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1. Park JW, Lee JK, Phillips JW, Huang P, Cheng D, Huang J, Witte ON: Prostate epithelial cell of origin determines cancer differentiation state in an organoid transformation assay. Proc Natl Acad Sci U S A; 2016 Apr 19;113(16):4482-7
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  • [Title] Prostate epithelial cell of origin determines cancer differentiation state in an organoid transformation assay.
  • The cell of origin for prostate cancer remains a subject of debate.
  • We found that c-Myc/myrAKT1-transduced luminal xenografts exhibited histological features of well-differentiated acinar adenocarcinoma, with strong androgen receptor (AR) and prostate-specific antigen (PSA) expression.
  • In contrast, c-Myc/myrAKT1-transduced basal xenografts were histologically more aggressive, with a loss of acinar structures and low/absent AR and PSA expression.
  • Our findings imply that distinct subtypes of prostate cancer may arise from luminal and basal epithelial cell types subjected to the same oncogenic insults.
  • Tumors derived in this fashion with defined genetics can be used in the preclinical development of targeted therapeutics.

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  • eScholarship, California Digital Library, University of California. Full text from University of California eScholarship .
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  • (PMID = 27044116.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA195505; United States / NCI NIH HHS / CA / R01 CA181242; United States / NCI NIH HHS / CA / U01 CA164188-01A; United States / NCI NIH HHS / CA / 1R01 CA181242-01A1; United States / NCI NIH HHS / CA / T32CA09056; United States / NCI NIH HHS / CA / U01 CA164188; United States / NCI NIH HHS / CA / 5R01 CA172603-02; United States / NCI NIH HHS / CA / P50 CA092131; United States / NCI NIH HHS / CA / P30 CA016042; United States / NCI NIH HHS / CA / T32 CA009056; United States / NCI NIH HHS / CA / 1R01 CA195505; United States / NCI NIH HHS / CA / 2P30 CA016042-39; United States / NCI NIH HHS / CA / R01 CA172603
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AR protein, human; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptors, Androgen; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.4.21.- / Kallikreins; EC 3.4.21.- / kallikrein-related peptidase 3, human; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Other-IDs] NLM/ PMC4843433
  • [Keywords] NOTNLM ; cancer differentiation / cells of origin / human prostate cancer / luminal cell / oragnoid culture
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2. Amin A, Epstein JI: Pathologic stage of prostatic ductal adenocarcinoma at radical prostatectomy: effect of percentage of the ductal component and associated grade of acinar adenocarcinoma. Am J Surg Pathol; 2011 Apr;35(4):615-9
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  • [Title] Pathologic stage of prostatic ductal adenocarcinoma at radical prostatectomy: effect of percentage of the ductal component and associated grade of acinar adenocarcinoma.
  • It is unknown whether ductal adenocarcinomas are more aggressive when matched for Gleason score (assigning the ductal component as Gleason pattern 4).
  • Of 18,552 radical prostatectomies performed from 1995 to 2008, 93 cases with a ductal adenocarcinoma component were identified.
  • Cases were classified based on their ductal/acinar ratio (<10%; ≥10% and <50%; ≥50%).
  • There was no difference in the distribution of Gleason score 3+4=7 versus 4+3=7 between ductal and nonductal tumors, such that cases were combined as Gleason score 7.
  • There was no age, race, and serum prostate-specific antigen difference between patients with and without ductal adenocarcinoma.
  • Cases with ductal adenocarcinoma were less likely to be organ confined (36.6% vs 65.6%) and more likely to show seminal vesicle invasion (SVI) (19.3% vs 5.3%), P<0.0001.
  • In this group, there was no statistically significant difference in SVI or lymph node involvement between Gleason score 7 ductal and nonductal tumors.
  • This study shows that ductal adenocarcinoma admixed with Gleason pattern 3 is more aggressive than Gleason score 7 acinar cancer, as long as the ductal component is ≥10%.
  • In addition, Gleason score 8 to 10 tumors with ductal features are not significantly more aggressive that acinar Gleason score 8 to 10 cancers in which the pure high-grade tumor, regardless of ductal features, determines the behavior.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Carcinoma, Ductal / secondary. Prostate / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 21383610.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS682077; NLM/ PMC4425125
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3. Basturk O, Hong SM, Wood LD, Adsay NV, Albores-Saavedra J, Biankin AV, Brosens LA, Fukushima N, Goggins M, Hruban RH, Kato Y, Klimstra DS, Klöppel G, Krasinskas A, Longnecker DS, Matthaei H, Offerhaus GJ, Shimizu M, Takaori K, Terris B, Yachida S, Esposito I, Furukawa T, Baltimore Consensus Meeting: A Revised Classification System and Recommendations From the Baltimore Consensus Meeting for Neoplastic Precursor Lesions in the Pancreas. Am J Surg Pathol; 2015 Dec;39(12):1730-41
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  • International experts met to discuss recent advances and to revise the 2004 recommendations for assessing and reporting precursor lesions to invasive carcinomas of the pancreas, including pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasm (IPMN), mucinous cystic neoplasm, and other lesions.
  • Thus, "high-grade dysplasia" is to be reserved for only the uppermost end of the spectrum ("carcinoma in situ"-type lesions). (2) Current data indicate that PanIN of any grade at a margin of a resected pancreas with invasive carcinoma does not have prognostic implications; the clinical significance of dysplasia at a margin in a resected pancreas with IPMN lacking invasive carcinoma remains to be determined. (3) Intraductal lesions 0.5 to 1 cm can be either large PanINs or small IPMNs.
  • The term "incipient IPMN" should be reserved for lesions in this size with intestinal or oncocytic papillae or GNAS mutations. (4) Measurement of the distance between an IPMN and invasive carcinoma and sampling of intervening tissue are recommended to assess concomitant versus associated status.
  • Conceptually, concomitant invasive carcinoma (in contrast with the "associated" group) ought to be genetically distinct from an IPMN elsewhere in the gland. (5) "Intraductal spread of invasive carcinoma" (aka, "colonization") is recommended to describe lesions of invasive carcinoma invading back into and extending along the ductal system, which may morphologically mimic high-grade PanIN or even IPMN. (6) "Simple mucinous cyst" is recommended to describe cysts >1 cm having gastric-type flat mucinous lining at most minimal atypia without ovarian-type stroma to distinguish them from IPMN. (7) Human lesions resembling the acinar to ductal metaplasia and atypical flat lesions of genetically engineered mouse models exist and may reflect an alternate pathway of carcinogenesis; however, their biological significance requires further study.
  • [MeSH-minor] Biopsy. Carcinoma in Situ / chemistry. Carcinoma in Situ / pathology. Carcinoma, Pancreatic Ductal / chemistry. Carcinoma, Pancreatic Ductal / pathology. Consensus. Cooperative Behavior. Humans. International Cooperation. Neoplasm Grading. Neoplasm Invasiveness. Neoplasms, Cystic, Mucinous, and Serous / chemistry. Neoplasms, Cystic, Mucinous, and Serous / pathology. Predictive Value of Tests. Tumor Burden

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  • (PMID = 26559377.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 103721; United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / P50 CA62924
  • [Publication-type] Consensus Development Conference; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS709550 [Available on 12/01/16]; NLM/ PMC4646710 [Available on 12/01/16]
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4. Yamada S, Nabeshima A, Noguchi H, Nawata A, Nishii H, Guo X, Wang KY, Hisaoka M, Nakayama T: Coincidence between malignant perivascular epithelioid cell tumor arising in the gastric serosa and lung adenocarcinoma. World J Gastroenterol; 2015 Jan 28;21(4):1349-56
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  • [Title] Coincidence between malignant perivascular epithelioid cell tumor arising in the gastric serosa and lung adenocarcinoma.
  • Since biopsy samples from the lung and abdomen revealed poorly differentiated adenocarcinoma and malignant tumor, clinicians first interpreted the abdominal mass as metastatic carcinoma, and a right lower lobectomy with following resection of the mass was performed.
  • On microscopic examination, the lung tumor was composed of a proliferation of highly atypical epithelial cells having abundant eosinophilic cytoplasm, predominantly arranged in an acinar or solid growth pattern with vessel permeation, while the abdominal tumor consisted of sheets or nests with markedly atypical epithelioid cells having pleomorphic nuclei and abundant eosinophilic to clear cytoplasm focally in a radial perivascular or infiltrative growth pattern.
  • Therefore, we finally made a diagnosis of malignant perivascular epithelioid cell tumor (PEComa) arising in the gastric serosa, combined with primary lung adenocarcinoma.
  • Furthermore, small papillary carcinoma of the thyroid gland was identified.
  • The current case describes the coincidence of malignant PEComa with other carcinomas, posing a challenge in distinction from metastatic tumor disease.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Neoplasms, Multiple Primary / pathology. Perivascular Epithelioid Cell Neoplasms / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Abdominal Pain / etiology. Adult. Back Pain / etiology. Biomarkers, Tumor / analysis. Biopsy. Carcinoma / pathology. Diagnosis, Differential. Gastrectomy. Humans. Immunohistochemistry. Male. Pneumonectomy. Predictive Value of Tests. Thyroid Neoplasms / pathology. Tomography, X-Ray Computed

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  • (PMID = 25632212.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; Adenocarcinoma of lung; Thyroid cancer, papillary
  • [Other-IDs] NLM/ PMC4306183
  • [Keywords] NOTNLM ; Gastric serosa / Lung adenocarcinoma / Malignant / Metastatic carcinoma / Perivascular epithelioid cell tumor
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5. Ghazy SE, Helmy IM, Baghdadi HM: Maspin and MCM2 immunoprofiling in salivary gland carcinomas. Diagn Pathol; 2011;6:89
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  • [Title] Maspin and MCM2 immunoprofiling in salivary gland carcinomas.
  • BACKGROUND: The pathogenesis of salivary gland carcinomas is very complex and prognostic markers are difficult to find in these carcinomas of which the different subtypes have varying malignant potential.
  • The study was conducted to examine the cellular distribution of maspin and MCM2 in salivary gland carcinomas and their value to predict lymph node metastasis.
  • MATERIALS AND METHODS: Fifty three paraffin blocks of different lesions (15 muco-epidermoid carcinoma, 14 adenoid cystic carcinoma, 3 epi-myoepithelial carcinoma, 5 salivary duct carcinoma, 5 malignant pleomorphic adenoma, 6 polymorphous low grade adenocarcinoma and 5 acinic cell carcinoma) were prepared for immunohistochemical staining with maspin and MCM2 antibodies.
  • RESULTS: All salivary gland carcinomas express maspin and MCM2 with variable cellular localization.
  • There was a significant difference in the expression of each antibody between mucoepidermoid carcinoma, adenoid cystic carcinoma and polymorphous low grade adenocarcinoma.
  • CONCLUSIONS: Salivary gland carcinomas express maspin and MCM2 with variable levels and cellular localization, consisting important markers of biological behavior in these tumors.
  • The level of MCM2 expression can be used in the differential diagnosis of adenoid cystic carcinoma and polymorphous low grade adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenoma, Pleomorphic / metabolism. Biomarkers, Tumor / analysis. Cell Cycle Proteins / analysis. Nuclear Proteins / analysis. Salivary Gland Neoplasms / metabolism. Serpins / analysis

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  • (PMID = 21943228.001).
  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Nuclear Proteins; 0 / SERPIN-B5; 0 / Serpins; EC 3.6.4.12 / MCM2 protein, human; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 2
  • [Other-IDs] NLM/ PMC3191357
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6. Canberk S, Onenerk M, Sayman E, Goret CC, Erkan M, Atasoy T, Kilicoglu GZ: Is DOG1 really useful in the diagnosis of salivary gland acinic cell carcinoma? - A DOG1 (clone K9) analysis in fine needle aspiration cell blocks and the review of the literature. Cytojournal; 2015;12:18
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  • [Title] Is DOG1 really useful in the diagnosis of salivary gland acinic cell carcinoma? - A DOG1 (clone K9) analysis in fine needle aspiration cell blocks and the review of the literature.
  • INTRODUCTION: DOG1 is a transmembrane protein originally "discovered on gastrointestinal stromal tumors," works as a calcium-activated chloride channel protein.
  • There is a limited number of studies on the potential usage of this antibody in the diagnosis of salivary gland tumors on routine practice in cell blocks.
  • The aim of this study was to search for the usefulness of K9 clone in oncocytic type tumors and review of the literature.
  • MATERIALS AND METHODS: Sixty-nine fine needle aspiration (FNA) cytologic materials of predominantly oncocytic morphology salivary gland tumors; acinic cell carcinoma (AciCC) (n = 8), adenoid cystic carcinoma (n = 2), pleomorphic adenoma (PA) (n = 22), Warthin tumor (WT) (n = 20), myoepithelioma (ME) (n = 5), benign oncocytoma (BeO) (n = 3), mucoepidermoid carcinoma (MEC) (n = 7), mammary analog salivary gland carcinoma (n = 2) were immunostained with DOG1 (clone K9) stain.
  • RESULTS: Of the 8 AciCCs, 7 were observed apical-luminal positive staining, demonstrating 1-3 + intensity, and involving 40-70% of the tumor cells.
  • One MEC of 7 (14%), 1 ME of 5 (20%), and 4 PA of 22 (18%) showed weak (1+) cytoplasmic granular staining in 5-10% of the tumor cells.
  • CONCLUSIONS: FNA is a common tool in the diagnosis and management of salivary gland tumors.
  • DOG1-K9 clone was very useful with a unique staining pattern of apical-luminal positivity in the differential diagnosis of AciCC from other oncocytic salivary gland tumors.

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  • (PMID = 26425134.001).
  • [ISSN] 1742-6413
  • [Journal-full-title] CytoJournal
  • [ISO-abbreviation] Cytojournal
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC4564987
  • [Keywords] NOTNLM ; Acinic cell carcinoma / DOG1 / clone K9 / fine needle aspiration biopsy / salivary gland
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7. Mohammadi A, Porghasem J, Esmaeili A, Ghasemi-Rad M: Spontaneous rupture of a pancreatic acinar cell carcinoma presenting as an acute abdomen. Int J Surg Case Rep; 2012;3(7):293-5
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  • [Title] Spontaneous rupture of a pancreatic acinar cell carcinoma presenting as an acute abdomen.
  • INTRODUCTION: Pancreatic acinar cell carcinoma is a rare malignant pancreatic neoplasm.
  • To the best of our knowledge, there has been no report on spontaneous rupture of acinar cell carcinoma.
  • Emergent abdominal operation was performed and histopathology revealed acinar cell carcinoma of the pancreas.
  • DISCUSSION: Pancreatic acinar cell carcinoma (ACC) usually presents with abdominal pain, nausea and vomiting.
  • CONCLUSION: Pancreatic carcinoma may present as acute abdomen due to rupture of underlying neoplasm.

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  • [Copyright] Crown Copyright © 2012. Published by Elsevier Ltd. All rights reserved.
  • (PMID = 22543229.001).
  • [ISSN] 2210-2612
  • [Journal-full-title] International journal of surgery case reports
  • [ISO-abbreviation] Int J Surg Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC3356555
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8. Gaujoux S, Tissier F, Ragazzon B, Rebours V, Saloustros E, Perlemoine K, Vincent-Dejean C, Meurette G, Cassagnau E, Dousset B, Bertagna X, Horvath A, Terris B, Carney JA, Stratakis CA, Bertherat J: Pancreatic ductal and acinar cell neoplasms in Carney complex: a possible new association. J Clin Endocrinol Metab; 2011 Nov;96(11):E1888-95
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  • [Title] Pancreatic ductal and acinar cell neoplasms in Carney complex: a possible new association.
  • CONTEXT: Carney complex (CNC) is a rare disease inherited as an autosomal dominant trait, associated with various tumors, and caused most frequently by inactivation of the PRKAR1A gene.
  • This possible association and PRKAR1A's possible involvement in pancreatic tumor have not been reported previously.
  • RESULTS: Three men and three women with a mean age of 49 yr (range 34-75 yr) had acinar cell carcinoma (n = 2), adenocarcinoma (n = 1), and intraductal pancreatic mucinous neoplasm (n = 3).
  • Five patients had a germline PRKAR1A mutation, including two patients with acinar cell carcinoma, for whom mutations were found in a hemizygous state in the tumor, suggesting loss of heterozygosity.
  • PRKAR1A expression was not detected in five of the six pancreatic neoplasms from CNC patients, whereas the protein was amply expressed on other sporadic pancreatic tumors and normal tissue.
  • CONCLUSION: An unexpectedly high prevalence of rare pancreatic tumors was found among CNC patients.
  • Immunohistochemistry and loss-of-heterozygosity studies suggest that PRKAR1A could function as a tumor suppressor gene in pancreatic tissue, at least in the context of CNC.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Acinar Cell / genetics. Carcinoma, Pancreatic Ductal / genetics. Carney Complex / genetics. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / genetics. Pancreatic Neoplasms / genetics

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  • (PMID = 21900385.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human
  • [Other-IDs] NLM/ PMC3205895
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9. Lowery MA, Klimstra DS, Shia J, Yu KH, Allen PJ, Brennan MF, O'Reilly EM: Acinar cell carcinoma of the pancreas: new genetic and treatment insights into a rare malignancy. Oncologist; 2011;16(12):1714-20
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  • [Title] Acinar cell carcinoma of the pancreas: new genetic and treatment insights into a rare malignancy.
  • BACKGROUND: Acinar cell carcinoma (ACC) of the pancreas is a rare neoplasm, accounting for 1% of all pancreatic neoplasms.
  • There remains a lack of data regarding the use of systemic therapy in this disease.
  • The median age at diagnosis was 65 years (range, 16-87 years).
  • The median overall survival (OS) time for patients with localized, resectable disease was 56.9 months and the OS time for patients with metastatic ACC (n = 18) was 19.6 months.
  • Six patients with metastatic or recurrent ACC had a partial response to chemotherapy and five patients had stable disease for ≥6 months on systemic chemotherapy.
  • CONCLUSIONS: ACC is moderately chemoresponsive to agents that have activity in pancreatic adenocarcinoma and colorectal carcinoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Acinar Cell. Pancreatic Neoplasms

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  • (PMID = 22042785.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / G-T mismatch-binding protein
  • [Other-IDs] NLM/ PMC3248770
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10. Barasch N, Gong X, Kwei KA, Varma S, Biscocho J, Qu K, Xiao N, Lipsick JS, Pelham RJ, West RB, Pollack JR: Recurrent rearrangements of the Myb/SANT-like DNA-binding domain containing 3 gene (MSANTD3) in salivary gland acinic cell carcinoma. PLoS One; 2017;12(2):e0171265
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  • [Title] Recurrent rearrangements of the Myb/SANT-like DNA-binding domain containing 3 gene (MSANTD3) in salivary gland acinic cell carcinoma.
  • Pathogenic gene fusions have been identified in several histologic types of salivary gland neoplasia, but not previously in acinic cell carcinoma (AcCC).
  • In preliminary functional studies, engineered MSANTD3 overexpression in rodent salivary gland epithelial cells did not enhance cell proliferation, but led to significant upregulation of gene sets involved in protein synthesis.
  • Our findings newly identify MSANTD3 rearrangement as a recurrent event in salivary gland AcCC, providing new insight into disease pathogenesis, and identifying a putative novel human oncogene.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Carcinoma, Acinar Cell / genetics. Gene Rearrangement. Salivary Gland Neoplasms / genetics
  • [MeSH-minor] Adult. Animals. Cell Line, Tumor. Conserved Sequence. Gene Expression Profiling. Gene Fusion. Humans. Rats. Up-Regulation

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  • (PMID = 28212443.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA128836
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / CNPY2 protein, human
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