lyn-Cook, Wise C., Patterson T., Blann E., Green B., Poirier L.A. and W. Slikker. Divisions of Molecular Epidemiology and Neurotoxicology, FDA/NCTR, Jefferson, Arkansas 72079-9502. | Mar-98 | ||||
| ACC is a rare tumor of salivary glands characterized by an indolent clinical course with the potential for both local recurrence and metastatic spread when tracked for decades. Published mortality rates vary from 6 to 50%. Histopathologic features do not reliably predict biologic behavior. | Acinic cell carcinoma presenting as an upper lip mass. | Author: Kenner JR; Benson PM; Sinha C; Willard CC; Harrington AC; Sau P Source: Dermatol Surg, 24(2):283-5 | Feb-98 | P. Nagesh Rao, Ph.D. | ||||
| No molecular evidence of p53 mutation was
found in any of the tumor DNAs and immunohistochemical data were regarded
as negative. This study provides evidence that acinar cell carcinogenesis in both humans and transgenic mice is independent of p53 mutation. |
Evaluation of p53 mutation in pancreatic acinar cell
carcinomas of humans and transgenic mice. |
Terhune PG, Memoli VA, Longnecker DS - Pancreas 1998 Jan;16(1):6-12 | Jan-98 | |||||
| DEFINITION * A neoplastic growth of epithelial cells showing serous acinar differentiation CLINICAL FEATURES: * Occurs most commonly in parotid gland * Occurs unilaterally. May occur bilaterally. * Occurs more frequently in women than men (3:2) * Occurs in young and old individuals * Slowly growing, mobile or fixed mass of various durations * Asympotatic * Pain or tenderness * Facial muscle weakness GROSS FEATURES: * Single, well circumscribed to multinodular and ill-defined * Firm to cystic * 0.5-13 cm * Lobular, red to tan cut surface |
GO TO THIS SITE AND COMPARE FEATURES WITH OTHER SALIVARY GLAND CANCERS. | SALIVARY GLAND TUMORS; CLINICAL AND PATHOLOGICAL FEATURES | S Tabibzadeh BioScience.org - FRONTIERS IN BIOSCIENCE; LECTURE SERIES [Vol 3, z1-129, January 1, 1998] Dept of Pathology, Moffitt Cancer Center and University of South Florida, 12902 Magnolia Drive, Tampa, FL 33612 http://www.bioscience.org/lecture/tabibza/list.htm |
Jan. 1 1998 | Informative site on salivary gland cancers of all types. | |||
| MICROSCOPIC FEATURES * Patterns * Sheets * Cysts, some with papillary growth * Microcystic * Acini * Ducts * Glands * Follicles (similar to thyroid) * Epithelium * Large polygonal * Lightly basophilic cytoplasm * Uniform to variable eccentic nuclei MICROSCOPIC FEATURES * Acinar epithelium * Large polygonal * Lightly basophilic cytoplasm (blue dot tumors) * Protuberance of luminal membrane producing a tombstone appearance * Uniform to variable eccentic nuclei * Cytoplasmic granules (PAS positive-diastase resistant; mucicarcmine positive) * Hemosiderin * Duct epithelium * Eosinophilic cytoplasm * Variable cell size * Central lumen of various size MICROSCOPIC FEATURES * Vacuolated cells * Eosinophilic to amphophilic cytoplasm * Clear vacuoles * PAS and mucicarmine negative * Clear cells * Lack of glycogen * Glandular cells * Round to polgonal * Eosinophilic to amphophilic cytoplasm * Lack of cytoplasmic granules or PAS positivity * Nuclear pleomorphism |
GO TO THIS SITE AND COMPARE FEATURES WITH OTHER SALIVARY GLAND CANCERS. | SALIVARY GLAND TUMORS; CLINICAL AND PATHOLOGICAL FEATURES | S Tabibzadeh BioScience.org - FRONTIERS IN BIOSCIENCE; LECTURE SERIES [Vol 3, z1-129, January 1, 1998] Dept of Pathology, Moffitt Cancer Center and University of South Florida, 12902 Magnolia Drive, Tampa, FL 33612 http://www.bioscience.org/lecture/tabibza/list.htm |
Jan. 1 1998 | Informative site on salivary gland cancers of all types. | |||
| MICROSCOPIC FEATURES * Vacuolated cells * Eosinophilic to amphophilic cytoplasm * Clear vacuoles * PAS and mucicarmine negative * Clear cells * Lack of glycogen * Glandular cells * Round to polgonal * Eosinophilic to amphophilic cytoplasm * Lack of cytoplasmic granules or PAS positivity * Nuclear pleomorphism MICROSCOPIC FEATURES * Stroma * Delicate fibrovascular tissue * Collagenous tissue * Lymphoid infiltration (in some cases) * Hemorrhage * Hemosiderin * Psammoma bodies ULTRASTRUCTUAL FEATURES * Main epithelial cells * Multiple round, membrane bound, electron dense cytoplasmic granules * Vacuoles * Lumina * Apical junctional complexes * Few microvilli * Clear cells * Dilated ER * Lipid inclusions * Intracytoplasmic pseudolumina * Myoepithelial cells * Elongated * Microfilaments *Dense bodies |
GO TO THIS SITE AND COMPARE FEATURES WITH OTHER SALIVARY GLAND CANCERS. | SALIVARY GLAND TUMORS; CLINICAL AND PATHOLOGICAL FEATURES | S Tabibzadeh BioScience.org - FRONTIERS IN BIOSCIENCE; LECTURE SERIES [Vol 3, z1-129, January 1, 1998] Dept of Pathology, Moffitt Cancer Center and University of South Florida, 12902 Magnolia Drive, Tampa, FL 33612 http://www.bioscience.org/lecture/tabibza/list.htm |
Jan. 1 1998 | Informative site on salivary gland cancers of all types. | |||
| IMMUNOHSITOCHEMICAL FEATURES * Cytokeratin(present) * CEA (present) * alpha 1 antitrypsin (present) * alpha 1 antichymotrypsin (present) * Leu-M1 (present) * Amylase (present) * Transferrin (present) * Lactoferrin (present) * Vasocactive intestinal polypeptide (present) * S-100 (some) * GFAP (some) DIFFERENTIAL DIAGNOSIS * Papillary-cystic and follicular type * Cystadenocarcinoma (lack of microcycstic and vacuolated cells) * Mucoepidermoid carcinoma (presence of mucous cells) * Metastatic thyroid carcinoma (presence of thyroglobulin) * Polmorphous low-grade adencarcinoma (perineural invasion, homogeneous cell population, single cell infiltration at the periphery) |
GO TO THIS SITE AND COMPARE FEATURES WITH OTHER SALIVARY GLAND CANCERS. | SALIVARY GLAND TUMORS; CLINICAL AND PATHOLOGICAL FEATURES | S Tabibzadeh BioScience.org - FRONTIERS IN BIOSCIENCE; LECTURE SERIES [Vol 3, z1-129, January 1, 1998] Dept of Pathology, Moffitt Cancer Center and University of South Florida, 12902 Magnolia Drive, Tampa, FL 33612 http://www.bioscience.org/lecture/tabibza/list.htm |
Jan. 1 1998 | Informative site on salivary gland cancers of all types. | |||
| It was recently found that cholecystokinin (CCK) activates mitogen-activated protein kinases (MAPK) in isolated rat pancreatic acini. The present study evaluates whether one or both types of CCK receptors are capable of MAPK activation in pancreatic AR42J acinar cells as well as CHO cells transfected with CCK-A or CCK-B receptors. CCK significantly increased p44 MAPK and p42 MAPK activities in AR42J cells. Minimal, half-maximal, and maximal responses were observed at 30 and 500 pM and 10 nM, respectively, after CCK-8 stimulation and at 100 pM and 1.5 and 30 nM, respectively, after gastrin stimulation. Glycine-extended gastrin had no effect at 100 nM and a small but significant effect at 1 microM. The CCK-B receptor antagonist L365,260 almost totally blocked MAPK activation in AR42J cells after stimulation with gastrin and glycine-extended gastrin and substantially reduced the activation of both kinases by CCK-8, while the CCK-A receptor antagonist L364,718 was much less effective. (more) | Stimulation of both CCK-A and CCK-B receptors
activates MAP kinases in AR42J and receptor-transfected CHO cells. |
Dabrowski A, Detjen KM, Logsdon CD, Williams JA Department of Physiology, University of Michigan, Ann Arbor 48109-0622, USA. |
1998 | |||||
| (cont'd) The CCK-A-selective agonist A71376, however, was an effective stimulant of MAPK activity. In an alternative approach, stably transfected CHO cells bearing either CCK-A or CCK-B receptors were stimulated with CCK-8. Each receptor induced a time-dependent increase in activity of both MAPKs by five- to sixfold in CCK-A- and CCK-B-bearing cells. In conclusion, both CCK-A and CCK-B receptors activate MAPK in AR42J cells and in transfected CHO cells. | Stimulation of both CCK-A and CCK-B receptors
activates MAP kinases in AR42J and receptor-transfected CHO cells. |
Dabrowski A, Detjen KM, Logsdon CD, Williams JA Department of Physiology, University of Michigan, Ann Arbor 48109-0622, USA. |
1998 | |||||
| (unclear if acinic cell in study) | Nine cases of salivary duct carcinomas reviewed: P53 protein nuclear immunostaining was positive in 66.6%, c-erbB-2 overexpression was observed in 100% of tumors, Ki67 positivity ranges from 6.75% to 47.5% (mean 21.3%), DNA aneuploidy was found in 4 tumors (44.4%), DNA diploidy in 5 (55.5%). | Salivary duct carcinoma: clinicopathological and immunohistochemical studies | Martinez-Barba E, Cortes-Guardiola JA, Minguela-Puras A, et al - Jour Craniomaxillofacial Surgery - 25(6): 328-34 | Dec-97 | P. Nagesh Rao, Ph.D. | |||
| The simian virus 40 large T antigen induces tumors in a wide variety of tissues in transgenic mice, the precise tissues depending on the tissue specificity of the upstream region controlling T-antigen expression. Expression of mutant T antigens that contain a subset of the protein's activities restricts the spectrum of tumors induced. Others showed previously that expression of a mutant large T antigen containing the N-terminal 121 amino acids (T1-121) under control of the lymphotropic papovavirus promoter resulted in slow-growing choroid plexus tumors, whereas full-length T antigen under the same promoter induced rapidly growing CPR tumors, T-cell lymphomas, and B-cell lymphomas. In those instances, the alteration in tumor induction or progression correlated with inability of the mutant large T antigen to bind the tumor suppressor p53. (more) | A simian virus 40 large T-antigen segment containing
amino acids 1 to 127 and expressed under the control of the rat elastase-1 promoter produces pancreatic acinar carcinomas in transgenic mice. |
Tevethia MJ, Bonneau RH, Griffith JW, Mylin L Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey 17033, USA. - J Virol 1997 Nov;71(11):8157-66 |
Nov-97 | COULD BE VERY USEFUL BASIC RESEARCH TO LEAD TO CURE? | ||||
| (cont'd): In the study reported here, we investigated the capacity of an N-terminal T antigen segment (T1-127) expressed in conjunction with small t antigen under control of the rat elastase-1 (E1) promoter to induce pancreatic tumors. The results show that pancreases of transgenic mice expressing T1-127 and small t antigen display acinar cell dysplasia at birth that progresses to neoplasia. The average age to death in these mice is within the range reported for transgenic mice expressing full-length T antigen under control of the E1 promoter. These results indicate that sequestering p53 by binding is not required for the development of rapidly growing acinar cell carcinomas. In addition, we provide evidence that small t antigen is unlikely to be required. Finally, we show that the p53 protein in acinar cell carcinomas is wild type in conformation. | A simian virus 40 large T-antigen segment containing
amino acids 1 to 127 and expressed under the control of the rat elastase-1 promoter produces pancreatic acinar carcinomas in transgenic mice. |
Tevethia MJ, Bonneau RH, Griffith JW, Mylin L Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey PA 17033, USA. - J Virol 1997 Nov;71(11):8157-66 |
Nov-97 | COULD BE VERY USEFUL BASIC RESEARCH TO LEAD TO CURE? | ||||
| Pathology of Edgar's Biopsy - Metastatic Site right posterior auricular (excisional
biopsy), 1997: Sections of the tumour show a well circumscribed nodule
composed of nests and sheets of tumour cells with interspersed fibrovascular
septa. The tumour cells have granular cytoplasm and have small nuclei. |
UCLA Pathologist: Sunita Bhuta, M.D - UCLA | 9/5/97 | ||||||
| Article details various factors for histological classification. No details available in abstract. | (Diagnosis and prognosis of salivary gland tumours. An interpretation of new revised WHO classification.) - Authour- Seifert,G | Mund Kiefer Gesichtschir, 1(5):252-67 | Sep-97 | |||||
| Several peroxisome proliferators have been shown to produce pancreatic acinar cell hyperplasia/adenocarcinomas in 2-year bioassays with rats: ammonium perfluorooctanoate (C8), clofibrate, methylclofenapate, HCFC-123, and Wyeth-14,643 (WY). We have used in vitro (C8, WY) and in vivo (WY) approaches to examine several possible mechanisms of pancreatic tumorigenesis by peroxisome proliferating compounds. These mechanisms include cholecystokinin receptor agonism (CCK(A)), trypsin inhibition, alterations in gut fat content, cholestasis, and altered bile flow/composition. All of these mechanisms enhance pancreatic growth either by binding to the CCK(A) receptor or by increasing plasma CCK levels. In vitro experiments using a receptor competition binding assay demonstrated that WY and C8 do not bind directly to the CCK(A) receptor. In a continuous spectrophotometric assay, WY and C8 also failed to inhibit trypsin, a common mechanism for increasing plasma CCK levels. These in vitro results suggested (more) | Mechanisms for the pancreatic oncogenic effects of
the peroxisome proliferator Wyeth-14,643. |
Toxicol Appl Pharmacol 1997 Aug;145(2):425-36 -
Obourn JD, Frame SR, Bell RH Jr, Longnecker DS, Elliott GS, Cook JC Haskell Laboratory for Toxicology and Industrial Medicine, E.I. du Pont de Nemours and Company, Newark, Delaware 19714, USA. |
Aug-97 | |||||
| (cont'd): that WY was not acting via the two most common mechanisms for modulation of pancreas growth. Two types of in vivo experiments were conducted. The subchronic study (2-month duration) was designed primarily to detect early changes in pancreatic growth such as those mediated by compounds that inhibit trypsin or act as CCK(A) receptor agonists. The chronic study (6 months) was designed primarily to evaluate whether the pancreatic lesions were secondary to hepatic changes such as cholestasis and/or altered bile flow/composition. In the in vivo experiments, male Crl:CDBR rats were fed diets containing 0 or 100 ppm WY. In the subchronic study WY-treated rats had a twofold increase in mean relative liver weights, an eightfold increase in hepatic peroxisomal proliferation, and a fourfold increase in hepatocyte cell proliferation after 1 week which remained elevated throughout the 2 months of treatment. In contrast, no pancreatic weight effects, increases in plasma CCK, or acinar cell proliferation was seen through 2 months in the WY group when compared to the control group. (more) | Mechanisms for the pancreatic oncogenic effects of
the peroxisome proliferator Wyeth-14,643. |
Toxicol Appl Pharmacol 1997 Aug;145(2):425-36 -
Obourn JD, Frame SR, Bell RH Jr, Longnecker DS, Elliott GS, Cook JC Haskell Laboratory for Toxicology and Industrial Medicine, E.I. du Pont de Nemours and Company, Newark, Delaware 19714, USA. |
Aug-97 | |||||
| (cont'd): Fecal fat concentrations were also measured at 2 months and demonstrated no difference between control and WY-treated animals. The absence of any early pancreas changes in the subchronic study is consistent with the in vitro data which demonstrated that WY is not a CCK(A) agonist or a trypsin inhibitor. The chronic study demonstrated increases in pancreatic weights at 3 months (6% above control) and 6 months (17% above control), as well as increased CCK plasma levels in the WY-treated group. Liver effects in the chronic study paralleled those of the subchronic time points. Clinical pathology endpoints including increased serum concentrations of bile acids, alkaline phosphatase, and bilirubin were indicative of cholestasis in the chronic WY-treated group. The cholestasis may be responsible for the downward trend in total bile acid output, both of which may contribute to the modest increases in plasma CCK levels. These results indicate that chronic exposure to WY causes liver alterations such as cholestasis, which may increase plasma concentrations of CCK. (more to right) | (cont'd. from left) Hence, WY may induce pancreatic acinar cell adenomas/ adenocarcinomas via a mild but sustained increase in CCK levels secondary to hepatic cholestasis. | Mechanisms for the pancreatic oncogenic effects of
the peroxisome proliferator Wyeth-14,643. |
Toxicol Appl Pharmacol 1997 Aug;145(2):425-36 -
Obourn JD, Frame SR, Bell RH Jr, Longnecker DS, Elliott GS, Cook JC Haskell Laboratory for Toxicology and Industrial Medicine, E.I. du Pont de Nemours and Company, Newark, Delaware 19714, USA. |
Aug-97 | ||||
| A case of dedifferentiated acinic cell carcinoma of the parotid gland is presented... Histologically, the tumor was a composite of a usual low-grade acinic cell carcinoma and high-grade, poorly differentiated carcinoma. Cervical lymph node metastases were composed entirely of high-grade carcinoma. Immunohistochemically, both low and high-grade malignant components were negative for p53 oncoprotein expression. Moreover, polymerase chain reaction and nonisotopic single-stranded conformational polymorphism analyses were consistent with a germ line configuration of the p53 gene, exons five through eight, in both low- and high-grade elements of the tumor. The literature on this unusual variant of acinic cell carcinoma is reviewed. | Dedifferentiated acinic cell carcinoma of the
parotid gland: a distinct rarely described entity |
Henley JD, Geary WA, Jackson CL, Wu CD, Gnepp DR - Dept. of Pathology, Rhode Island Hospital and Brown University School of Medicine, Providence 02903, USA - Hum Pathol 1997 Jul;28(7):869-73 | Jul-97 | |||||
| Acinic Cell Carcinoma is a rare salivary gland tumour, making up 4% of all minor salivary gland tumours. Typically it is composed of acinic cells, although transitional and duct-like cells are also identified. In the present study, a panel of antibodies was applied to eight minor salivary gland ACCs. Antibodies tested wre: cytokeratins 7,8,13,14,18,19, vimrntin and actin(HHF35). Immunohistochemical staining revealed that cytokeratin 8, among the tested antibodies, was the more specific to neoplastic cells, with a pattern of distribution quite variable and peculiar. This staining may be useful in the recognition of neolastic acinic cells. | Immunohistochemical study of acinic cell carcinoma of minor salivary gland. | Crivelini MM, de Sousa SO, de Araujo VC - Oral Oncol, 33(3):204-8 | May-97 | |||||
| The cytologic findings in fine-needle
aspiration (FNA) biopsies obtained from 40 primary and 18 recurrent
acinic-cell carcinomas (ACC) were retrospectively analyzed. Cytomorphologically, ACC is characterized by acinar
differentiated tumor cells. In addition to these diagnostic clue cells, other
types of neoplastic cells including vacuolated cells, cells resembling
oncocytes, and nonspecific glandular cells are encountered. A pronounced lymphocytic reaction is a hallmark in 10% of ACC
aspirates. Both the variety of tumor cell differentiation and the pronounced
lymphocytic reaction observed in ACC aspirates may result in confusion with
other salivary gland lesions. The differential
diagnosis of ACC encompasses adenocarcinoma, mucoepidermoid carcinoma,
pleomorphic adenoma, Warthin tumor, sebaceous lymphadenoma, benign
lymphoepithelial lesion, sialoadenosis, sialadenitis caused by radiotherapy,
and lymphadenitis. (more below) |
Cytologic diagnosis of acinic-cell carcinoma of salivary glands. | Nagel H; Laskawi R; B¨uter JJ; Schr¨oder M; Chilla R; DroeseM - Diagn Cytopathol, 16(5):402-12 | 1997 May | |||||
| (cont'd) Primary ACCs were correctly diagnosed in 68%; additionally, ACC was suspected or included in the differential diagnosis in 15%. Increased familiarity with the spectrum of cytomorphologic findings and the potential diagnostic pitfalls in ACC will improve the cytodiagnosis of this neoplasm. | Cytologic diagnosis of acinic-cell carcinoma of salivary glands. | Nagel H; Laskawi R; B¨uter JJ; Schr¨oder M; Chilla R; DroeseM - Diagn Cytopathol, 16(5):402-12 | 1997 May | |||||
| OBJECTIVE: This study investigates the
distribution of the alpha chain of the integrin family of extracellular
matrix receptors in a series of adenomas and carcinomas of salivary gland origin to determine if the malignant phenotype is associated with modification of the expression of these receptors. STUDY DESIGN: Cryostat sections of 36 tumor specimens were stained by a standard streptavidin-biotin-peroxidase technique using primary monoclonal antibodies against alpha 1-6 and alpha v integrin chains. The immunohistochemical reaction was scored using a three-point scale and the results were analyzed using Fisher's exact test. RESULTS: In salivary adenomas, alpha 2, alpha 3, alpha 4, alpha 6, and alpha v chains were widely expressed in most of the cases studied. The alpha 1 subunit was prominently expressed by the epithelial cells of Warthin's tumor, whereas a minority of pleomorphic adenomas showed immunoreactivity for this antigen. We observed alpha 5 subunit expression only in the mesenchymal-like component of pleomorphic adenomas. (more to right) |
(from left) In salivary
carcinomas, integrin alpha chain expression was heterogeneous, varying
greatly between different histotypes and within the same histotype. The distribution of the antigens was
similar to that of adenomas, except for the alpha 6 chain, which localized
not only at the interface between cell and matrix, but also at sites of
cell-cell contact. When the immunohistochemical levels of integrin alpha
chain expression were compared in adenomas and carcinomas, expression
significantly decreased for the alpha 6 and alpha v chains (p = 0.0007; p =
0.002, respectively). CONCLUSIONS: Loss of alpha 6
and alpha v integrin subunits occurring in salivary gland carcinomas could
modify the adhesive properties of malignant cells, contributing to the
invasive potential of these tumors. |
Comparison of integrin alpha chain expression in benign and malignant salivary gland tumors. | Franchi A, Santoro R, Paglierani M, Bondi R - Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997 May;83(5):588-95 | 1997 May | ||||
| Bcl-2 protein and Ki-67 (MIB-1) were studied in 32 acinic cell carcinomas (ACCs), all with a minimum of 5 years' clinical follow-up. Tumour apoptosis was evaluated by TdT dUTP nick end labelling (TUNEL) and by morphological criteria. Five patients died of their disease. Patients with stage I tumours had significantly better survival compared with other stages (P < 0.05). Patients with MIB-1-negative tumours had significantly better survival than patients with MIB-1-positive tumours (P = 0.05). This study confirms a previous report that MIB-1 is an independent prognostic factor for survival in patients with ACC. Stage I tumours had high expression of bcl-2 protein, but there was no difference when compared with other stages. TUNEL positivity was most prevalent in stage I tumours, compared with stages II, III, and IV (P < 0.05), probably indicating more apoptosis. This could imply a capacity of stage I tumours ('early tumours') for early selection of tumour cells for elimination by apoptosis. (more below) | Tumour growth fraction and apoptosis in salivary
gland acinic cell carcinomas. Prognostic implications of Ki-67 and bcl-2
expression and of in situ end labelling (TUNEL). |
Hellquist HB; Sundelin K; Di Bacco A; Tytor M;
Manzotti M; Viale G Address: Department of Pathology II, University Hospital, Link¨oping, Sweden. henrik.hellquist@pat.liu.se Source: J Pathol, 181(3):323-9 1997 Mar |
Mar-97 | |||||
| (cont'd.) There was no significant difference between expression of bcl-2 and TUNEL, between these parameters and clinical outcome, or between any parameter and morphological subclassification. We conclude that MIB-1 has prognostic value in ACC. Clinical staging, bcl-2, and TUNEL are also potentially useful as prognostic markers. | Tumour growth fraction and apoptosis in salivary
gland acinic cell carcinomas. Prognostic implications of Ki-67 and bcl-2 expression and of in situ end labelling (TUNEL). |
Hellquist HB; Sundelin K; Di Bacco A; Tytor M;
Manzotti M; Viale G Address: Department of Pathology II, University Hospital, Link¨oping, Sweden. henrik.hellquist@pat.liu.se Source: J Pathol, 181(3):323-9 1997 Mar |
Mar-97 | |||||
| Acinar cell carcinoma (ACC) of the
pancreas is a rare malignancy accounting for < 1% of pancreatic neoplasms.
We report the clinical and biological characteristics of this carcinoma from
two cases that were of interest because of their similar presentation: extensive subcutaneous fat necroses from excessive lipase
production by these tumors. Immunohistochemical and
ultrastructural analyses of both tumors were consistent with an acinar cell
line origin. Recognition of the association between
subcutaneous panniculitis and pancreatic neoplasm may prevent long delays in
the diagnosis and treatment of this malignancy. |
Pancreatic Acinic/Acinar Cell - Accounts for < 1% of pancreatic neoplasms. | Functioning pancreatic acinar cell carcinoma:
immunohistochemical and ultrastructural analyses. |
Am J Clin Oncol 1997 Feb;20(1):101-7 - Kuerer H, Shim H, Pertsemlidis D, Unger P - Department of Surgery, The Mount Sinai School of Medicine, New York, NY 10029, USA. |
Feb-97 | ||||
| The imaging findings of two children with acinic cell carcinoma of the parotid gland are presented. Ultrasonic features are emphasized. One of these children, a 6-year-old boy, suffers from the oculocerebrorenal syndrome of Lowe, a rare congenital, inherited condition manifested by defects of the nervous system (mental retardation, hypotonia), eyes (cataracts, glaucoma) and kidneys. To date, no known association exists between these two rare entities. The other child, a 10-year-old girl, was otherwise well. The ultrasound findings of both cases demonstrate features more classic for a benign intraparotid mass than for a potentially malignant lesion. The possibility of acinic cell carcinoma should be considered if a well-defined, relatively homogenously hypo-echoic intraparotid mass is encountered in a child, especially if cystic spaces are present. | Acinic cell carcinoma of the parotid in children. | Australas Radiol 1997 Feb;41(1):44-8 - Jones AO, Lam AH, Martin HC | Feb-97 | |||||
| This study evaluated the action of menadione on cell proliferation and integrity of the rat pancreatic acinar cell line, AR4-2J. Menadione at 1-20 microM dose- and time-dependently inhibited cell proliferation of AR4-2J cells. In contrast, a high concentration of menadione (100 microM) caused rapid cell death (> 90% of cells took up trypan blue within 4-h). While the high concentration of menadione (100 microM) induced DNA smear in electrophoresis indicative of necrosis, lower concentrations (10-20 microM) induced a DNA ladder indicative of apoptosis. Similar results were obtained using a DNA fragmentation ELISA. Glutathione (1 mM), the calcium chelator EGTA (500 microM), and the cysteine protease inhibitor NCO-700 (5 mM) partly inhibited the effect of 1-10 microM menadione on cell proliferation and DNA fragmentation. Menadione at1-20 microM induced wild-type P53, whereas the 100 microM menadione had a minor effect on wild-type P53. It is concluded that menadione induced necrosis at high concentrations and apoptosis at low concentrations in AR4-2J cells. Apoptosis induced by lower concentrations of menadione may be mediated by wild-type P53, intracellular calcium, and mechanisms which decrease the intracellular concentration of reduced glutathione. | Menadione induces both necrosis and apoptosis in rat pancreatic acinar AR4-2J cells. | Sata N, Klonowski-Stumpe H, Han B, Haussinger D, Niederau C ,Department of Gastroenterology, University of Dusseldorf, Germany. beaglen@t3.rim.or.jp - Free Radic Biol Med 1997;23(6):844-50 | 1997 | |||||
| Adenosine 3',5'-cyclic monophosphate (cAMP) regulates growth and/or differentiation of some tumor cells in culture. The effects of cAMP on human parotid acinar cells have never been studied. Results showed that 2HPC8 (non-tumorigenic cells derived from human pleomorphic parotid adenoma) were more sensitive to dibutyryl cAMP, an analog of cAMP, and RO20-1724, an inhibitor of cyclic nucleotide phosphodiesterase, than 2HP1G cells (derived from spontaneous transformation of 2HPC8 cells), suggesting that human parotid adenoma cells maintain a higher degree of cAMP-responsiveness than parotid carcinoma cells. Prostaglandin E1 (PGE1), a stimulator of adenylate cyclase, which increased cAMP levels in 2HPC8 cells, but not in 2HP1G cells, caused a greater degree of growth inhibition in 2HP1G cells than in 2HPC8 cells, suggesting that this effect of PGE1 on tumorigenic cells is not related to cAMP. In the normal parotid and parotid adenoma cell cultures, about 5-10% of cells were small and round, whereas in tumorigenic cell cultures, all cells were small and round. (more to right) | (cont'd from left) Some indirect evidence suggests that these round cells may be the primary target for transformation. These tumor cells formed cytoplasmic processes of variable length after treatment with cAMP stimulating agents and prostaglandin E1. | Effect of adenosine 3',5'-cyclic monophosphate (cAMP) on human non-tumorigenic and tumorigenic parotid acinar cells in culture. | Cancer Lett 1996 Nov 12;108(1):73-9 - Krause G, Kumar R, Meyers A, Prasad KN - Center for Vitamins and Cancer Research, School of Medicine, University of Colorado Health Sciences Center, Denver 80262, USA. | Nov. 12, 1996 | ||||
| Transglutaminase C (TGase C), a family of Ca(2+)-dependent enzymes and an essential component in the cross-linking of peptide bonds, has been found to be a marker of epithelial differentiation with a possible role in cellular apoptosis, extracellular matrix stabilisation and Ca2+ binding, thereby having a potential role in tumour growth, differentiation and invasive behaviour. The expression of TGase C was evaluated in normal human salivary glands and their neoplastic lesions. Adenoid cystic carcinomas had tumour cells in the luminal cells of tubular and cribriform structures and the acinic cell carcinoma had from low to moderate immunoreactivity in the tumour cell component and a diffuse immunoreactivity in the stroma for TGase C. As the presence of TGase C in salivary gland tumours was confined to those tumour cells which form the predominant histomorphology in each tumour subtype, it may be suggested that these enzymes may have a potential role in the regulation of cellular function in neoplastic salivary tissues affecting tumour growth, differentiation and neoplastic behaviour. | Immunohistochemical evaluation of transglutaminase C in tumours of salivary glands. | Eur J Cancer B Oral Oncol 1996 Nov;32B(6):401-6 - Lee CH, Lee SK, Chi JG, Park SC, Chung SI, Saitoh M, Shrestha P, Mori M | Nov-96 | |||||
| IgA-, IgG, and IgM-producing plasma cells as well as 3- and T-lymphocytes were immunophenotyped and quantitated in a series of 216 benign and malignant salivary gland tumors, with special emphasis placed on the clinical behavior of the tumors. No IgA-immunoreactivity was found in adenoid cystic, undifferentiated, acinic cell, carcinoma in pleomorphic adenoma, and mucoepidermoid carcinomas. In logistic regression analysis, IgG- and IgM-producing plasma cells in malignant salivary gland tumors were related to an increased tumor diameter (p = 0.022 and 0.046, respectively). In benign tumors, neither clinical nor prognostic value could be attributed to the distribution of plasma cells. T-cells and B-cells were present in 63.9% and 33.8% of all tumors, found in 63.8% and 26.7% (p = 0.0048) of the benign tumors, and in 64.1% and 41.7% (not significant) of the malignant tumors, respectively. (more below) | adenoid cystic, undifferentiated, carcinoma in pleomorphic adenoma, and mucoepidermoid carcinomas. | Immunocompetent cells in benign and malignant salivary gland tumors. | Gen Diagn Pathol, 142(2):75-81 1996 Oct - Karja VJ, Syrjanen KJ, Syrjanen SM | Oct-96 | ||||
| (cont'd.): The presence of T- of B-lymphocytes was of no prognostic significance in malignant tumors. In benign tumors, however, the mean age of the patients was significantly higher (p = 0.010) and the mean time to recurrence significantly shorter (p = 0.018) in patients with tumors containing T-cells than in those devoid of these cells. In conclusion, the cell-mediated immunity (T-cells and their subsets) seems to play a more important role in pathogenesis and prognostication of salivary gland neoplasms than do the cells of the B-cell lineage, and, clearly, further studies are needed to elucidate these issues. | Immunocompetent cells in benign and malignant salivary gland tumors. | Gen Diagn Pathol, 142(2):75-81 1996 Oct - Karja VJ, Syrjanen KJ, Syrjanen SM | Oct-96 | |||||
| We report CT and MRI bindings in two cases of acinic cell carcinoma of the parotid glands which behaved differently on T2-weighted images. Differences in signal intensities were considered to reflect the histology ofthe lesion, although a histological diagnosis could not be made on imaging grounds alone. | Acinic cell Carcinoma of the parotid gland: CT and MRI | Sakai O; Nakashima N; Takata Y; Furuse M Address: Department of Radiology, Jichi Medical School and Hospital, Tochigi, Japan. Source: Neuroradiology, 38(7): 675-9 | Oct-96 | |||||
| Helioid bodies are exceedingly rare, intranuclear, rounded inclusions with peripheral radiating filaments. These structures, which were formerly observed in only three cases of proliferative breast epithelial lesions, appeared in 0.5-1% of the neoplastic cells of a case of dedifferentiated acinic cell carcinoma of the parotid gland. Helioid bodies are related to rough endoplasmic reticulum cisternae, which suggests that they are the result of the condensation and partial crystallization of their contents when sequestrated into the nuclear compartment of the cell. The presence of helioid bodies may be related to secretory dysfunction of the tumor cells associated with the process of neoplastic dedifferentiation. | EXCEEDINGLY rare characteristic | Helioid inclusions in dedifferentiated acinic cell carcinoma of the parotid gland. | Nunes JF; Fonseca I; Soares J - Departmento de
Patologia Morfol´ogica, Instituto Portugu^es de Oncologia de Francisco Gentil, Lisboa, Portugal. Source Ultrastruct Pathol, 20(5):443-9 |
Sept/Oct. 1996 | ||||
| Cellular proliferation activity in a series of salivary gland malignant tumors was evaluated using the index of proliferation cellular nuclear antigen (PCNA) immunoreactivity. A streptavidin-biotin immunoperoxidase method (ABC) using a monoclonal antibody PC10 demonstrated nuclear staining with varying intensity and distribution in all tumor specimens. Acinic cell carcinoma (n = 5) and polymorphous low-grade adenocarcinoma (n = 1) showed relatively low proliferation fractions. Tumor cell differentiation appears to be more important than proliferation in determining biological behavior and prognosis. | polymorphous low-grade adenocarcinoma | Anticancer Res 1996 Sep-Oct;16(5A):2693-8 - Zhao M, Zhao QX, Saitoh M, Ohmura H, Okamoto Y, Shrestha P, Mori M | Sept/Oct. 1996 | |||||
| Fourteen salivary gland type tumors were analyzed with a combination of conventional cytogenetics via GTG-banding, molecular cytogenetics via fluorescent in situ hybridization, and chromosome morphometry. Nine tumors were benign (eight pleomorphic adenomas and one Warthin tumor) five tumors were malignant (one carcinoma ex pleomorphic adenoma, two adenoid cystic carcinomas including one from the breast, a basal cell adenocarcinoma, and an acinic cell carcinoma). Of the four malignant tumors with karyotypes, the acinic cell carcinoma and one adenoid cystic carcinoma were normal, the second adenoid cystic carcinoma showed a normal polymorphic variant... In conclusion, 66% of the benign tumors and 25% of the malignant tumors demonstrated abnormal karyotypes. | adenoid cystic carcinoma | Cytogenetic analysis of salivary gland type tumors. | Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996 Aug;82(2):187-92 - Mark HF, Hanna I, Gnepp DR | Aug-96 | ||||
| Cell proliferation, assessed with the MIB 1 antibody, that recognizs the Ki67 antigen in proliferating cells, represents a significant prognostic factor for acinic cell carcinomas and mucoepidermoid carcinomas of salivary gland origin. Š. Thus assessment of cell proliferation in salivary gland tumours using the MIB1 antibody and PCNA in paraffin-embedded tissue should be incorporated into routine immunohistologic evaluation of histologically difficult cases of salivary gland tumours. | mucoepidermoid carcinomas of salivary gland origin | Cell proliferation in salivary gland tumours. | Sk'alov'a A, Leivo I - Gen Diagn Patho; 142(1): 7-16 | Jun-96 | ||||
| A group of 19 malignant salivary gland neoplasms of various histological types (mucoepidermoid carcinoma, acinic cell carcinoma, adenoid cystic carcinoma, epithelial-myoepithelial carcinoma, myoepithelial carcinoma, basal cell adenocarcinoma, carcinoma ex-pleomorphic adenoma, ductal carcinoma, adenocarcinoma not otherwise specified and undifferentiated carcinoma) were cytogenetically investigated. Previous karyotypic information revealed deletion of the long arm of chromosome 6, loss of chromosome Y and the gain of chromosome 8 as the most recurrent deviations found in these neoplasms. Clonal chromosome aberrations were detected in 11 cases of this series. In 7 of them there were only numerical deviations (gain of chromosomes 2, 7, 8, 10 and X and loss of chromosomes 18, 21 and Y) without concomitant structural anomalies. Structural rearrangements such as t(2;7), t(6;16), t(6;9) and t(1;1) translocations were found in two mucoepidermoid carcinomas, one adenoid cystic carcinoma and one ductal carcinoma, respectively. (more below) | Malignant salivary gland neoplasms: a cytogenetic study of 19 cases. | Eur J Cancer B Oral Oncol 1996 Mar;32B(2):128-32 - Martins C, Fonseca I, Roque L, Pinto AE, Soares J | Mar-96 | |||||
| (cont'd): The wide spectrum of changes found in this group of neoplasms may reflect the diversity in their histogenesis and differentiation phenotypes. NOTE: GET FULL TEXT | Malignant salivary gland neoplasms: a cytogenetic study of 19 cases. | Eur J Cancer B Oral Oncol 1996 Mar;32B(2):128-32 - Martins C, Fonseca I, Roque L, Pinto AE, Soares J | Mar-96 | |||||
| No acinic cell specifically mentioned. | To elucidate the genetic alterations that occur in salivary gland tumors, we screened every autosomal arm (and the X-chromosome) of 29 primary human salivary gland neoplasms (11 pleomorphic adenomas, 10 adenoid cystic carcinomas, 5 mucoepidermoid carcinomas, and 3 carcinoma ex-mixed tumors) for allelic loss using 86 microsatellite markers. A minimum of two microsatellite markers were used per chromosomal arm to achieve informativity of at least 60% (excluding X). The pleomorphic adenomas demonstrated few areas of allelic loss; the most prominent chromosomal arm involved was 12q, lost in more than 35% of informative cases. The most significant allelic losses in adenoid cystic carcinoma were 1p, 2p, 6q, 17p, and 20p (> 20% of informative cases) and 19q (40% of informative cases). (more below) | Allelotype of Salivary Gland Tumors | Cancer Research 56, March 1 1996, 1151-1154 - American Association for Cancer Research 1996 - Michael M. Johns III, William H. Westra, Joseph A. Califano, David Eisele, Wayne M. Koch, and David Sidransky - Department of Otolaryngology, Division of Head and Neck Cancer Research [M. M. J., J. A. C., D. E., W. M. K., D. S.], and Department of Pathology [W. W.], The Johns Hopkins University, Baltimore, Maryland 21205 | 3/1/96 (received 11/13/95) | Found online at American Association for Cancer Research site. | |||
| No acinic cell specifically mentioned. | (cont'd from above) Mucoepidermoid carcinoma showed 50% or greater loss at 2q, 5p, 12p, and 16q. Although losses at 9p, 3p, and 17p are common in squamous cell carcinoma of the head and neck, only the carcinoma ex-mixed tumors demonstrated loss at these loci, consistent with progression to a more aggressive phenotype. Salivary gland tumors display allelic loss patterns different from many other tumor types, suggesting distinct genetic pathways in the progression of these tumors. | Allelotype of Salivary Gland Tumors1 | American Association for Cancer Research 1996 - Michael M. Johns III, William H. Westra, Joseph A. Califano, David Eisele, Wayne M. Koch, and David Sidransky - Department of Otolaryngology, Division of Head and Neck Cancer Research [M. M. J., J. A. C., D. E., W. M. K., D. S.], and Department of Pathology [W. W.], The Johns Hopkins University, Baltimore, Maryland 21205 | 1/15/96 | Found online at American Association for Cancer Research site. | |||
| The effects of individual and multiple
antioxidant vitamins on growth and morphology of human nontumorigenic
(2HPC8) and tumorigenic (2HP1G) parotid acinar cells in culture have not been investigated. Our study showed that tumorigenic acinar cells were more sensitive than non-tumorigenic acinar cells to individual vitamins such as vitamin C, beta-carotene (BC), d-alpha-tocopheryl succinate (alpha-TS), and retinoic acid (RA) and a mixture of four vitamins (vitamin C, BC, alpha-TS, and RA). The effect of individual vitamins on tumorigenic acinar cells depended on the dose and the type of vitamins. Vitamin C at a low concentration stimulated growth, but at a high concentration it inhibited growth. BC was most effective in reducing growth, and it alone caused extensive morphological changes in tumorigenic acinar cells. A mixture of four vitamins at appropriate doses was more effective than a mixture of two or three vitamins at the same doses in reducing the growth of tumorigenic acinar cells. (more below) |
Effect of individual and multiple antioxidant vitamins on growth and morphology of human nontumorigenic and tumorigenic parotid acinar cells in culture. | Nutr Cancer 1996;26(1):11-9 - Prasad KN, Kumar R - Department of Radiology, School of Medicine, University of Colorado Health Sciences Center, Denver 80262, USA. | 1996 | TREATMENT RELATED - IMPORTANT ! | ||||
| (cont'd) The extent of growth inhibition depended on the dose and the type of vitamins. Our results suggest that the use of multiple antioxidant vitamins is essential for a maximal reduction in cancer incidence among a high-risk population. The use of one or two vitamins may be ineffective or even harmful. | Effect of individual and multiple antioxidant vitamins on growth and morphology of human nontumorigenic and tumorigenic parotid acinar cells in culture. | Nutr Cancer 1996;26(1):11-9 - Prasad KN, Kumar R - Department of Radiology, School of Medicine, University of Colorado Health Sciences Center, Denver 80262, USA. | 1996 | TREATMENT RELATED - IMPORTANT ! | ||||
| The neoplastic cells were immunoreactive with anti-lysozyme and anti-salivary-type amylase antisera and contained electron-dense cytoplasmic globules similar to those seen in acinic cell carcinoma of salivary glandsŠ. This appears to be the first case of carcinoma of acinic cell-like features reported in the breast. | Breast Cancer | Acinic cell-like carcinoma of the breast. | Virchows Arch; 429(1) 69-74 | 1996 | ||||
| This study reports the isolation and characterization of a rat nontumorigenic parotid acinar cell clone (2RSG), a human nontumorigenic parotid acinar cell clone (2HPC8), and a human tumorigenic acinar clone (2HP1G). The levels of alpha-amylase mRNAs detected when using alpha-amylase cDNA of 1176 and 702 bp for hybridization were higher in 2RSG and 2HPC8 cells than their respective whole parotid glands. The level of these mRNAs decreased in 2HP1G cells. In contrast to alpha-amylase mRNAs levels, the alpha-amylase activity in cultured acinar cells was extremely low in comparison to whole glands, irrespective of species or cell status. The levels of proline-rich protein (PRP) mRNA and parotid secretory protein (PSP) mRNA detected when using PRP cDNA of 600 bp and PSP cDNA of 805 bp for hybridization were higher in 2RSG cells than those in rat parotid glands; the reverse was observed in 2HPC8 cells and human parotid glands. The levels of PRP mRNA and PSP mRNA in 2HPC8 and 2PH1G acinar cells were similar. (more to right) | (cont'd from left) The level of mRNA was not detectable in murine neuroblastoma cells (NBP2) using the same alpha-amylase cDNA, PRP cDNA and PSP cDNA for hybridization. The PSP level in rat parotid gland was lower than that found in 2RSG cells; the reverse was observed in 2HPC8 cells and human parotid glands. The level of PSP in 2HP1G cells was higher than that found in 2HPC8 cells. Isoproterenol increased the cAMP level in 2RSG, 2HPC8, and 2HP1G clones, being most effective in 2RSG cells, and least effective in 2HPG cells. Prostaglandin E1 (PGE1) also increased cAMP level, being most effective in 2HPC8 cells and ineffective in 2HP1G cells, suggesting that the PGE1 receptor-linked adenylate cyclase becomes inactive upon transformation. These results suggest that the three clonal acinar cells from rat and human parotid glands reported here can be useful in comparative studies on regulation of growth, differentiation, and transformation. | In Vitro Cell Dev Biol Anim 1995 Nov;31(10):767-72 - Prasad KN, Kumar S, Carvalho E, Edwards-Prasad J, Kumar R, La Rosa FG, Larsen BB, Ann D - Department of Radiology, School of Medicine, University of Colorado Health Sciences Center, Denver 80262-0278, USA. | Nov-95 | |||||
| The biological behaviour of acinic cell carcinomas, even if well differentiated, is unpredictableŠ The presence of a predominantly solid architecture was strongly associated with poor outcome (P<0.01) and this was the only independent prognostic variable when log rank testing was performed. Tumor size (>2.75 cm) was a significant predictor of recurrent deep parotid lobe involvement, the presence of cervical nodal disease and lymphocytic infiltration, although not significant, factors showed a tendency towards recurrence. For acinic cell carcinoma, the predominant solid architecture would appear to be a strong predictor of recurrence. | Clinico-pathological predictors of recurrence for acinic cell carcinoma. | Clin Otolaryngol 1995 Oct;20(5):396-401 - Timon CI, Dardick I, Panzarella T, Thomas J, Ellis G, Gullane P | Oct-95 | GET FULL TEXT VERSION AND INPUT | ||||
| Unusual filamentous inclusion bodies in the cytoplasm of metastatic tumor cells are described. Their presence (intermingled with zymogen granules) seems rather restricted to cells of metastatic acinar cell carcinoma of the pancreas, acinic cell carcinoma of salivary gland (parotid gland) and Paneth cells (neoplastic or in zinc deficiency state). For the time being, the real nature of these inclusions (deranged zymogen granules?) is unclear. | acinar cell carcinoma of the pancreas and Paneth cells (neoplastic or in zinc deficiency state) | Unusual intracytoplasmic inclusions in metastatic carcinoma. Discussion of their possible significance. | van Haelst UJ,Pruszczynski M (Department of Pathology, Medical Faculty, Nijmegen, The Netherlands) - Pathol Res Pract, 191(6): 535-40 July 1995 | Jul-95 | POSSIBLY VERY IMPORTANT | |||
| Interleukin-6 (IL-6) is a multifunctional cytokine that regulates immune responses and acute phase reactions. It has demonstrated a growth factor function in several tumors, including those of salivary, plasma cell, and renal origin. We performed immunohistochemical staining for IL-6 localization on 57 salivary tumors. Reactivity was scored by intensity (0 to 4+) and percentage of cells staining, and the tumors were classified into three groups representing low (0 to 1+, 0% to 30%), moderate (2 to 3+, 31% to 75%), or high (> 3 to 4+, 76% to 100%) reactors. Low reactivity characterized all acinic cell carcinomas (N = 3) and mucoepidermoid carcinomas (N = 3) as well as six of nine primary adenoid cystic carcinomas and all metastatic adenoid cystic carcinomas (N = 3). A pattern emerged in which the benign and low grade malignant tumors showed stronger reactivity than the metastatic or high grade malignant tumors. This suggests an inverse relationship between the presence of IL-6 and the biological aggressiveness of salivary gland tumors. The function of IL-6 in salivary gland neoplasia awaits further study and elucidation. | mucoepidermoid carcinomas as well as primary adenoid cystic carcinomas and metastatic adenoid cystic carcinomas | Immunolocalization of interleukin-6 in salivary gland tumors. | Hum Pathol 1995 May;26(5):501-3 - Gandour-Edwards R, Kapadia SB, Gumerlock PH, Barnes L | May-95 | ||||
| Acinic Cell results UNKNOWN from abstract - GET FULL TEXT AND CHECK. Regarding parotid gland carcinoma in general: BACKGROUND. Recent studies of the molecular biology of cancer have demonstrated that p53 tumor suppressor gene aberration is associated with the development and progression of several different cancer types. METHODS. To analyze the expression of the p53 oncoprotein in parotid gland neoplasms, 72 parotid gland tumors (including 46 malignant and 26 benign cases) were studied immunocyto- chemically using the murine monoclonal DO-7 anti-p53 antibody. In parotid gland cancers, no and low expression (-/+) or moderate and high expression (++/+++) of the p53 oncoprotein were examined for correlation with patient survival and other clinicopathologic features, including clinical stage, tumor size, regional lymph node status, facial nerve paralysis, local infiltration, and distant failures. RESULTS. Positive staining was observed focally in 3 of 26 (11%) benign tumors and in 31 (67%) of 46 malignant tumors. Cancers showing moderate and high expression of p53... (more to right) | (cont'd from left) ...tended to be more advanced and larger than those with no expression or low expression, and presented at diagnosis more frequently, with signs of local aggressiveness. Tumors with moderate and high expression of p53 were associated more frequently with regional and distant metastases (P = 0.07 and P = 0.004, respectively). Multiple logistic regression analysis showed that regional and distant metastases were associated independently with p53 expression (P = 0.068 and P = 0.047, respectively). Moreover, patients whose cancers had moderate or high p53 expression had lower disease free and overall actuarial survival rates than those with no or low p53 expression (P = 0.021 and P = 0.033, respectively). Univariate and multivariate analysis confirmed the independent predictive prognostic value of p53 expression in patients with parotid gland cancer (P = 0.044 and P = 0.039, respectively). (more below) | p53 oncoprotein expression in parotid gland carcinoma is associated with clinical outcome. | Gallo O, Franchi A, Bianchi S, Boddi V, Giannelli E, Alajmo E - Institute of Otolaryngology-Head & Neck Surgery, University of Florence, Italy - Cancer 1995 Apr 15;75(8):2037-44 | Apr-95 | GET FULL TEXT AND CHECK FOR ACINIC CELL CARCINOMA REFERENCES. | |||
| Acinic Cell results UNKNOWN from abstract - GET FULL TEXT AND CHECK. | (cont'd from above) Furthermore, p53 expression did not correlate positively with patients' smoking habits in this series. CONCLUSION: The p53 tumor suppressor gene may be involved in salivary gland carcinogenesis, and its oncoprotein expression is an independent indicator of clinical aggressiveness in patients with carcinoma of the parotid gland. | p53 oncoprotein expression in parotid gland carcinoma is associated with clinical outcome. | Gallo O, Franchi A, Bianchi S, Boddi V, Giannelli E, Alajmo E - Institute of Otolaryngology-Head & Neck Surgery, University of Florence, Italy - Cancer 1995 Apr 15;75(8):2037-44 | Apr-95 | ||||
| Stimulation of rat lacrimal acinar cells with ATP and acetylcholine (ACh) induced a rapid accumulation of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] and its degradation products, resulting in an initial release of Ca2+ from intracellular stores. However, after pretreating the acini with U73122 no increase in the intracellular free Ca2+ concentration ([Ca2+]i) or Ins(1,4,5)P3 production was observed. A short pretreatment with the phorbol ester 4-beta-phorbol-12-beta-myristate-13-alpha-acetate (PMA) significantly attenuated the ATP- and ACh-induced increase in [Ca2+]i and overall inositol phosphate production. In contrast, staurosporine enhanced Ins(1,4,5)P3 and inositol 1,3,4-trisphosphate [Ins(1,3,4)P3] production and [Ca2+]i above control values in ATP- and ACh-stimulated cells. Stimulation of phospholipase C by ionomycin-evoked changes in [Ca2+]i were unaltered by pretreatment with staurosporine and PMA. The data show that a change in protein kinase C activity during cell stimulation affects the inositol phosphate metabolism and thereby the cellular Ca2+ signalling processes in lacrimal acinar cells. | Role of protein kinase C in the regulation of inositol phosphate production and Ca2+ mobilization evoked by ATP and acetylcholine in rat lacrimal acini. | Gromada J, Jorgensen TD, Dissing S - Pflugers Arch 1995 Feb;429(4):578-86 Department of Medical Physiology, Panum Institute, University of Copenhagen, Denmark. | Feb-95 | |||||
| Re: Cathepsin-D and tumour associated antigen DF3 - Acinic Cell Carcinomas and polymorphous low-grade adenocarcinomas were mostly negative. (Cathepsin-D is normally overexpressed in cancer cells, where its concentration in primary tumour is correlated with increased risk of metastases.) | polymorphous low-grade adenocarcinoma | Cathepsin-D and tumour associated antigen DF3 in salivary gland neoplasia. Differential diagnostic and prognostic applications. | Pathol Res Pract, 190 (12):1174-84 | Dec-94 | ||||
| DNA flow cytometry showed that very few of the above mentioned three types of malignant neoplasms revealed aneuploid DNA stemlines, indicating that this is not a relevant prognostic tumor marker within the groupsŠ. Among confirmed acinic cell, mucoepidermoid and adenoid cystic carcinomas, the S-phase fraction was a significant prognostic factor, as it was among all tumors examined. | adenoid cystic and mucoepidermoid carcinomas. | DNA flow Cytometry of Reclassified Subtypes of Malignant Salivary Gland Tumors | Bang G, Donath K, et al - J Oral Pathol Med, 23 (7): 291-7 | Aug-94 | ||||
| Cell proliferation correlates with prognosis in ACC of salivary gland origin. | Cell proliferation correlates with prognosis in ACC of salivary gland origin. Immunohistochemical study of 30 cases using the MIB 1 antibody in formalin-fixed paraffin sections. | Skalova A. Leivo I, et al - Journal of Pathology, 173(1):13-21 | May-94 | |||||
| Acinic Cell Carcinoma exhibited greatest level of c-erB-2 Oncogene Overexpression. Study confirms that c-erB-2 oncogene is overexpressed at the mRNA level in salivary gland tumours. | Mucoepidermoid carcinomas and pleomorphic adenomas were also signficantly greater in level of c-erB-2 cellular mRNA than normal salivary glands (non-tumour). | Demonstration of c-erB-2 oncogene overexpression in salivary gland neoplasms by in situ hybridization. | Jordan R, Dardick I, Lui E, Birek C - Journal of Oral Path Med, 23(5): 226-31 - May 1994 | May-94 | ||||
| The resultsŠare important in showing that data on DNA content, cell cycle, and nuclear limits useful in other neoplasms are of limited practical application in establishing predictors of time to recurrence or time to death in acinic cell carcinomas. | Acinic cell carcinoma of salivary glands: Prognostic relevance of DNA flow cytomtry and nucleolar organizer regions. | Arch Otolaryngol Head Neck Surg; 120(7): 727-33 | 1994 | |||||
| Pathology of Edgar's Biopsy - Acinic Cell Carcinoma, Metastatic Site Anterior to Ear, 1993: No detailed report available. | Aug-93 | |||||||
| Pathology of Edgar's Biopsy - Acinic Cell Carcinoma, Metastatic Pelvic Site, 1993: No detailed report available. | Apr-93 | |||||||
| Basic Characteristics: Acinic Cell carcinomas are usually well differentiated and account for about 13% of the cancers arising in the parotid glands. Lymph node metastases occurs in about 16% of cases. Local recurrences and distant metastases many years after treatment are common. | Adenoid Cystic Carcinoma (Cylindromas) account for approx. 12% of parotid gland cancers... Although these tumors often follow an indolent course, as many as 40% of patients ultimately develop regional and/or distant metastases. | Neoplasms of the Head and Neck; Salivary Gland | Cancer Medicine, 3rd Edition - Holland, Frei III, Bast Jr., Kufe, Morton, Weichselbaum; pp 1240-1242 | Jun-09 | ||||
| Immunoreactivity of proliferating cell
nuclear antigen (PCNA) was assessed to evaluate growth potential in
surgically resected tissue specimens from 70 cases of benign and malignant salivary gland tumours. Three stage streptavidin-biotin immunoperoxidase immunostaining using monoclonal antibody to PCNA showed a heterogeneity of PCNA index and distribution. In normal salivary gland specimens, PCNA was demonstrated in the nuclei of few ductal and acinar cells. In pleomorphic adenoma a multiple nodular growth pattern was observed with positive immunoreactivity restricted to the nuclei of tubulo-ductal structures. Warthin's tumour had positive nuclei in the outer cuboidal cells of epithelial component and germinal centres of lymphoid tissue. Myoepithelioma and acinic cell carcinoma showed slightly differing values and a statistically significant difference in the value of the index was observed in tumour cell aggregates of the cribiform type of adenoid cystic carcinoma and the solid undifferentiated type and between low/ interme-diate and high-grade mucoepidermoid tumours.(more to rt.) |
Myoepithelioma (cont'd from left) PCNA is a useful marker of tumour cell proliferation; the index correlates with the grade of malignancy in salivary gland tumours. | Immunoreactivity of proliferating cell nuclear antigen in salivary gland tumours: an assessment of growth potential. | Yang L, Hashimura K, Qin C, et al - Virchows Arch A Pathol Anat Histopathol, 422(6): 481-6 | 1993 | ||||
| Primary malignant tumors in the salivary glands are rare. The most frequent sites of distant metastases were in the lungs, bones, central nervous system, and mediastinum. The time until development of recurrence was longest for patients with acinic cell carcinomas. Although almost half of the patients with acinic cell... had tumors with local extension, none had high grade malignancy, and these patients showed the best 10-year corrected survival. Average months to recurrence: 53. | Malignant Parotid Tumors in 110 Consecutive Patients: Treatment Results and Prognosis | Pedersen D, Overgaard J, et al - Laryngoscope 102 ; 1064-1069 | Sept. -1992 | |||||
| Eight cases of acinic cell carcinoma of
the salivary glands were histologically reclassified and
their immunohistochemical expression and distribution for various tissue
antigens were examined. The epithelial elements were divided into
tubuloglandular components, microcystic patterns and solid nests. The
authors' results indicated the following: 1) The
duct luminal cells of tubuloglandular components have distinct epithelial
features with cytokeratin (KL 1), alpha 1-antichymotrypsin (alpha 1-ACT),
transferrin, lactoferrin, IgA, and carcinoembryonic antigen (CEA) positivity.
2) The cyst-lining cells of microcystic pattern expressed immunophenotypes
similar to those of the duct luminal cells. 3) The acinic cells in solid
nests had positive results for KL 1, alpha 1-antitrypsin (alpha 1-AT),
transferrin, lactoferrin and vasoactive intestinal polypeptide (VIP). 4) The
clear cells in solid areas had positive results for KL 1, alpha 1-AT,
transferrin and VIP. (more below) |
Distribution of tissue markers in acinic cell carcinomas of salivary gland. | Pathol Res Pract 1992 Aug;188(6):692-700- Takahashi
H, Fujita S, Okabe H, Tsuda N, Tezuka F |
Aug-92 | |||||
| (cont'd from above)
Both the clear cells and the neoplastic acinic cells showed
a rather similar pattern of immunoreactivity. Therefore, the clear cells may
transform from the neoplastic acinic cells. 5) Secretory products in
tubuloglandular and microcystic patterns had positive results for alpha
1-ACT, lactoferrin, IgA and CEA. 6) The basement membrane-like material
between the neoplastic islands has distinct positivity for alpha 1-AT. The
result suggests that alpha 1-AT is a useful marker of basement membrane-like
material. |
Distribution of tissue markers in acinic cell carcinomas of salivary gland. | Pathol Res Pract 1992 Aug;188(6):692-700- Takahashi
H, Fujita S, Okabe H, Tsuda N, Tezuka F |
Aug-92 | |||||
| All tumors were classified according to the criteria of Abrams et al. As solid, microcystic, papillary-cystic and follicular. The cytological pattern of the tumor was classified as acinic, intercalated-duct, clear, vacuolated and non-specific-glandular, depending on the predominant neoplastic cell type. The tumor was considered aneuploid when the majority of cells had a DNA index above or below 2c or if there was dispersion of values, none of the peaks having more than 20% of the cells. The results obtained by means of cytophotometry DNA analysis of the six cases evaluated, showed a typical 'diploid' distribution. In the present series we verified a high local recurrence rate, which contrasts with most of the published results... Metastases are infrequent... The occurence of secondary deposits seems to be related to the incapacity to control the disease locally and with the number of recurrences. The low aggressiveness of this tumor is apparent from the indolent course of the metastases. | Acinic Cell Carcinoma of the Salivary Glands. A Long-Term follow-up study of `15 cases | Oliveira P, Fonseca I, Soares J - European Journal of Surgical Oncology - 18: 7-15 | 1992 | |||||
| Fifty-one salivary gland tumours (23
pleomorphic adenomas, 5 Warthin's tumours, 12 mucoepidermoid carcinomas, 7
adenoid cystic carcinomas, 3 undifferentiated carcinomas and 1 acinic cell tumour) and 27 lung
carcinomas (18 squamous cell carcinomas) were analysed immunohistochemically
for the expression of p53 nuclear phosphoprotein. Eight out of 51 (16%)
salivary gland tumours were p53 positive... The results show that mutations of the p53 gene may be infrequent in salivary gland tumours when compared with lung carcinomas. The relatively indolent course of some histological types of malignant salivary gland tumours could be associated with the preservation of the non-mutated p53 gene in most of these tumours. |
Low p53 protein expression in salivary gland tumours compared with lung carcinomas | Soini Y, Kamel D, Nuorva K, Lane DP, Vahakangas K, Paakko P (Department of Pathology, University of Oulu, Finland) - Virchows Arch A Pathol Anat Histopathol 1992;421(5):415-20 | 1992 | |||||
| A study was made on the effects of long-term dietary administration of beta-carotene, vitamin C, vitamin E and selenium, either alone or in combination, on azaserine-induced pancreatic carcinogenesis in rats. Rats maintained on a diet high in either beta-carotene, vitamin C or selenium developed significantly less atypical acinar cells nodules, adenomas and carcinomas as compared to controls. The number of tumour-bearing animals was significantly lower in the groups fed the diet high in beta-carotene or selenium. In animals of the group given a diet high in all micronutrients investigated, both the number and incidence of pancreatic tumours was lower than in all other groups. It was concluded that selenium, beta-carotene and vitamin C, alone as well as in combination, have an inhibitory effect on pancreatic carcinogenesis induced in rats by azaserine. | pancreatic Acinic/Acinar Cell tested specifically | Inhibitory effects of micronutrients on pancreatic carcinogenesis in azaserine-treated rats. | Appel MJ, Roverts G, Woutersen RA - Department of Biological Toxicology, TNO Toxicology and Nutrition Institute, Zeist, The Netherlands. - Carcinogenesis 1991 Nov;12(11):2157-61 | Nov-91 | Take those vitamins! | |||
| The findings of this study indicate that the protein product of the c-erbB-2 proto-oncogene is infrequently expressed in salivary gland tumors, and when it is localized on the tumor cell surface membrane, there is no clear evidence that this determines the biological behaiour of the tumour. (Positive staining, as defined in previous studies, was present in five tumours; three cases of poorly differentiated adenocarcinoma, one mucoepidrmoid carcinoma, and one adenoid cystic carcinoma.) | Some other salivary gland tumours. | Expression of c-erbB-2 Oncoprotein in Salivary Gland Tumours: An immunohistochemical Study | Kernohan NM, Blessing K, King G, Corbett IP, Miller ID - J Pathol 1991 Jan; 163(1): 77-80 | Jan-91 | ||||
| Acinic Cell tumours, adenocarcinomas, mucoepidermoid tumours and squamous cell carcinomas (for comparison taken from other regions in the head and neck area) presented a clear destruction of the basal membrane as visualized by antibodies against collagen IV and laminin. | adenocarcinomas, mucoepidermoid tumours and squamous cell carcinomas (?) | Basal Membrane associated substances in human salivary glands and salivary gland tumours. | J Craniomaxillofac Surg; 19(6): 260-6 | 1991 | ||||
| Vitamin B12 R-binder, a specific binding protein for vitamin B12, was studied immunohistochemically in normal and 106 neoplastic salivary gland tissues with a monoclonal antibody against vitamin B12 R-binder (R-binder). In normal salivary glands, R-binder localization was restricted to the ductal systems and to mucous acinar cells; serous acinar cells, myoepithelial cells and stromal connective tissues were consistently negative. Among salivary gland tumors, R-binder was present in 87% of pleomorphic adenomas, 100% of monomorphic adenomas, and 40% of adenoid cystic carcinomas; positivity was observed only on luminal surfaces of small ductular elements, indicating that the components closely related to ductal differentiation were rather small in population. R-binder could be detected both in lacunar and non-lacunar cells within chondroid areas of pleomorphic adenomas, suggesting the possibility that chondroid regions arise from metaplastic changes in ductal epithelial cells. In mucoepidermoid tumors, mucous cells and focal squamous cells exhibited cytoplasmic staining. (more below) | Immunohistochemical localization of vitamin B12 R-binder in salivary gland tumors. Implications for cell differentiation. | Ogawa K, Ogawa O, Koshiba M, Sugiyama T, Wakatsuki Y, Kudo H, Kim YC, Nakashima Y, Yamabe H - Department of Pathology, Faculty of Medicine, Kyoto University, Japan - Pathol Res Pract 1990 Dec;186(6):751-8 | Dec-90 | |||||
| (cont'd): The staining pattern for R-binder in epithelial components of adenolymphomas showed close similarities to those found in normal large excretory ducts. Two acinic cell tumors and one case each of myoepithelioma and malignant myoepithelioma exhibited negative reactivity for R-binder, showing that these neoplasms are solely composed of tumor cells without the characteristics of ductular differentiation. Theimmunohistochemical examination of salivary gland tumors, employing a monoclonal anti-R-binder antibody, may have some implications for cellular heterogeneity and differentiation in various tumors. | myoepithelioma and malignant myoepithelioma | Immunohistochemical localization of vitamin B12 R-binder in salivary gland tumors. Implications for cell differentiation. | Ogawa K, Ogawa O, Koshiba M, Sugiyama T, Wakatsuki Y, Kudo H, Kim YC, Nakashima Y, Yamabe H - Department of Pathology, Faculty of Medicine, Kyoto University, Japan - Pathol Res Pract 1990 Dec;186(6):751-8 | Dec-90 | ||||
| Acinic cell carcinomas display varied cytoarchitectural patterns of growth that should allow for formulation of histopathologic grading. Grading of these carcinomas may serve to identify subsets whose biologic behavior is more aggressive than the usually accepted low-grade behavior of acinic cell carcinomas as a group. To that end, a three-level histopathologic grading scheme is presented. | Histopathologic grading of salivary gland neoplasms: II. Acinic cell carcinomas | Author: Batsakis JG; Luna MA; el-Naggar AK - Ann OtolRhinol Laryngol | Nov-90 | |||||
| Basic Histology - Consists of 2 cell types; granulated secretory cells and precursor duct cells. ENTER MORE INFO. FROM THIS SOURCE | Batsakis JG, et al. - Annals of Otology, Rhinology & Laryngology 99:929 | 1990 | Have to get full text from library, it seems. | |||||
| Dietary influences on carcinogenesis have
been shown in various tissues on the basis of epidemiological and
experimental approaches. The
present paper demonstrates that the oral application of fructose over long
periods to rats previously treated with N-nitrosomorpholine increases the
incidence of atypical acinar cell nodules (AACN) in the pancreas. Whereas an increase in AACN was statistically significant (P
less than 0.005), no effect on ductule-like structures was detectable. AACN
have been regarded as precursor lesions of the acinar cell carcinoma.
Although the AACN observed frequently exhibited severe atypia and numerous
mitotic figures, no clearcut evidence for malignancy could be detected under
our experimental conditions. |
Dietary fructose enhances the development of atypical acinar cell nodules in the pancreas of rats pretreated with N-nitrosomorpholine | Enzmann H Dettler T Ohlhauser D Stumpf H Bannasch P - Arch-Geschwulstforsch. 1990; 60(4): 283-7 1990 0003-911X | 1990 | Fructose no good? | ||||
| Fifteen acinic cell carcinomas from an
equal number of patients were analysed for their DNA content and
proliferative (S-phase) index by flow cytometry from archival tissues. Seven of the carcinomas manifested a diploid DNA content. None of the patients with diploid acinic cell carcinomas died of their carcinomas and none developed metastases in follow-up periods extending for 10 or more years. Four of eight patients with aneuploid acinic cell carcinomas have died because of their malignancies within a 10 year period after the first surgical removal of the carcinoma. Five of the eight patients exhibited metastases. Although the number of cases does not permit strong correlations between histopathological features, abnormalities in DNA content and outcome of patients, it was noted that carcinomas with prominent necrosis, tubuloductal differentiation and 'dedifferentiated' areas displayed more aggressive biological courses. |
DNA flow cytometry of acinic cell carcinomas of major salivary glands. |
el-Naggar AK, Batsakis JG, Luna MA, McLemore D,
Byers RM. Department of Pathology, University of Texas MD Anderson Cancer Center, Houston. J Laryngol Otol 1990 May;104(5):410-6 |
May-90 | GET FULL TEXT | ||||
| Acinic cell carcinomas of the Salivary Gland Registry, Institute of Pathology, University of Hamburg, West Germany, from 1965 to 1980 (n = 55) were evaluated retrospectively with respect to histologic, cytophotometric, and clinical data. The majority of the tumors (92.8%) were located in the parotid gland. Two thirds of the patients were female; one third were male. Mean age at primary diagnosis was 55.4 years. The tumors were graded into highly differentiated (76%) or less differentiated forms (24%) according to classic histologic and cytologic criteria. The clinical course was characterized by no recurrence in 15 cases; in 17 cases, recurrences developed, and 12 patients died of their tumor, some as late as 240 months after primary diagnosis. Differentiation showed a weak correlation with the clinical course. (more below) | Acinic cell carcinoma of the salivary glands: the
prognostic relevance of DNA cytophotometry in a retrospective study of long
duration (1965-1987). |
Hamper K, Mausch HE, Caselitz J, Arps H, Berger J,
Askensten U, Auer G, Seifert G. Institute of Pathology, University-Hospital Hamburg-Eppendorf, West Germany. Oral Surg Oral Med Oral Pathol 1990 Jan;69(1):68-75 |
Jan. 1990 | GET FULL TEXT | ||||
| (cont'd) In 35 cases, nuclear DNA content of tumor cells was assessed cytochemically. The tumors were "diploid" or "near-diploid" in 34 cases; DNA content showed no correlation to the clinical course. As a result of long-term follow-up, it becomes evident that acinic cell carcinoma is prone to develop recurrences and metastases. Complete tumor removal during the primary operation seems to be important for controlling the disease inasmuch as the ostensible prognostic predictors evaluated here proved to be unreliable. |
Acinic cell carcinoma of the salivary glands: the
prognostic relevance of DNA cytophotometry in a retrospective study of long
duration (1965-1987). |
Hamper K, Mausch HE, Caselitz J, Arps H, Berger J,
Askensten U, Auer G, Seifert G. Institute of Pathology, University-Hospital Hamburg-Eppendorf, West Germany. Oral Surg Oral Med Oral Pathol 1990 Jan;69(1):68-75 |
Jan. 1990 | GET FULL TEXT | ||||
| Basic Characteristics: Acinic Cell Tumors are typically slow-growing,low-grade neoplasms that appear in all age groups and are most common in women. They wil recur after inadequate removal, sometimes as long as 25 to 30 years after initial treatment. Metastases occur in a small precentage of cases, but cannot be predicted by the histologic picture. | Adenoid Cystic Carcinoma is uncommon in the major salivary glands. It varies in growth rate from slow to fast. Metastases to regional lymph nodes and distant sites occur; perineural involvement is characteristic; and recurrences may appear many years after initial treatment. | Cancer of the Head and Neck | Cancer; Principles and Practice of Oncology ; DeVita VT, Hellman S, Rosenberg SA - pp 574-590 | 1989 | ||||
| The distribution of various tissue antigens was studied in mucoepidermoid carcinomas (n = 74) and acinic cell carcinomas (n = 38) by means of immunocytochemistry. Mucoepidermoid carcinomas were generally positive for cytokeratin and showed double expression for cytokeratin and vimentin in 31.1% and triple expression for cytokeratin, vimentin and GFAP in 24.1%. CEA was studied using new monoclonal antibodies which distinguish between epitopes that are present on CEA alone and those which are present on nonspecific cross reacting antigens as well. The monospecific CEA antibody was completely negative in mucoepidermoid carcinomas, while nonspecific cross reacting antigens (NCAs) were positive in mucoepidermoid carcinomas to a varying degree. Alpha 1-antichymotrypsin, a marker formerly thought to be specific for tissues for histiocytic origin, was positive in 85.1% of mucoepidermoid carcinomas. Twenty three percent of mucoepidermoid carcinomas showed focal infiltration by S-100 positive dendritic stromal cells, tumour cell being negative. (more below) | Mucoepidermoid carcinoma showed similarities to acinic cell carcinoma, with a number of tissue antigens, including: cytokeratin, vimentin, NCAs, alpha 1-antichymotrypsin, and others. | Multiple expression of tissue markers in mucoepidermoid carcinomas and acinic cell carcinomas of the salivary glands. | Virchows Arch A Pathol Anat Histopathol 1989;414(5):407-13 - Hamper K, Schmitz-Watjen W, Mausch HE, Caselitz J, Seifert G | 1989 | ||||
| (cont'd from above) Leu-M1 antigen was positive in 58.1% of mucoepidermoid carcinomas. Acinic cell carcinomas were generally positive for cytokeratin and in single cases showed double expression for cytokeratin and vimentin and triple expression for cytokeratin, vimentin and GFAP. Monospecific CEA antibody positivity could be demonstrated in 24.2% of acinic cell carcinoma, while nonspecific cross reacting antigens (NCAs) were positive in acinic cell carcinomas to a varying degree. Alpha 1-antichymotrypsin was positive in 97.4% of acinic cell carcinomas. 2.5% of acinic cell carcinomas showed focal infiltration by S-100 positive dendritic stromal cells, 2.5% of acinic cell carcinomas were positive for S-100 protein with no dendritic stromal cells present. Leu-M1 antigen was positive in 86.8% of acinic cell carcinomas. For S-100 protein and Leu-M1, no correlation with the clinical course, as reported previously for other tumours, could be observed. | Mucoepidermoid carcinoma showed similarities to acinic cell carcinoma, with a number of tissue antigens, including: cytokeratin, vimentin, NCAs, alpha 1-antichymotrypsin, and others. | Multiple expression of tissue markers in mucoepidermoid carcinomas and acinic cell carcinomas of the salivary glands. | Virchows Arch A Pathol Anat Histopathol 1989;414(5):407-13 - Hamper K, Schmitz-Watjen W, Mausch HE, Caselitz J, Seifert G | 1989 | ||||
| Basic Characteristics: Acinic (Acinous) cell carcinoma is a well-differentiated tumor accounting for 13% of all malignancies of the parotid glands, and is rarely seen in other salivary tissues. This carcinoma ranks only behind Warthin's tumor in its frequency of bilateral parotid gland involvement, which is seen in approximately 3% of of these patients. Multinodularity seen in primary lesions is felt to represent multifocal origin. Lymph node metastases occur in only 16% of patients. It has been demonstrated by several investigators that recurrences as well as metastases in this tumor may occur may years later. | Tumors of the Major and Minor Salivary Glands | McNeese,MD, Fletcher GH | 1989 | |||||
| Human salivary gland tissue was analysed with respect to the distribution of basal membrane associated substances... Acinic Cell tumors, adenocarcinomas, mucoepidermoid tumors and squamous cell carcinomas (for comparison taken from other regions in the head and neck area) presented a clear destruction of the basal membrane as visualized by antibodies against collagen IV and laminin. | adenocarcinomas, mucoepidermoid tumors and squamous cell carcinomas | Basal Membrane associated substances in human salivary glands and salivary gland tumours. | Caselitz J, Schmitt P, Seifert G, Wustrow J Schuppan D - Pathol Res Pract, 183(4):386-94, Aug. 1988 | Aug-88 | ||||
| A monoclonal antibody to HLA-DR antigens
that is reactive in formalin-fixed tissues was used with the immunoperoxidase
method to evaluate 212 salivary gland lesions (normal, nonspecific, and
autoimmune inflammatory, benign, and malignant tumors). Results of
immunostaining showed that (1) intercalated ducts,
myoepithelial cells, and acinous cells of normal salivary glands express
HLA-DR antigens, (2) autoimmune salivary gland disease results in greater
HLA-DR expression than that seen in nonspecific
inflammatory lesions or normal glands, (3) stromal cells associated with
benign and malignant salivary gland tumors express HLA-DR antigens, and (4)
numerous benign and malignant salivary gland tumors express HLA-DR antigens.
It was of interest that lymphocyte-rich Warthin's tumors displayed epithelial
immunoreactivity, whereas oncocytomas devoid of a lymphocytic component were
invariably negative. This suggests a lymphocyte-mediated role in salivary
epithelial HLA-DR expression. (more below) |
intercalated ducts, myoepithelial cells |
HLA-DR antigens in normal, inflammatory, and neoplastic salivary glands. | Zarbo RJ; Regezi JA; Lloyd RV; Crissman JD; Batsakis JG Nov. 1987 | Nov. 1987 | ||||
| (cont'd.) It appears
that HLA-DR expression is both a normal and an inducible phenomenon in
salivary glands, salivary gland neoplasia, and the desmoplastic host
response. There is no discriminatory role in the immunologic detection of
HLA-DR for differential diagnosis of salivary gland tumors. |
intercalated ducts, myoepithelial cells |
HLA-DR antigens in normal, inflammatory, and neoplastic salivary glands. | Zarbo RJ; Regezi JA; Lloyd RV; Crissman JD; Batsakis JG Nov. 1987 | Nov. 1987 | ||||
| Acinic Cell Carcinomas, in some instances, contain a component of intercalated duct cells. However, the manner in which this element is integrated within the more obvious acinar cells, as well as the role neoplastic intercalated duct cells play in determining morphologic patterns in acinic cell tumours, has not been fully investigated. Ultrastructural study and immuno- staining with antibodies to cytokeratins and to S-100 protein carried out in 9 cases of parotid acinic cell carcinoma suggest two basic differentiation patterns. In three cases, the lesions were essentially composed of acinar cells (with variation in the number and form of secretory granules), and one of these tumours was unique in having ultrastructural evidence of differentiated myoepithelial cells. In the second group of six cases, there was light microscopic, ultra- structural, and immunohistochemical evidence of a significant component of intercalated duct cells. By means of immuno- staining (intercalated ducts were positive for keratin and S-100 protein; acinar cells were negative for both antigens) (more below) | Ultrastructural Morphology and Cellular Differentiation in Acinic Cell Carcinoma | Oral Surg Oral Med Oral Pathol; 63(3); 325-34 | 1987 | |||||
| (cont'd): and electron microscopy, flattened-to-cuboidal intercalated duct cells were noted to enclose and, presumably, to be involved in the formation of microcystic spaces. Acinic cell carcinomas with a more solid growth pattern contained groups of intercalated duct cells positive for keratin and S-100 protein. Ultrastructurally, these cells were organised into well-formed ducts related to nests of acinar cells. Acinic cell carcinoma is another class of salivary tumor in which there can be an integrated proliferation of intercalated duct and acinar cells and, infrequently, of myoepithelial cells, all organised in a simulation of the intercalated duct-acinar unit of the normal salivary gland. | Ultrastructural Morphology and Cellular Differentiation in Acinic Cell Carcinoma | Oral Surg Oral Med Oral Pathol; 63(3); 325-34 | 1987 | |||||
| The regulation of cholesterol
esterification during cell proliferation was studied. The serum free
cholesterol, cholesterol esters and lecithin: cholesterol acyltransferase (
LCAT) activity of nude mice with and without pancreatic acinar cell tumours
and rats with proliferating tissues were determined. In
addition, the apparent activity of acyl-CoA: cholesterol acyltransferase
(ACAT) in homogenates of nude mouse tumours and proliferating rat tissues
were determined and compared with those of normal nude mouse and rat tissues.
Serum cholesterol ester levels were significantly
lower in host nude mice with tumours and in rats
with regenerating liver, and increased significantly in pregnant rats when
compared with respective controls. Circulating LCAT activity levels decreased
in host nude mice, in pregnant rats, and in rats with regenerating pancreas
and regenerating liver. Apparent ACAT activity levels increased significantly in nude mouse tumours and in foetal and postnatal rat pancreata and also in postnatal liver. (more to right) |
(cont'd from left) At the same time, apparent ACAT activity levels decreased in foetal and regenerating rat livers when compared with respective control tissues. These results suggest that serum cholesterol esters, circulating LCAT and cellular ACAT levels are modulated during cell proliferation. | Acinar cell carcinoma of rat pancreas: regulation of cholesterol esterification | Rao KN Kottapally S Eskander ED Shinozuka H Dessi S
Pani P - Journal: Br-J-Cancer. 1986 Aug; 54(2): 305-10 1986 0007-0920 |
1986 | ||||
| Basic Characteristics: Acinic Cell Carcinomas develop slowly and occur almost exclusively in the parotid gland. There are four histologic types: solid, microsyctic, papillary cystic, and follicular. They made up 13% of 296 malignant salivary gland tumors in Blanck's series. Electron microscopy studies have shown a similarity between the Acinic carcinoma cell and serous acinar cell. | Serous Acinar Cell | Accessory Organs; Salivary Glands | Ackerman and Del Regato's Cancer; Diagnosis, Treatment and Prognosis | 1985 | ||||
| Acinic Cell Carcinomas, adenoid cystic carcinomas and low-grade mucoepidermoid carcinomas were excluded from study (of high grade malignancies of the parotid gland) because of their different biologic behavior. | Acinic Cell Carcinomas, adenoid cystic carcinomas and low-grade mucoepidermoid carcinomas | High Grade Malignancies of the Parotid Gland: Effective Use of Planned Combined Surgery and Irradiation | Laryngoscope; 95(9 pt. 1): 1059-63 | 1985 | ||||
| Basic Characteristics: (selected) It accounts for up to 5% of all parotid gland tumors and 15% of all parotid malignancies. The histogenesis...is not entirely certain. However, it probably arises from the acinar cells or the cells of the terminal tubule or intercalated ducts. The appearance is of normal salivary gland serous cells, containing secretory granules as well as ductlike structure that have clear cytoplasm. Recurrence may occur in up to half of patients, and tends to be local and multiple. Hematogenous spread may be noted in preterminal and long-standing cases with lung, liver, bone, and brain involved. ...larger tumors also appeared to be rapidly growing. | Diagnosis and Management of Head and Neck Neoplasia | Head and Neck Management of the Cancer Patient - pp. 218-229 | 1985 | |||||
| A retrospective chart review study was conducted on 498 patients with histopathologically confirmed carcinoma of the major salivary glands to ascertain the potential risk factors and to abstract the clinicopathologic and survival data. The distribution of histologic classification varied by race, sex, and history of benign salivary gland lesion (37 patients). Of the 57 patients who had a history of radiation exposure, 49 patients had been irradiated in a field encompassing the salivary gland area. Sixty-six patients had had a prior primary cancer. Of 43 instances of previous skin cancer, 37 occurred in male patients. The rationale for a possible relationship between cutaneous neoplasms and salivary carcinoma is explained embryologically and histogenetically. Tumor histology, anatomic site, race, and sex were important predictors of survival. | Major salivary gland carcinoma. Descriptive epidemiology and survival of 498 patients. | Arch Otolaryngol; 110(1):45-9 1984 UI: 84079177 - Spitz MR, Batsakis JG | 1984 | |||||
| Pathology of Edgar's Biopsy - Primary Site, 8/84, REPORT #1 OF 2: The neoplasm consists of
sheets of cells with abundant cytoplasm containing basophilic granules.
Nucei are uniform and round with occasional macronuclei. Scattered small
vessels are present within the neoplasm. Tumor cells and tumor cell nuclei
form linear arrays along these vessels. The tumor is focally present within
blood vessels. No mitoses are seen. Portions of the neoplasm contain
microcystic spaces. Occasional tumor cells have vacuolated or clear cytoplasm.
Small islands of tumor cells are focally present within the pseudo capsule
but it has not been definitively penetrated in the examined sections. PAS
positive diastase resistant cytoplasmic granular material is present in tumor
cells. These findings are compatible with an acinic cell adenocarcinoma of
the parotid gland, with a predominant microcystic and subordinate solid
pattern of growth. (more) |
Tumors of this size with intravascular invasion have been said to have a poorer prognosis | Pathologist: L. Thanning, M.D. / M. Mitchell, M.D. - SUNY at Stony Brook | 8/7/84 | |||||
| (cont'd.) The acinic cell type predominates. Review of the parotid biopsy (Specimen A) shows polygonal cells with granular cytoplasm. Although eosinophilic on frozen section, the permanent section of the specimen is basophilic and diagnostic of acinic cell carcinoma. | Pathologist: L. Thanning, M.D. / M. Mitchell, M.D. - SUNY at Stony Brook | 8/7/84 | ||||||
| Pathology of Edgar's Biopsy - Primary Site, 8/84, REPORT #2 OF 2: MICRO: Survey sections
for light microscopy are cut from 6 blocks, they reveal a tumor consisting of
large nests and perforated sheets of polygonal cells, with round central
nuclei. The cytoplasm is deeply staining. Some of the spaces in the nests
are filled with pale staining material and others are optically clear. No
ducts are recognized. Two representative areas are selected for electron microscopy. They are examined in order to determine whether the cells show features of secretory cell differentiation. At the ultrastructural level, the tumor cell nests rest on a delicate basal lamina. The cells are rich in mitochondria but contain large numbers of secretory granules as well. The secretory granules vary in size and shape. Some are small and dense, and others are large with lucent more granular matrix. Virtually all cells contain granules, although some cells have very large accumulation in one portion of the cytoplasm. (more) |
Pathologist: Bernard P. Lane, M.D. - SUNY at Stony Brook | 8/7/84 | ||||||
| The microcystic spaces within the cell
nests vary in content from faintly particulate to densely particulate with
visible secretory granules. These spaces are true glandular lumens
delineated by junctional complexes. Some cells which form the lumen are rich
in granules. Although there are others which have few or none. DIAGNOSIS:
Parotid gland tumor with ultrastructural features of acinic cell
adenocarcinoma. NOTE: This tumor corresponds to that described by Erlandson
and Tandler (Ultrastructural of acinic cell carcinoma of the parotid gland -
Arch Pathol 93: 130-140, 1972). They suggest that the tumor consists of 2
cell types; granulated secretory cells and precursor duct cells. |
Pathologist: , Bernard P. Lane, M.D. - SUNY at Stony Brook | 8/7/84 | ||||||
| Basic Histology - ENTER MORE INFO. FROM THIS SOURCE | Ellis et al. Cancer 52: 542-549 | 1983 | Article in Acinic Cell Binder - Med Research VI | |||||
| Substances with "marker" characteristics for tumors were studied in parotid gland neoplasms. The substances included intermediate-sized filaments, oncofetal and proliferation antigens, metalloproteins, antigens related to the blood group system, and enzymes and other cellular products. The immunoperoxidase technique was applied on the following kind of tissues: normal parotid glands, Morbus Sjogren, cystadenolymphomas, pleomorphic adenomas, adenocarcinomas, adenoid cystic carcinomas, salivary duct carcinomas, mucoepidermoid tumors, squamous cell carcinomas, and anaplastic carcinomas. The intermediate-sized filaments of the prekeratin type were demonstrated in the ducts and myoepithelial cells of the normal parotid glands, and in the epithelial tumors, which all were vimentin negative. Carcinoembryonic antigen was found in squamous cell carcinomas and glandular differentiated tumors, whereas lactoferrin was detected only in a part of glandular tumors. Amylase was seen in acinic cell tumors. | Tumor markers in parotid gland carcinomas:
immunohistochemical investigations. |
Cancer Detect Prev 1983;6(1-2):119-30 - Seifert G,
Caselitz J |
1983 | |||||
| Adenoid Cystic Carcinoma has been an uncommon, slow-growing tumor characterized by multiple recurrences. Biologically, Adenoid Cystic Carcinoma is characterized by slow growth, with insidious involvement in local structures. | Adenoid Cystic Carcinoma | Adenoid cystic carcinoma of the salivary gland. Sustained complete response to chemotherapy. | Budd GT; Groppe CW - Cancer, 51(4):589-90 1983 Feb 15 | 1983 | ||||
| The group of tumour markers contain antigens and cell products which can be demonstrated in tumour cells by immunocytochemical methods (immunofluorescence, immunoperoxidase) and can, thus, be analysed for the classification of tumour. In human salivary gland tumours the distribution of cytoplasmatic antigens as components of the cytoskeleton, the occurrence of cell membrane antigens and of enzymatic cell products is demonstrated. Prekeratin, as an intermediate-sized filament protein, is a specific marker of epithelial tumours, whereas vimentin is a marker of mesenchymal cells. A special feature is the occurrence of prekeratin and vimentin in spindle-shaped cells of pleomorphic adenomas. The tumour-associated carcinoembryonic antigen (CEA) is found in glandular tumours and highly differentiated keratinized squamous cell carcinomas. With regard to enzymatic cell products, lactoferrin is present in glandular tumours and amylase in acinic cell tumours, but lysozyme is not detectable. The implementation of tumour markers contributes not only to an improvement in tumour diagnosis, but opens up new aspects in the cyto- and histogenesis of tumours. | other glandular tumors? | [Use of tumor markers in the diagnosis of salivary
gland tumors]. |
Wien Klin Wochenschr 1982 Jul 9;94(14):372-5 -
Seifert G |
Jul-82 | ||||
| In general, acinic cell carcinoma can be defined as a tumour of low-grade malignancy, though not too rarely it may recur and occasionally metastasize. - GET FULL TEXT | comparisons with and against other cancers - GET FULL TEXT | Acinic Cell Carcinoma of Minor salivary glands: | Histopathology; 4(3): 331-343 | 1980 | Get Full Text | |||
| Basic Histology - ENTER MORE INFO. FROM THIS SOURCE | Acinic Cell Carcinoma Arising in Salivary Glands - A Clinicopathologic Study | Perzin et al. - Cancer 44: 1434 | 1979 | Article in Acinic Cell Binder - Med Research VI | ||||
| Basic Histology - ENTER MORE INFO. FROM THIS SOURCE | Acinic Cell Carcinoma of Salivary Origin | Spiro R, et al. - Cancer 41:924 | 1978 | Article in Acinic Cell Binder - Med Research VI | ||||
| In untreated patients with small tumors, clinical findings usually suggested a benign mixed tumorŠ Survival was most directly influenced by the clinical extent of the primary tumor, and also correlated with certain histologic features which are described. (GET FULL TEXT) | Acinic cell carcinoma of salivary origin. A clinicopathologic study of 67 cases. |
Spiro RH, Huvos AG, Strong EW. Cancer 1978 Mar;41(3):924-35 Abstract |
Mar-78 | GET FULL TEXT | ||||
| In a series of patients drawn from the Birmingham Regional Cancer Registry (England) with tumours of the salivary glands, a significant excess of second primary tumours was observed. For females, the excess was found mainly in breast and bronchus and, for males, in prostate and skin. In a parallel series of female breast-cancer patients, the observed number of second primary tumours in salivary glands significantly exceeded expectation. These results support the reported association between salivary gland and breast cancer, and suggest that other hormone-dependent sites are also at risk. | Breast | Second primary cancers in patients with tumours of the salivary glands. | Prior P; Waterhouse JA Br J Cancer, 36(3): 362-8 Sept. 1977 | Sep-77 | ||||
| The ultrastructure of an acinic cell
carcinoma, occurring in the left parotid gland of a 52-year-old woman and
causing a total facial nerve paralysis, is described. Histologically the tumour consisted of numerous granulated cells arranged around lumen-like openings and resembling a secretory system. Furthermore, areas with agranulated cells growing in a solid pattern were also encountered. In the electron microscope the cytoplasmic granules of the tumour cells displayed a varied appearance. Granules of a dense homogeneous type, as well as granules with a more electron lucid appearance were observed. Furthermore, numerous cytoplasmic granules displayed a bipartite structure with a dense central and a more electron lucid outer zone. In specimens primarily fixed in OSO4 or KMnO4 the granules displayed a 'leached out' appearance. (more below) |
Secretory breast carcinoma? | Some ultrastructural features of acinic cell carcinoma | Bloom GD, Carlsoo B, Henriksson R. - J Laryngol Otol 1977 Nov;91(11):947-958 | Nov. 1977 | ||||
(cont'd) The membrane-bounded of the tumour cells also showed a strong positive staining with the periodic acid-chromic silver technique of Rambourg et al. (1969). Other characteristic ultrastructural features of the tumour cells studied were: Smooth cell surfaces, the presence of subplasmalemmal bands of electron dense material, desmosome-like attachment areas between cells and grossly altered mitochondria. |
Some ultrastructural features of acinic cell carcinoma | Bloom GD, Carlsoo B, Henriksson R. - J Laryngol Otol 1977 Nov;91(11):947-958 | Nov. 1977 | |||||
| Basic Histology - Consists of 2 cell types; granulated secretory cells and precursor duct cells. | "Ultrastructural of acinic cell carcinoma of he parotid gland" | Erlandson and Tandler - Arch. Pathol 93: 130-140, 1972 | 1972 | |||||
| A thin but definite capsule could be made out, particularly in the primary tumors, from which connective tissue septa further subdivided the tumor, giving the neoplasm its characteristic lobulated appearance. On cut section, the color ranged from grayish white to reddish tan, with a glistening surface. The tumors were friable and occassionally cystic. On microscopic exam, the neoplastic tissue appeared to be made up almost entirely of well differentiated, rounded or polygonal epithelial cells with scanty stroma. In a typical tumor, the epithelial cells were in close contiguity to each other and frequently arranged into fairly well formed acini. Considerable variation from this pattern occurred. In some areas the epithelial cells formed gland-like structures, and in others a cystic papillary appearance dominated. The abundant, granular cytoplasm exhibited a strikingly basophilic cast. In two tumors the granularity was so pronounced as to suggest zymogenic granules. (more below) | Acinic Cell Carcinoma of the Parotid Gland: A Clinicopathologic Review of Eleven Cases | Grage TB, Lober PH, Arhelger SW - American Journal of Surgery, Vol. 102 Dec. 1961 | Dec. 1961 | |||||
| (cont'd) In other areas the cytoplasm of the epithelial cells was almost water clear. The nuclei were usually small, dark staining an in an eccentric position. However, in some tumors the nuclei were larger, but almost always of uniform size, and mitoses wre rarely seen. Throughout the tumor tissue numerous cellular spaces were noted, which frequently coalesced to form larger clear lareas... The strucural similarity of the neoplastic epithelial cells to the normal acinar cells of the parotid gland, the formation of acini the the tumors, and the absence of ductal elements point to the origin of this tumor from the serous cells of the parotid gland. This view is further supported by the cytochemical studies of Azzopardi and Smith, who found a striking correlation between the histochemical characteristics of the epithelial cells of an acinic cell carcinoma and the serous cells of the normal parotid gland. (more) | Acinic Cell Carcinoma of the Parotid Gland: A Clinicopathologic Review of Eleven Cases | Grage TB, Lober PH, Arhelger SW - American Journal of Surgery, Vol. 102 Dec. 1961 | Dec. 1961 | |||||
| (cont'd) The insidious nature of acinic cell carcinoma is well demonstrated by a 57 year old man who underwent excision of four discrete tumor nodules, which had been present for three years. The primary tumor had been excised thirty years previously, and the patient had been free of symptoms for twenty-seven years. In another patient, the time interval between excision and recurrence was nine years. | Acinic Cell Carcinoma of the Parotid Gland: A Clinicopathologic Review of Eleven Cases | Grage TB, Lober PH, Arhelger SW - American Journal of Surgery, Vol. 102 Dec. 1961 | Dec. 1961 |