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1. Klimstra DS: Nonductal neoplasms of the pancreas. Mod Pathol; 2007 Feb;20 Suppl 1:S94-112
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  • [Title] Nonductal neoplasms of the pancreas.
  • Although the majority of pancreatic neoplasms are infiltrating ductal adenocarcinomas or other neoplasms with ductal differentiation, neoplasms with acinar, endocrine, mixed, or uncertain differentiation constitute a diverse and distinctive group.
  • The most common and best-characterized nonductal neoplasms are pancreatic endocrine neoplasm, acinar cell carcinoma, pancreatoblastoma, and solid pseudopapillary neoplasm.
  • This review details the clinical and pathologic features of these nonductal neoplasms, highlighting diagnostic criteria including the use of specific immunohistochemical stains to define the cellular differentiation of the neoplasms.
  • [MeSH-major] Adenocarcinoma, Papillary / pathology. Adenoma, Islet Cell / pathology. Carcinoma, Acinar Cell / pathology. Carcinoma, Islet Cell / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor. Humans

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  • (PMID = 17486055.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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2. Hezel AF, Gurumurthy S, Granot Z, Swisa A, Chu GC, Bailey G, Dor Y, Bardeesy N, Depinho RA: Pancreatic LKB1 deletion leads to acinar polarity defects and cystic neoplasms. Mol Cell Biol; 2008 Apr;28(7):2414-25
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  • [Title] Pancreatic LKB1 deletion leads to acinar polarity defects and cystic neoplasms.
  • LKB1 is a key regulator of energy homeostasis through the activation of AMP-activated protein kinase (AMPK) and is functionally linked to vascular development, cell polarity, and tumor suppression.
  • In humans, germ line LKB1 loss-of-function mutations cause Peutz-Jeghers syndrome (PJS), which is characterized by a predisposition to gastrointestinal neoplasms marked by a high risk of pancreatic cancer.
  • The Lkb1-deficient pancreas, although grossly normal at birth, demonstrates a defective acinar cell polarity, an abnormal cytoskeletal organization, a loss of tight junctions, and an inactivation of the AMPK/MARK/SAD family kinases.
  • Rapid and progressive postnatal acinar cell degeneration and acinar-to-ductal metaplasia occur, culminating in marked pancreatic insufficiency and the development of pancreatic serous cystadenomas, a tumor type associated with PJS.
  • These genetic studies provide in vivo evidence of a key role for LKB1 in the establishment of epithelial cell polarity that is vital for pancreatic acinar cell function and viability and for the suppression of neoplasia.

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  • (PMID = 18227155.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084313; United States / NCI NIH HHS / CA / K08CA122835; United States / NCI NIH HHS / CA / P01 CA117969; United States / NCI NIH HHS / CA / P01 CA117969-01; United States / NCI NIH HHS / CA / K01 CA104647; United States / NCI NIH HHS / CA / U01CA084313-09; United States / NCI NIH HHS / CA / K01CA104647; United States / NCI NIH HHS / CA / P01CA117969-03; United States / NCI NIH HHS / CA / K08 CA122835
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.- / Protein Kinases; EC 2.7.1.- / AMP-activated protein kinase kinase; EC 2.7.1.- / Stk11 protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ PMC2268441
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3. Dewald GW, Smyrk TC, Thorland EC, McWilliams RR, Van Dyke DL, Keefe JG, Belongie KJ, Smoley SA, Knutson DL, Fink SR, Wiktor AE, Petersen GM: Fluorescence in situ hybridization to visualize genetic abnormalities in interphase cells of acinar cell carcinoma, ductal adenocarcinoma, and islet cell carcinoma of the pancreas. Mayo Clin Proc; 2009 Sep;84(9):801-10
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  • [Title] Fluorescence in situ hybridization to visualize genetic abnormalities in interphase cells of acinar cell carcinoma, ductal adenocarcinoma, and islet cell carcinoma of the pancreas.
  • OBJECTIVE: To use fluorescence in situ hybridization (FISH) to visualize genetic abnormalities in interphase cell nuclei (interphase FISH) of acinar cell carcinoma, ductal adenocarcinoma, and islet cell carcinoma of the pancreas.
  • PATIENTS AND METHODS: Between April 4, 2007, and December 4, 2008, interphase FISH was used to study paraffin-embedded preparations of tissue obtained from 18 patients listed in the Mayo Clinic Biospecimen Resource for Pancreas Research with a confirmed diagnosis of acinar cell carcinoma, ductal adenocarcinoma, islet cell carcinoma, or pancreas without evidence of neoplasia.
  • RESULTS: FISH abnormalities were observed in 12 (80%) of 15 patients with pancreatic cancer: 5 of 5 patients with acinar cell carcinoma, 5 of 5 patients with ductal adenocarcinoma, and 2 (40%) of 5 patients with islet cell carcinoma.
  • All 3 specimens of pancreatic tissue without neoplasia had normal FISH results.
  • Gains of CTNNB1 due to trisomy 3 occurred in each tumor with acinar cell carcinoma but in none of the other tumors in this study.
  • CONCLUSION: FISH abnormalities of CTNNB1 due to trisomy 3 were observed only in acinar cell carcinoma.
  • FISH abnormalities of genes implicated in familial cancer, tumor progression, and the 5-fluorouracil pathway were common but were not associated with specific types of pancreatic cancer.

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  • (PMID = 19720778.001).
  • [ISSN] 1942-5546
  • [Journal-full-title] Mayo Clinic proceedings
  • [ISO-abbreviation] Mayo Clin. Proc.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA102701; United States / NCI NIH HHS / CA / P50 CA102701-07; United States / NCI NIH HHS / CA / R01 CA097075; United States / NCI NIH HHS / CA / R01 CA97075
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2735430
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4. Radhi J, Tse F, Marcaccio M: Papillocystic variant of acinar cell pancreatic carcinoma. J Oncol; 2010;2010:242016

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Papillocystic variant of acinar cell pancreatic carcinoma.
  • Acinar cell pancreatic carcinoma is a rare solid malignant neoplasm.
  • We report a large 10 cm pancreatic tumor with papillocystic pathology features involving the pancreatic head.
  • The growth pattern of these tumors could be mistaken for intraductal papillary mucinous tumors or other pancreatic cystic neoplasms.

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  • (PMID = 20204128.001).
  • [ISSN] 1687-8469
  • [Journal-full-title] Journal of oncology
  • [ISO-abbreviation] J Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2831459
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5. Illyés G, Luczay A, Benyó G, Kálmán A, Borka K, Köves K, Rácz K, Tulassay T, Schaff Z: Cushing's syndrome in a child with pancreatic acinar cell carcinoma. Endocr Pathol; 2007;18(2):95-102
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  • [Title] Cushing's syndrome in a child with pancreatic acinar cell carcinoma.
  • A case of pancreatic acinar cell tumor (ACC) is presented in a 10-year-old boy.
  • The tumor manifested clinically with Cushing's syndrome, high serum adrenocorticotropic hormone (ACTH) and cortisol concentrations.
  • Periodic acid Schiff positive cytoplasmic granules, trypsinogen, keratins, alpha-1-antitrypsin, and AFP were identified in the tumor cells.
  • Using immunochemiluminometric assay, a high quantity of ACTH was found in the fresh frozen tumor extract.
  • Combined radiochemotherapy was temporarily effective in reducing the tumor mass and serum AFP.
  • [MeSH-major] Carcinoma, Acinar Cell / complications. Cushing Syndrome / etiology. Pancreatic Neoplasms / complications


6. Habbe N, Shi G, Meguid RA, Fendrich V, Esni F, Chen H, Feldmann G, Stoffers DA, Konieczny SF, Leach SD, Maitra A: Spontaneous induction of murine pancreatic intraepithelial neoplasia (mPanIN) by acinar cell targeting of oncogenic Kras in adult mice. Proc Natl Acad Sci U S A; 2008 Dec 2;105(48):18913-8
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  • [Title] Spontaneous induction of murine pancreatic intraepithelial neoplasia (mPanIN) by acinar cell targeting of oncogenic Kras in adult mice.
  • Pancreatic ductal adenocarcinoma (PDAC) is believed to arise through a multistep model comprised of putative precursor lesions known as pancreatic intraepithelial neoplasia (PanIN).
  • Recent genetically engineered mouse models of PDAC demonstrate a comparable morphologic spectrum of murine PanIN (mPanIN) lesions.
  • The most faithful genetic models activate an oncogenic Kras(G12D) knockin allele within the pdx1- or ptf1a/p48-expression domain of the entire pancreatic anlage during development, thus obscuring the putative cell(s)-of-origin from which subsequent mPanIN lesions arise.
  • In our study, activation of this knockin Kras(G12D) allele in the Elastase- and Mist1-expressing mature acinar compartment of adult mice resulted in the spontaneous induction of mPanIN lesions of all histological grades, although invasive carcinomas per se were not seen.
  • We observed no requirement for concomitant chronic exocrine injury in the induction of mPanIN lesions from the mature acinar cell compartment.
  • The acinar cell derivation of the mPanINs was established through lineage tracing in reporter mice, and by microdissection of lesional tissue demonstrating Cre-mediated recombination events.
  • We conclude that in the appropriate genetic context, the differentiated acinar cell compartment in adult mice retains its susceptibility for spontaneous transformation into mPanIN lesions, a finding with potential relevance vis-à-vis the origins of PDAC.

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  • (PMID = 19028870.001).
  • [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 / NIDDK NIH HHS / DK / DK56211; United States / NIDDK NIH HHS / DK / R21 DK072532-01; United States / NCI NIH HHS / CA / R01 CA113669-02; United States / NIDDK NIH HHS / DK / R21 DK072532-02; United States / NCI NIH HHS / CA / R01 CA113669-01; United States / NCI NIH HHS / CA / CA113669-02; United States / NCI NIH HHS / CA / CA113669-04; United States / NIDDK NIH HHS / DK / DK072532-01; United States / NCI NIH HHS / CA / CA113669-03; United States / NCI NIH HHS / CA / CA113669; United States / NIDDK NIH HHS / DK / DK55489; United States / NIDDK NIH HHS / DK / DK072532; United States / NIDDK NIH HHS / DK / R01 DK055489-11A1; United States / NIDDK NIH HHS / DK / R01 DK055489; United States / NCI NIH HHS / CA / R01 CA124586-04; United States / NCI NIH HHS / CA / R01 CA113669-05; United States / NIDDK NIH HHS / DK / DK61215; United States / NIDDK NIH HHS / DK / R21 DK072532; United States / NIDDK NIH HHS / DK / R01 DK061215; United States / NCI NIH HHS / CA / R01 CA113669-03; United States / NCI NIH HHS / CA / CA124586-04; United States / NIDDK NIH HHS / DK / T32 DK007713; United States / NCI NIH HHS / CA / R01 CA124586; United States / NIDDK NIH HHS / DK / T32DK007713; United States / NCI NIH HHS / CA / CA124586; United States / NIDDK NIH HHS / DK / DK055489-11A1; United States / NCI NIH HHS / CA / R01 CA113669; United States / NIDDK NIH HHS / DK / R01 DK056211; United States / NCI NIH HHS / CA / R01 CA113669-04; United States / NCI NIH HHS / CA / CA113669-05; United States / NIDDK NIH HHS / DK / DK072532-02; United States / NCI NIH HHS / CA / CA113669-01
  • [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 / Receptors, Notch; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ PMC2596215
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7. Pascual Mateo C, Luján Galán M, Rodríguez García N, Llanes González L, Berenguer Sánchez A: [Clinical significance of prostatic intraepithelial neoplasm and atypical small acinar proliferation: relationship with prostate cancer]. Actas Urol Esp; 2008 Jul-Aug;32(7):680-5
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  • [Title] [Clinical significance of prostatic intraepithelial neoplasm and atypical small acinar proliferation: relationship with prostate cancer].
  • [Transliterated title] Significado clínico de la neoplasia intraepitelial prostática y de la proliferación acinar focal atípica: relación con el cáncer de próstata.
  • INTRODUCTION: Prostatic intraepithelial neoplasia (PIN) and atypical small acinar proliferation (ASAP) in the setting of prostatic needle biopsies are considered premalignant although questions still remain.
  • [MeSH-major] Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Biopsy. Cell Proliferation. Humans. Male. Middle Aged. Retrospective Studies

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  • (PMID = 18788482.001).
  • [ISSN] 0210-4806
  • [Journal-full-title] Actas urologicas españolas
  • [ISO-abbreviation] Actas Urol Esp
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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8. Sanati S, Watson MA, Salavaggione AL, Humphrey PA: Gene expression profiles of ductal versus acinar adenocarcinoma of the prostate. Mod Pathol; 2009 Oct;22(10):1273-9
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  • [Title] Gene expression profiles of ductal versus acinar adenocarcinoma of the prostate.
  • Ductal adenocarcinoma is an uncommon variant of prostatic adenocarcinoma with a generally more aggressive clinical course than usual acinar adenocarcinoma.
  • However, the molecular distinction between ductal and acinar adenocarcinomas is not well characterized.
  • The aim of this investigation was to evaluate the relatedness of ductal versus acinar prostatic adenocarcinoma by comparative gene expression profiling.
  • Archived, de-identified, snap frozen tumor tissue from 5 ductal adenocarcinomas, 3 mixed ductal-acinar adenocarcinomas, and 11 acinar adenocarcinomas cases were analyzed.
  • All cases of acinar and ductal adenocarcinomas were matched by Gleason grade.
  • RNA from whole tissue sections of the 5 ductal and 11 acinar adenocarcinomas cases were subjected to gene expression profiling on Affymetrix U133Plus2 microarrays.
  • Independently, laser-capture microdissection was also performed on the three mixed ductal-acinar cases and five pure acinar cases to isolate homogeneous populations of ductal and acinar carcinoma cells from the same tumor.
  • Seven of these laser-capture microdissected samples (three ductal and four acinar cell populations) were similarly analyzed on U133Plus2 arrays.
  • Analysis of data from whole sections of ductal and acinar carcinomas identified only 25 gene transcripts whose expression was significantly and at least two-fold different between ductal and acinar adenocarcinomas.
  • A similar analysis of microdissected cell populations identified 10 transcripts, including the prolactin receptor, with more significant differences in expression of 5- to 27-fold between ductal and acinar adenocarcinomas cells.
  • Overexpression of prolactin receptor protein in ductal versus acinar adenocarcinoma was confirmed by immunohistochemistry in an independent set of tumors.
  • We conclude that ductal and acinar adenocarcinomas of the prostate are strikingly similar at the level of gene expression.
  • However, several of the genes identified in this study, including the prolactin receptor, represent targets for further investigations on the molecular basis for histomorphological and clinical behavioral differences between acinar and ductal adenocarcinomas.
  • [MeSH-major] Biomarkers, Tumor / genetics. Carcinoma, Acinar Cell / genetics. Carcinoma, Ductal / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Cluster Analysis. Humans. Immunohistochemistry. Male. Microdissection. Neoplasm Staging. Oligonucleotide Array Sequence Analysis. Predictive Value of Tests. Prostatectomy. RNA, Messenger / analysis. Receptors, Prolactin / analysis. Receptors, Prolactin / genetics

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  • (PMID = 19633648.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / Receptors, Prolactin
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9. Kinkor Z, Skálová A: [Acinic cell-like differentiation in invasive ductal carcinoma and in ductal hyperplasia of the breast--report of two cases]. Cesk Patol; 2005 Jan;41(1):29-33
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  • [Title] [Acinic cell-like differentiation in invasive ductal carcinoma and in ductal hyperplasia of the breast--report of two cases].
  • [Transliterated title] "Acinic cell-like" diferenciace v invazivním duktálním karcinomu a duktální hyperlazii mlécné zlázy--popis dvou prípadů.
  • Described are two epithelial lesions of the breast displaying extremely rare, widespread acinic cell-like differentiation (metaplasia).
  • Two women, 70 and 40-year-old, one with invasive ductal papillocarcinoma, the other one with conventional intraductal hyperplasia without atypia, both demonstrated massive diffuse, PAS positive, granular eosinophilic transformation of the cell cytoplasm.
  • This unusual cell appearance closely simulated acinar cells in normal serous salivary gland/acinic cell carcinoma or Paneth cells.
  • Both extensive expression of lysozyme and finding of numerous zymogen granules ultrastructurally confirmed the acinic cell-like fenotype.
  • Discussed is differential diagnosis of the breast neoplasm containing overt eosinophilic and granular cytoplasm.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Acinar Cell / pathology. Carcinoma, Ductal, Breast / pathology


10. Mansfield A, Tafur A, Smithedajkul P, Corsini M, Quevedo F, Miller R: Mayo Clinic experience with very rare exocrine pancreatic neoplasms. Pancreas; 2010 Oct;39(7):972-5
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  • [Title] Mayo Clinic experience with very rare exocrine pancreatic neoplasms.
  • OBJECTIVES: Limited data are available to guide the management of very rare exocrine neoplasms of the pancreas (VREP).
  • The most commonly identified neoplasms were acinar cell carcinoma (n = 15), small cell carcinoma (n = 12), and squamous cell carcinoma (n = 8).
  • [MeSH-major] Pancreatic Neoplasms / mortality. Pancreatic Neoplasms / therapy. Rare Diseases / mortality. Rare Diseases / therapy
  • [MeSH-minor] Adult. Aged. Carcinoma, Acinar Cell / mortality. Carcinoma, Small Cell / mortality. Carcinoma, Squamous Cell / mortality. Female. Humans. Male. Middle Aged. Neoplasm Staging

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  • (PMID = 20622706.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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11. Komorski JA, Nienartowicz JM: [Acinic cell carcinoma of glandule parotidea presenting untypical clinical symptoms and their bad prognosis]. Otolaryngol Pol; 2009 Sep-Oct;63(5):442-7
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  • [Title] [Acinic cell carcinoma of glandule parotidea presenting untypical clinical symptoms and their bad prognosis].
  • [Transliterated title] Acinic cell carcinoma ślinianki przyusznej o nietypowym obrazie klinicznym i niekorzystnym przebiegu.
  • In the case of neck tumours, these are unfortunately late signs, but in patients with a primary neoplastic focus within the head and neck, neck tumour is often the first sign of the disease.
  • The authors describe a clinical case of neck tumour with initially unclear etiology.
  • The preoperative diagnostics including ultrasonography, thin-needle puncture, MRI, carotid angiography and videostroboscopy was significant for surgical treatment planning; yet it was the intraoperative clinical picture which indicated that the tumour derived from the inferior parotid pole.
  • The histopathological examination confirmed non-cornifying basal cell epithelioma only in the essential lesion with no metastases to lymph nodes and surrounding tissue margins free of infiltrates.
  • Two and a half years after the procedure, the patient presented with a tumour localized on the front thoracic wall and two rapidly enlarging tumours in the nape of the neck.
  • In the collected specimen of the tumour on the front thoracic wall, a diagnosis of acinic cell carcinoma was made.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / surgery. Parotid Neoplasms / pathology. Parotid Neoplasms / surgery
  • [MeSH-minor] Aged. Head and Neck Neoplasms / secondary. Humans. Male. Neck Dissection / methods. Neoplasm Staging. Palliative Care. Prognosis. Thoracic Wall / pathology

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  • (PMID = 20169911.001).
  • [ISSN] 0030-6657
  • [Journal-full-title] Otolaryngologia polska = The Polish otolaryngology
  • [ISO-abbreviation] Otolaryngol Pol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
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12. Stelow EB, Shaco-Levy R, Bao F, Garcia J, Klimstra DS: Pancreatic acinar cell carcinomas with prominent ductal differentiation: Mixed acinar ductal carcinoma and mixed acinar endocrine ductal carcinoma. Am J Surg Pathol; 2010 Apr;34(4):510-8
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  • [Title] Pancreatic acinar cell carcinomas with prominent ductal differentiation: Mixed acinar ductal carcinoma and mixed acinar endocrine ductal carcinoma.
  • BACKGROUND: Pancreatic acinar cell carcinomas (ACCs) are clinically and pathologically distinct from pancreatic ductal adenocarcinomas (PDAs).
  • All cases showed significant evidence of both acinar and ductal differentiation, estimated to be at least 25% of the neoplastic cells, and 3 cases in addition had endocrine differentiation in more than 25% of cells.
  • Five cases were predominately acinar with intracellular and sometimes extracellular mucin ("mucinous acinar cell carcinoma" pattern).
  • Six cases seemed more mixed with areas recapitulating typical PDAs whereas the other portions of the tumors seemed akin to typical acinar cell carcinomas ("combined acinar and ductal" pattern).
  • CONCLUSION: Despite the early embryologic divergence of acinar and ductal cell lineages, rare pancreatic tumors have both acinar and ductal differentiation, usually predominantly the former.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Carcinoma, Islet Cell / pathology. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Combined Modality Therapy. DNA Mutational Analysis. DNA, Neoplasm / analysis. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Mucins / metabolism. Mutation. Neoplasms, Multiple Primary. New York / epidemiology. Pancreatectomy. Proto-Oncogene Proteins / genetics. Survival Rate. Virginia / epidemiology. ras Proteins / genetics

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  • (PMID = 20182344.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / KRAS protein, human; 0 / Mucins; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
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13. Sipos B, Klöppel G: [Acinar cell carcinomas and pancreatoblastomas: related but not the same]. Pathologe; 2005 Feb;26(1):37-40
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  • [Title] [Acinar cell carcinomas and pancreatoblastomas: related but not the same].
  • Acinar cell carcinomas and pancreatoblastomas are malignant tumors of the pancreas, showing predominantly acinar differentiation characterized by the immunohistochemical expression of pancreatic enzymes.
  • Histologically, they usually display acinar and/or solid patterns, but may occasionally also exhibit cystic structures.
  • Acinar cell carcinomas predominantly occur in adults, pancreatoblastomas in children.
  • Both tumor types commonly show allelic losses on chromosome 11p and mutations in the APC/beta-catenin signaling pathway.
  • Pancreatoblastomas, in contrast to acinar cell carcinomas, are potentially curable.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Cell Differentiation. Diagnosis, Differential. Female. Humans. Male. Prognosis. Sex Characteristics

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  • (PMID = 15614488.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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14. Stelow EB, Bardales RH, Shami VM, Woon C, Presley A, Mallery S, Lai R, Stanley MW: Cytology of pancreatic acinar cell carcinoma. Diagn Cytopathol; 2006 May;34(5):367-72
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  • [Title] Cytology of pancreatic acinar cell carcinoma.
  • Acinar cell carcinoma (ACC) of the pancreas is extremely uncommon and its cytologic features have rarely been described.
  • Original cytologic diagnoses included "acinar cell carcinoma," "pancreatic endocrine tumor," "favor neuroendocrine tumor, low-grade" and "non-diagnostic specimen."
  • The cytologic features included small to moderate-sized loose groups with numerous single cells, prominent acinar formation, little anisonucleosis and prominent nucleoli.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Biopsy, Fine-Needle. Female. Humans. Keratins / analysis. Liver Neoplasms / chemistry. Liver Neoplasms / secondary. Lymph Nodes / pathology. Male. Middle Aged. Pancreas / chemistry. Pancreas / pathology

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  • (PMID = 16604543.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 68238-35-7 / Keratins
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15. Mizuno Y, Sumi Y, Nachi S, Ito Y, Marui T, Saji S, Matsutomo H: Acinar cell carcinoma arising from an ectopic pancreas. Surg Today; 2007;37(8):704-7
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  • [Title] Acinar cell carcinoma arising from an ectopic pancreas.
  • We herein report a rare case of ectopic pancreatic acinar cell carcinoma (ACC) which presented as a submucosal tumor of the pylorus.
  • Esophago-gastroduodenal endoscopy showed no mucosal lesions, but a submucosal tumor was observed around the pylorus.
  • We diagnosed a gastrointestinal stromal tumor or malignant lymphoma preoperatively, and decided to perform an operation in order to confirm the diagnosis and select the optimal treatment.
  • The resected specimen showed the 7.6 x 4.9-cm size tumor to mainly originate from the pylorus.
  • Histopathologically, the tumor was identified as pancreatic ACC with lymph node metastasis.
  • The tumor cells were labeled by immunohistochemical staining for alpha1-antitrypsin.
  • Because of the tumor location, we considered the tumor to have originated from the ectopic pancreatic tissue in the stomach.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology. Pylorus / pathology. Stomach Neoplasms / secondary

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  • (PMID = 17643220.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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16. Basturk O, Zamboni G, Klimstra DS, Capelli P, Andea A, Kamel NS, Adsay NV: Intraductal and papillary variants of acinar cell carcinomas: a new addition to the challenging differential diagnosis of intraductal neoplasms. Am J Surg Pathol; 2007 Mar;31(3):363-70
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  • [Title] Intraductal and papillary variants of acinar cell carcinomas: a new addition to the challenging differential diagnosis of intraductal neoplasms.
  • The recognition and differential diagnosis of pancreatic intraductal neoplasms (IN) have gained importance in the past few years, as the incidence of these tumors (especially intraductal papillary mucinous neoplasms-IPMNs) have risen to >10% of pancreatic resections, and their significance as precursors of invasive cancer is better appreciated.
  • Acinar cell carcinomas (ACCs) are typically solid tumors; however, we have recently encountered 7 ACCs with either intraductal growth and/or a papillary/papillocystic pattern that could be mistaken for IN.
  • Four patients were male and 3 female, with a mean age of 59 and mean tumor size of 4.9 cm (as compared with 10 cm in conventional ACCs).
  • In 5 cases, the tumors had nodular growth of sheet-forming acinar cells, some of which were within ducts, as evidenced by the polypoid nature of the process, partial ductal lining, and presence of small tributary ducts in the walls.
  • In 3 cases, the tumor had papillary and/or papillocystic growth, at least focally.
  • In such cases, attention to morphologic details described above, and immunohistochemistry are helpful.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Papillary / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Periodic Acid-Schiff Reaction. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 17325477.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50-CA62924
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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17. Matos JM, Schmidt CM, Turrini O, Agaram NP, Niedergethmann M, Saeger HD, Merchant N, Johnson CS, Lillemoe KD, Grützmann R: Pancreatic acinar cell carcinoma: a multi-institutional study. J Gastrointest Surg; 2009 Aug;13(8):1495-502
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  • [Title] Pancreatic acinar cell carcinoma: a multi-institutional study.
  • INTRODUCTION: The presentation and outcome of patients with acinar cell carcinoma (ACC) of the pancreas compared to the more common ductal cell adenocarcinoma (DCA) may be distinct.
  • Mean tumor size was 5.3 cm.
  • American Joint Commission on Cancer tumor stages were stage I (two), stage II (eight), stage III (four), and stage IV (three).
  • This is in contrast to 1,608 patients with ductal cell adenocarcinoma who underwent resection identified from recent literature reports where the average median survival was only 24 months.
  • CONCLUSION: Acinar cell carcinoma of the pancreas is rare and appears to have a presentation and outcome distinct from the more common pancreatic DCA.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Biopsy. Cholangiopancreatography, Endoscopic Retrograde. Diagnosis, Differential. Follow-Up Studies. Germany / epidemiology. Humans. Incidence. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging. Pancreatectomy / methods. Prognosis. Prospective Studies. Survival Rate. United States / epidemiology

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  • (PMID = 19495891.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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18. Tsutsumi M: [Differential genetic pathway of duct and acinar carcinomas of the pancreas]. Gan To Kagaku Ryoho; 2005 May;32(5):593-8
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  • [Title] [Differential genetic pathway of duct and acinar carcinomas of the pancreas].
  • There are many differences in the genetic pathway between duct carcinogenesis and acinar carcinogensis.
  • [MeSH-major] Carcinoma, Acinar Cell / genetics. Carcinoma, Pancreatic Ductal / genetics. Genes, ras. Pancreatic Neoplasms / genetics

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  • (PMID = 15918556.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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19. Yamaguchi R, Okabe Y, Jimi A, Shiota K, Kodama T, Naito Y, Yasunaga M, Kinoshita H, Kojiro M: Pancreatic acinar cell carcinoma extending into the common bile and main pancreatic ducts. Pathol Int; 2006 Oct;56(10):633-7
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  • [Title] Pancreatic acinar cell carcinoma extending into the common bile and main pancreatic ducts.
  • Acinar cell carcinoma (ACC) of the pancreas is relatively rare, accounting for only approximately 1% of all exocrine pancreatic tumors.
  • Magnetic resonance cholangiopancreatography showed defect of the lower common bile duct (CBD) due to obstruction by the tumor cast.
  • Histopathologically, the pancreatic head tumor invaded the main pancreatic duct (MPD) and CBD with extension into the CBD in a form of tumor cast.
  • The tumor cells consisted of a solid proliferation with abundant eosinophilic cytoplasm and round nuclei in an acinar and trabecular fashion.
  • Histopathologically, the tumor was encapsulated by fibrous capsule and had extensive central necrosis with solid areas in the tumor periphery, and invaded with extension into the MPD in a form of tumor cast.
  • The tumor cells resembled acinar cells in solid growths.
  • Two resected cases of ACC with unusual tumor extension into the CBD and the MPD, respectively, are reported.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Common Bile Duct / pathology. Common Bile Duct Neoplasms / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Humans. Male. Middle Aged. Neoplasm Invasiveness / pathology

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  • (PMID = 16984622.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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20. Kawakami H, Kuwatani M, Onodera M, Hirano S, Kondo S, Nakanishi Y, Itoh T, Asaka M: Primary acinar cell carcinoma of the ampulla of Vater. J Gastroenterol; 2007 Aug;42(8):694-7

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  • [Title] Primary acinar cell carcinoma of the ampulla of Vater.
  • Acinar cell carcinoma of the pancreatobiliary system is a relatively rare malignant neoplasm arising usually in the pancreatic parenchyma.
  • The patient underwent a curative surgical operation, and histopathological examination revealed that the tumor was confined to the ampulla of Vater with no continuity to the pancreatic parenchyma.
  • The tumor cells showed acinar or tubular arrangement with eosinophilic to basophilic granular cytoplasm, findings identical to those of acinar cell carcinoma of the pancreas.
  • Immunohistochemically, the tumor cells were positive for lipase.
  • From these findings, we concluded that the tumor was primary acinar cell carcinoma arising in the ampulla of Vater, probably originating from heterotopic pancreatic tissue.
  • This is the first reported case of primary acinar cell carcinoma in the ampulla of Vater.
  • [MeSH-major] Ampulla of Vater. Carcinoma, Acinar Cell / diagnosis. Common Bile Duct Neoplasms / diagnosis

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  • (PMID = 17701134.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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21. Zhu L, Shi G, Schmidt CM, Hruban RH, Konieczny SF: Acinar cells contribute to the molecular heterogeneity of pancreatic intraepithelial neoplasia. Am J Pathol; 2007 Jul;171(1):263-73
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  • [Title] Acinar cells contribute to the molecular heterogeneity of pancreatic intraepithelial neoplasia.
  • A number of studies have shown that pancreatic ductal adenocarcinoma develops through precursor lesions termed pancreatic intraepithelial neoplasia (PanIN).
  • What remains unanswered is the identification of the individual cell type(s) that contributes to pancreatic ductal adenocarcinoma formation.
  • To follow the cellular and molecular changes that occur in acinar and duct cell properties on Kras(G12D) expression, we took advantage of LSL-Kras(G12D/+)/p48(Cre/+) mice, which faithfully mimic the human disease.
  • In young animals (4 weeks), the predominant cellular alteration in the exocrine pancreas was acinar metaplasia in which individual acini consisted of acinar cells and duct-like cells.
  • Metaplastic acinar structures were highly proliferative, expressed Notch target genes, and exhibited mosaic expression patterns for epidermal growth factor receptor, ErbB2, and pErk.
  • This expression pattern paralleled the expression pattern detected in mouse PanINs, suggesting that mouse PanINs and acinar-ductal metaplasia follow similar molecular pathways.
  • Indeed, immunofluorescence studies confirmed the presence of acinar cells within mPanIN lesions, raising the possibility that Kras(G12D)-induced mPanINs develop from acinar cells that undergo acinar-ductal metaplasia.
  • Identification of an acinar contribution to PanIN formation offers new directions for successful targeted therapeutic approaches to combat this disease.

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  • (PMID = 17591971.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA062924; United States / NIDDK NIH HHS / DK / DK55489; United States / NCI NIH HHS / CA / P50 CA62924; United States / NIDDK NIH HHS / DK / R01 DK055489; United States / NCI NIH HHS / CA / R01 CA124586
  • [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 / Carrier Proteins; 0 / Erbb2ip protein, mouse; 0 / Interferon-Stimulated Gene Factor 3, gamma Subunit; 0 / Isgf3g protein, mouse; 0 / Receptors, Notch
  • [Other-IDs] NLM/ PMC1941579
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22. Sabbagh C, Fuks D, Chatelain D, Flamant M, Delcenserie R, Yzet T, Regimbeau JM: [Acinar cell carcinoma of the pancreas: a rare tumor with particular clinical and paraclinical presentation]. Rev Med Interne; 2008 Dec;29(12):1046-9
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  • [Title] [Acinar cell carcinoma of the pancreas: a rare tumor with particular clinical and paraclinical presentation].
  • Acinar cell carcinoma of the pancreas is a rare tumour with specific clinical and paraclinical presentation.

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  • (PMID = 18433943.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin
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23. Kolb-van Harten P, Rosien U, Klöppel G, Layer P: Pancreatic acinar cell carcinoma with excessive alpha-fetoprotein expression. Pancreatology; 2007;7(4):370-2
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  • [Title] Pancreatic acinar cell carcinoma with excessive alpha-fetoprotein expression.
  • We report a case of acinar cell carcinoma of the pancreas associated with excessively elevated levels of serum alpha-fetoprotein (>32,000 ng/ml).
  • This regimen was associated with clinical improvement and dramatic decreases in both tumor size and serum alpha-fetoprotein.
  • [MeSH-major] Carcinoma, Acinar Cell / metabolism. Pancreatic Neoplasms / metabolism. alpha-Fetoproteins / metabolism

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  • [Copyright] 2007 S. Karger AG, Basel and IAP
  • (PMID = 17703084.001).
  • [ISSN] 1424-3911
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / alpha-Fetoproteins; 0W860991D6 / Deoxycytidine; 50SG953SK6 / Mitomycin; B76N6SBZ8R / gemcitabine
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24. Bostwick DG, Meiers I: Atypical small acinar proliferation in the prostate: clinical significance in 2006. Arch Pathol Lab Med; 2006 Jul;130(7):952-7
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  • [Title] Atypical small acinar proliferation in the prostate: clinical significance in 2006.
  • About 2% of contemporary prostate needle biopsy specimens contain collections of small acini that are suspicious for cancer but that fall below the diagnostic threshold and are reported as atypical small acinar proliferation suspicious for but not diagnostic of malignancy.
  • Prostate cancer has been identified in specimens from subsequent biopsies in up to 60% of cases of atypical small acinar proliferation, indicating that this finding is a significant predictor of cancer.
  • Identification of atypical small acinar proliferation warrants repeat biopsy for concurrent or subsequent invasive carcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Precancerous Conditions / pathology. Prostate / pathology. Prostatic Hyperplasia / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Biopsy, Needle. Cell Proliferation. Diagnosis, Differential. Follow-Up Studies. Humans. Male

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  • (PMID = 16831049.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 32
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25. Klock C, Gomes R, João M, Netto G: Prostate melanosis associated with acinar adenocarcinoma. Int J Surg Pathol; 2010 Oct;18(5):379-80
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  • [Title] Prostate melanosis associated with acinar adenocarcinoma.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Melanosis / pathology. Prostate / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 19098014.001).
  • [ISSN] 1940-2465
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Melanins
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26. Liu Y, Chen N, Cui X, Zheng X, Deng L, Price S, Karantza V, Minden A: The protein kinase Pak4 disrupts mammary acinar architecture and promotes mammary tumorigenesis. Oncogene; 2010 Nov 4;29(44):5883-94
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  • [Title] The protein kinase Pak4 disrupts mammary acinar architecture and promotes mammary tumorigenesis.
  • The Pak4 serine/threonine kinase is highly expressed in many cancer cell lines and human tumors.
  • Epithelial cancers are associated not only with changes in cell growth but also with changes in the cellular organization within the three-dimensional (3D) architecture of the affected tissues.
  • In this study we used immortalized mouse mammary epithelial cells (iMMECs) as a model system to study the role for Pak4 in mammary tumorigenesis. iMMECs are an excellent model system for studying breast cancer, as they can grow in 3D-epithelial cell culture, in which they form acinar structures that recapitulate in vivo mammary morphogenesis.
  • In this study we found that overexpression of Pak4 in iMMECs leads to changes in 3D acinar architecture that are consistent with oncogenic transformation.
  • These include decreased central acinar cell death, abrogation of lumen formation, cell polarity alterations and deregulation of acinar size and cell number.
  • This is likely to be owing to the ability of Pak4 to inhibit apoptosis and promote cell survival and thus subsequent uncontrolled proliferation, and to its ability to deregulate cell shape and polarity.

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  • (PMID = 20697354.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / L30 CA116898; United States / NCI NIH HHS / CA / L30 CA116898-01; United States / NCI NIH HHS / CA / R00 CA133181; United States / NCI NIH HHS / CA / CA116898-01; United States / NCI NIH HHS / CA / R01 CA076342; United States / NCI NIH HHS / CA / R01 CA076342-11; United States / NCI NIH HHS / CA / CA076342-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.11.1 / Pak4 protein, mouse; EC 2.7.11.1 / p21-Activated Kinases
  • [Other-IDs] NLM/ NIHMS218926; NLM/ PMC2974003
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27. Ayub SB, Dodge J: Lipid-rich variant of pancreatic endocrine neoplasms: a case report. Acta Cytol; 2010 Sep-Oct;54(5 Suppl):829-34
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  • [Title] Lipid-rich variant of pancreatic endocrine neoplasms: a case report.
  • BACKGROUND: Pancreatic endocrine neoplasms (PENs) are a well-defined and well-characterized group of tumors.
  • The cells in the cell block were immunoreactive (positive) for cytokeratin AE1/AE3, synaptophysin, and chromogranin A.
  • An elective resection of the tumor was performed, which confirmed the diagnosis of lipid-rich variant of PENs.
  • CONCLUSION: Its mimickers include adrenal cortical carcinoma, metastatic clear-cell renal cell carcinoma, clear-cell PEN, foamy gland pattern of pancreatic ductal carcinoma, solid pseudopapillary tumor, and acinar cell carcinoma.
  • The distinguishing morphologic and immunohistochemical features of each are described.
  • [MeSH-major] Endocrine Gland Neoplasms / pathology. Lipids / chemistry. Pancreatic Neoplasms / pathology

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  • (PMID = 21053550.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Lipids
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28. Pradhan S, Liu C, Zhang C, Jia X, Farach-Carson MC, Witt RL: Lumen formation in three-dimensional cultures of salivary acinar cells. Otolaryngol Head Neck Surg; 2010 Feb;142(2):191-5
The Lens. Cited by Patents in .

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  • [Title] Lumen formation in three-dimensional cultures of salivary acinar cells.
  • Cell viability and phenotype were examined.
  • Prior studies demonstrated differentiation of acinar cells into lobular structures that mimicked intact glands when cultured on PlnDIV peptide-coated surfaces.
  • [MeSH-minor] Cell Differentiation. Cells, Cultured. Heparan Sulfate Proteoglycans / pharmacology. Humans. Laryngeal Neoplasms / complications. Laryngeal Neoplasms / radiotherapy. Lung Neoplasms / complications. Lung Neoplasms / radiotherapy. Microscopy, Electron, Transmission. Microscopy, Phase-Contrast. Morphogenesis. Pharyngeal Neoplasms / complications. Pharyngeal Neoplasms / radiotherapy. Radiotherapy, Adjuvant / adverse effects. Salivary Ducts / cytology. Salivary Ducts / growth & development. Xerostomia / etiology. Xerostomia / therapy

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  • [Copyright] Copyright 2010 American Academy of Otolaryngology-Head and Neck Surgery Foundation. Published by Mosby, Inc. All rights reserved.
  • (PMID = 20115973.001).
  • [ISSN] 1097-6817
  • [Journal-full-title] Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery
  • [ISO-abbreviation] Otolaryngol Head Neck Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Heparan Sulfate Proteoglycans; 143972-95-6 / perlecan
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29. Kebir FZ, Lahmar A, Arfa N, Manai S, El Ouaer MA, Bouraoui S, Gouttalier C, Mezabi-Regaya S: Acinar cell carcinoma of the pancreas in a young patient with chronic pancreatitis. Hepatobiliary Pancreat Dis Int; 2010 Feb;9(1):103-6
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  • [Title] Acinar cell carcinoma of the pancreas in a young patient with chronic pancreatitis.
  • BACKGROUND: Acinar cell carcinoma (ACC) is a rare malignancy of the pancreas arising from acinar cells.
  • Unlike ductal adenocarcinoma, this tumor rarely presents with pancreatitis.
  • CONCLUSIONS: The clinical presentation of ACC of the pancreas is not specific and the tumor can be under-diagnosed when associated with chronic pancreatitis.
  • Data regarding course, treatment, and prognosis of this tumor are generally lacking.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Neoplasms / diagnosis. Pancreatitis, Chronic / complications

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  • (PMID = 20133240.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
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30. Sorscher SM: Metastatic acinar cell carcinoma of the pancreas responding to gemcitabine, 5-fluorouracil and leucovorin therapy: a case report. Eur J Cancer Care (Engl); 2009 May;18(3):318-9
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  • [Title] Metastatic acinar cell carcinoma of the pancreas responding to gemcitabine, 5-fluorouracil and leucovorin therapy: a case report.
  • Acinar cell carcinoma of the pancreas is rare tumour with a generally poor prognosis.
  • There are very few reports of tumour regression following chemotherapy.
  • In this case report, a patient with metastatic acinar cell carcinoma in the liver developed progressive disease after cisplatin/etoposide and then had progressive disease after weekly paclitaxel chemotherapy.
  • However, his tumour then responded to gemcitibine/5-flourouracil/leucovorin chemotherapy.
  • Herein, previously described chemotherapy regimens used for this rare tumour are reviewed.
  • This case represents the first reported metastatic acinar cell carcinoma responding to this regimen.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Liver Neoplasms / drug therapy. Pancreatic Neoplasms
  • [MeSH-minor] Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Drug Resistance, Neoplasm. Fluorouracil / administration & dosage. Humans. Leucovorin / administration & dosage. Male. Middle Aged. Treatment Outcome. Vitamin B Complex / administration & dosage

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  • (PMID = 19445023.001).
  • [ISSN] 1365-2354
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; 12001-76-2 / Vitamin B Complex; B76N6SBZ8R / gemcitabine; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
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31. Martin SK, Agarwal G, Lynch GR: Subcutaneous fat necrosis as the presenting feature of a pancreatic carcinoma: the challenge of differentiating endocrine and acinar pancreatic neoplasms. Pancreas; 2009 Mar;38(2):219-22
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  • [Title] Subcutaneous fat necrosis as the presenting feature of a pancreatic carcinoma: the challenge of differentiating endocrine and acinar pancreatic neoplasms.
  • In our review of the published reports of tumor types associated with pancreatic panniculitis, we found that immunohistochemical staining and electron microscopy can and should be used in conjunction with clinical correlation to accurately differentiate neuroendocrine tumors from carcinomas with acinar cell features.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Fat Necrosis / pathology. Neuroendocrine Tumors / pathology. Pancreatic Neoplasms / pathology. Panniculitis / pathology. Skin / pathology

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  • (PMID = 19238022.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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32. Chiaravalli AM, Finzi G, Bertolini V, La Rosa S, Capella C: Colonic carcinoma with a pancreatic acinar cell differentiation. A case report. Virchows Arch; 2009 Dec;455(6):527-31
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  • [Title] Colonic carcinoma with a pancreatic acinar cell differentiation. A case report.
  • A case of a colonic carcinoma showing a pancreatic acinar cell differentiation is described for the first time.
  • A 65-year-old woman underwent surgical resection for an ulcerated protruding tumour of 4 x 2.5 cm in size on the anterior wall of the sigmoid colon.
  • Histologically, tumour cells were organized in acinar structures resembling pancreatic acini and in solid nests and ribbons or diffusely infiltrated as poorly cohesive cells.
  • The ultrastructural analysis of the primary tumour indicated the presence of zymogen-like granules in the cytoplasm of tumour cells.
  • Immunohistochemically, both acinar and diffuse patterns of growth showed an intense staining for trypsin, chymotrypsin and BCL10 and a weaker immunoreactivity for lipase and carboxyl ester hydrolase.
  • Most tumour cells were cytokeratin 20, CDX2 and p53 positive; whereas, mucin (MUC)2 immunoreactivity was observed only in the signet ring cells present in the diffuse pattern and chromogranin A in rare isolated tumour cells.
  • There was no evidence of a pancreatic acinar cell carcinoma or of heterotopic pancreatic tissue.
  • A colonic origin ought to be suspected when a metastatic carcinoma of unknown primary shows an acinar differentiation.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Colonic Neoplasms / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Cell Differentiation. Fatal Outcome. Female. Homeodomain Proteins / metabolism. Humans. Immunohistochemistry. Keratin-20 / metabolism. Lymphatic Metastasis. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19908063.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Keratin-20; 0 / Tumor Suppressor Protein p53
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33. Sawey ET, Johnson JA, Crawford HC: Matrix metalloproteinase 7 controls pancreatic acinar cell transdifferentiation by activating the Notch signaling pathway. Proc Natl Acad Sci U S A; 2007 Dec 4;104(49):19327-32
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  • [Title] Matrix metalloproteinase 7 controls pancreatic acinar cell transdifferentiation by activating the Notch signaling pathway.
  • Acinar-to-ductal metaplasia in the pancreas is associated with an increased risk for tumorigenesis.
  • Molecular dissection of this process in vitro has shown that primary acinar cells, in response to EGF receptor ligands, can transdifferentiate into duct-like epithelia, passing through a nestin-positive intermediate, in a Notch pathway-dependent manner.
  • Here, we show that in vitro acinar transdifferentiation depends on matrix metalloproteinase 7 (MMP-7), a proteinase expressed in most metaplastic epithelia in vivo.
  • MMP-7 was found to be required for Notch activation, which leads to dedifferentiation of acinar cells to the nestin-positive transitional cell.
  • Besides being necessary for acinar transdifferentiation, it was found that MMP-7 activity was sufficient to induce the process, indicating that molecular signals capable of initiating MMP-7 expression also have the potential to induce formation of metaplastic epithelia in the pancreas.

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  • (PMID = 18042722.001).
  • [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 CA100126; United States / NCI NIH HHS / CA / R01CA100126
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intermediate Filament Proteins; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Receptors, Notch; EC 3.4.24.23 / Matrix Metalloproteinase 7
  • [Other-IDs] NLM/ PMC2148289
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34. Kataoka Y, Nio Y, Yano S, Koike M, Hashimoto K, Itakura M, Itagaki T, Nishi T, Endo S, Higami T: [Pancreatic acinar cell carcinoma successfully treated with combination of oral TS-1 and intra-arterial cisplatin]. Gan To Kagaku Ryoho; 2006 Apr;33(4):525-8
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  • [Title] [Pancreatic acinar cell carcinoma successfully treated with combination of oral TS-1 and intra-arterial cisplatin].
  • Pancreatic acinar cell carcinomas are rare, and little is reported on their chemotherapy.
  • We report a 49-year old male patient with pancreatic acinar cell carcinoma and multiple liver metastases, which responded to oral TS-1 and hepatic arterial infusion of cisplatin.
  • The patient underwent a partial hepatectomy, MCT abrasions and excision of the pancreatic tumor.
  • Postoperative pathological studies revealed metastases of acinar cell carcinoma to the liver and lymph nodes; the primary lesion was undetermined.
  • Abdominal CT one year after surgery revealed a pancreatic body tumor, which was surgically removed.
  • Pathological studies showed primary pancreatic acinar cell carcinoma, while previous metastases remained under control.
  • To summarize, TS-1 and cisplatin can be effective treatments for pancreatic acinar cell carcinomas.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Cisplatin / administration & dosage. Combined Modality Therapy. Drug Administration Schedule. Drug Combinations. Hepatectomy. Humans. Infusions, Intra-Arterial. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Liver Neoplasms / surgery. Male. Middle Aged. Oxonic Acid / administration & dosage. Pyridines / administration & dosage. Tegafur / administration & dosage

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  • (PMID = 16612167.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Pyridines; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; Q20Q21Q62J / Cisplatin
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35. Minakawa K, Oka K, Nihei T, Sando N, Oikawa H, Toda J, Hosokawa Y, Matsumoto T, Yanagisawa A: Pancreatic endocrine tumor with partial acinar cell differentiation. APMIS; 2006 Oct;114(10):720-5
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  • [Title] Pancreatic endocrine tumor with partial acinar cell differentiation.
  • We examined a 70-year-old woman in whom a pancreatic endocrine tumor with partial acinar cell differentiation had been diagnosed.
  • The tumor was located in the pancreatic tail and measured 12.5 x 9.5 x 8 cm.
  • The cells had proliferated in islet-like solid medullary, trabecular, acinar, and papillary patterns.
  • The tumor may be considered an amphicrine tumor.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Islet Cell / diagnosis. Neoplasms, Multiple Primary / diagnosis. Pancreas / pathology. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Biomarkers, Tumor / metabolism. Biopsy, Needle. Cytoplasmic Granules / ultrastructure. Female. Humans. Immunohistochemistry. Secretory Vesicles / ultrastructure. Synaptophysin / analysis. Synaptophysin / metabolism. alpha 1-Antitrypsin / analysis. alpha 1-Antitrypsin / metabolism

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  • (PMID = 17004975.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Synaptophysin; 0 / alpha 1-Antitrypsin
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36. López JI: Prostate adenocarcinoma detected after high-grade prostatic intraepithelial neoplasia or atypical small acinar proliferation. BJU Int; 2007 Dec;100(6):1272-6
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  • [Title] Prostate adenocarcinoma detected after high-grade prostatic intraepithelial neoplasia or atypical small acinar proliferation.
  • OBJECTIVE: To review specific histological variables in patients with prostate cancer who previously had diagnoses of high-grade prostatic intraepithelial neoplasia (HGPIN) and/or atypical small acinar proliferation (ASAP), compared with those who had no such diagnoses.
  • Similarly, patients with these previous diagnoses had a lower Gleason score (P = 0.017 and <0.001, respectively) and lower tumour volume variables (fewer tumour foci, P = 0.033 and 0.041, respectively) and shorter cancer (P = 0.048 and 0.030) in core biopsies than those without.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Prostate / pathology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Biopsy, Needle. Cell Proliferation. Humans. Immunohistochemistry. Male. Retrospective Studies

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  • (PMID = 17850386.001).
  • [ISSN] 1464-410X
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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37. Roldo C, Missiaglia E, Hagan JP, Falconi M, Capelli P, Bersani S, Calin GA, Volinia S, Liu CG, Scarpa A, Croce CM: MicroRNA expression abnormalities in pancreatic endocrine and acinar tumors are associated with distinctive pathologic features and clinical behavior. J Clin Oncol; 2006 Oct 10;24(29):4677-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA expression abnormalities in pancreatic endocrine and acinar tumors are associated with distinctive pathologic features and clinical behavior.
  • PURPOSE: We investigated the global microRNA expression patterns in normal pancreas, pancreatic endocrine tumors and acinar carcinomas to evaluate their involvement in transformation and malignant progression of these tumor types.
  • Recent evidence indicates that microRNAs can contribute to tumor development and progression and may have diagnostic and prognostic value in several human malignancies.
  • MATERIALS AND METHODS: Using a custom microarray, we studied the global microRNA expression in 12 nontumor pancreas and 44 pancreatic primary tumors, including 12 insulinomas, 28 nonfunctioning endocrine tumors, and four acinar carcinomas.
  • RESULTS: Our data showed that a common pattern of microRNA expression distinguishes any tumor type from normal pancreas, suggesting that this set of microRNAs might be involved in pancreatic tumorigenesis; the expression of miR-103 and miR-107, associated with lack of expression of miR-155, discriminates tumors from normal; a set of 10 microRNAs distinguishes endocrine from acinar tumors and is possibly associated with either normal endocrine differentiation or endocrine tumorigenesis; miR-204 is primarily expressed in insulinomas and correlates with immunohistochemical expression of insulin; and the overexpression of miR-21 is strongly associated with both a high Ki67 proliferation index and presence of liver metastasis.
  • CONCLUSION: These results suggest that alteration in microRNA expression is related to endocrine and acinar neoplastic transformation and progression of malignancy, and might prove useful in distinguishing tumors with different clinical behavior.
  • [MeSH-major] Carcinoma, Acinar Cell / genetics. Carcinoma, Acinar Cell / pathology. Insulinoma / genetics. Insulinoma / pathology. MicroRNAs / metabolism. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Cell Transformation, Neoplastic. Gene Expression Profiling. Humans. Liver Neoplasms / secondary. Pancreas / metabolism. Prognosis. Survival

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  • (PMID = 16966691.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01CA76259; United States / NCI NIH HHS / CA / P01CA81534
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs
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38. McEvoy MP, Rich B, Klimstra D, Vakiani E, La Quaglia MP: Acinar cell cystadenoma of the pancreas in a 9-year-old boy. J Pediatr Surg; 2010 May;45(5):e7-9
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  • [Title] Acinar cell cystadenoma of the pancreas in a 9-year-old boy.
  • This report describes a rare benign cystic lesion of the pancreas known as acinar cell cystadenoma.
  • [MeSH-major] Cystadenoma / pathology. Pancreatic Neoplasms / pathology

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20438912.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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39. Zhang N, Lyons S, Lim E, Lassota P: A spontaneous acinar cell carcinoma model for monitoring progression of pancreatic lesions and response to treatment through noninvasive bioluminescence imaging. Clin Cancer Res; 2009 Aug 1;15(15):4915-24
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  • [Title] A spontaneous acinar cell carcinoma model for monitoring progression of pancreatic lesions and response to treatment through noninvasive bioluminescence imaging.
  • PURPOSE: We have generated an EL1-luc/TAg transgenic mouse model that develops spontaneous and bioluminescent acinar cell carcinomas.
  • We applied this model to noninvasively monitor tumor development and drug response.
  • Tumor development was monitored through bioluminescence imaging and necropsy at the study end point.
  • RESULTS: EL1-luc/TAg transgenic mice showed pancreas-specific bioluminescence signal before tumor progression and produced increasing light emission from the onset of the pancreatic acinar cell carcinomas.
  • The latency of tumor development ranged from 10 to >20 weeks of age in these mice.
  • Progression of the primary acinar cell carcinoma was accompanied by emergence of metastatic lesions in the abdominal organs, including liver and gastrointestinal fat tissues.
  • Rapamycin treatment suppressed tumor development.
  • CONCLUSIONS: The EL1-luc/TAg mouse provides a noninvasive approach for monitoring spontaneous acinar cell carcinoma development and comprises a convenient tool for the evaluation of novel therapeutics against pancreatic cancers.
  • Tumor growth suppression through inhibition of the mammalian target of rapamycin pathway further validates this model as clinically relevant.
  • [MeSH-major] Antibiotics, Antineoplastic / metabolism. Carcinoma, Acinar Cell / metabolism. Drug Monitoring. Pancreas / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 19622581.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; W36ZG6FT64 / Sirolimus
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40. Lakhani A, Maas L: Necrotizing panniculitis: a skin condition associated with acinar cell carcinoma of the pancreas. South Med J; 2008 May;101(5):554-5
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  • [Title] Necrotizing panniculitis: a skin condition associated with acinar cell carcinoma of the pancreas.
  • Thorough investigation revealed stage IV acinar cell carcinoma of the pancreas.
  • [MeSH-major] Carcinoma, Acinar Cell / complications. Pancreatic Neoplasms / complications. Panniculitis / etiology

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  • (PMID = 18414166.001).
  • [ISSN] 1541-8243
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.1.1.3 / Lipase; EC 3.2.1.- / Amylases
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41. Lin YC, Lee PH, Yao YT, Hsiao JK, Sheu JC, Chen CH: Alpha-fetoprotein-producing pancreatic acinar cell carcinoma. J Formos Med Assoc; 2007 Aug;106(8):669-72
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  • [Title] Alpha-fetoprotein-producing pancreatic acinar cell carcinoma.
  • A pancreatic tail tumor, instead of liver tumor, was detected.
  • He underwent elective distal pancreatectomy and splenectomy and the pathology turned out to be acinar cell carcinoma of the pancreas.
  • Alpha-fetoprotein is commonly used as a tumor marker to screen for hepatocellular carcinoma in high-risk patients.
  • However, elevated alpha-fetoprotein could occur in a much rarer disease, acinar cell carcinoma of the pancreas.

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  • (PMID = 17711801.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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42. Distler M, Rückert F, Dittert DD, Stroszczynski C, Dobrowolski F, Kersting S, Grützmann R: Curative resection of a primarily unresectable acinar cell carcinoma of the pancreas after chemotherapy. World J Surg Oncol; 2009;7:22
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  • [Title] Curative resection of a primarily unresectable acinar cell carcinoma of the pancreas after chemotherapy.
  • BACKGROUND: Acinar cell carcinoma (ACC) represents only 1-2% of pancreatic cancers and is a very rare malignancy.
  • MRI-imaging showed a tumor within the head of the pancreas concomitant with Serum-Lipase and CA19-9.
  • Endosonographic fine needle biopsy confirmed an acinar cell carcinoma.
  • Laparotomy presented an locally advanced tumor with venous infiltration that was consequently deemed unresectable.
  • Twelve months later, the patient was in stable condition, and CT-scanning showed an obvious reduction in the size of the tumor.
  • Histopathological examination gave evidence of a diffuse necrotic ACC-tumor, all resection margins were found to be negative.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Carcinoma, Acinar Cell / surgery. Fluorouracil / therapeutic use. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Aged. Combined Modality Therapy. Humans. Magnetic Resonance Imaging. Male. Neoplasm Staging. Prognosis. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 19239719.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2657786
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43. Kereszturi E, Sahin-Tóth M: Intracellular autoactivation of human cationic trypsinogen mutants causes reduced trypsinogen secretion and acinar cell death. J Biol Chem; 2009 Nov 27;284(48):33392-9
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  • [Title] Intracellular autoactivation of human cationic trypsinogen mutants causes reduced trypsinogen secretion and acinar cell death.
  • In the present study, we characterized the cell biological effects of these mutants using human embryonic kidney 293T and AR42J rat acinar cells.
  • Acinar cells expressing the p.D22G mutant detached from the culture plate over time, became terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive, and exhibited elevated levels of the proapoptotic transcription factor CHOP.
  • The observations indicate that activation peptide mutants of human cationic trypsinogen undergo autoactivation intracellularly, which leads to decreased trypsinogen secretion and eventual acinar cell death.

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  • (PMID = 19801634.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK058088; United States / NIDDK NIH HHS / DK / DK058088; United States / NIDDK NIH HHS / DK / R01 DK058088-08; United States / NIDDK NIH HHS / DK / R01 DK058088-07; United States / NIDDK NIH HHS / DK / R01 DK058088-09; United States / NIDDK NIH HHS / DK / DK058088-07; United States / NIDDK NIH HHS / DK / DK058088-04; United States / NIDDK NIH HHS / DK / R01 DK058088-03; United States / NIDDK NIH HHS / DK / DK058088-08; United States / NIDDK NIH HHS / DK / R01 DK058088-04; United States / NIDDK NIH HHS / DK / DK058088-03
  • [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 / DDIT3 protein, human; 147336-12-7 / Transcription Factor CHOP; EC 3.4.21.4 / PRSS1 protein, human; EC 3.4.21.4 / Trypsin; EC 3.4.22.1 / Cathepsin B
  • [Other-IDs] NLM/ PMC2785183
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44. Mathieu A, Clerc P, Portolan G, Bierkamp C, Lulka H, Pradayrol L, Seva C, Fourmy D, Dufresne M: Transgenic expression of CCK2 receptors sensitizes murine pancreatic acinar cells to carcinogen-induced preneoplastic lesions formation. Int J Cancer; 2005 May 20;115(1):46-54
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  • [Title] Transgenic expression of CCK2 receptors sensitizes murine pancreatic acinar cells to carcinogen-induced preneoplastic lesions formation.
  • Previous studies have demonstrated that transgenic expression of the CCK2 receptor in acinar cells of ElasCCK2 mice plays a role in the development of pancreatic neoplasia.
  • Transition of acinar cells into duct-like cells expressing Pdx1 and gastrin, as well as proliferation of acinar cells, were transiently observed in both transgenic and control mice.
  • Indeed, treated ElasCCK2 mice exhibited larger areas of pancreatic acinar-ductal transition, increased cellular proliferation as well as larger adenomas areas vs. control mice.
  • [MeSH-major] Carcinoma, Acinar Cell / etiology. Carcinoma, Acinar Cell / genetics. Pancreatic Neoplasms / etiology. Pancreatic Neoplasms / genetics. Receptor, Cholecystokinin B / genetics. Receptor, Cholecystokinin B / physiology. Transgenes
  • [MeSH-minor] Adenoma / metabolism. Animals. Antimetabolites, Antineoplastic / pharmacology. Azaserine / chemistry. Azaserine / pharmacology. Bromodeoxyuridine / pharmacology. Carcinogens. Cell Proliferation. Coloring Agents / pharmacology. Homeodomain Proteins / metabolism. Homozygote. Immunohistochemistry. Inflammation. Lymphocytes / metabolism. Mice. Mice, Transgenic. Phenotype. Precancerous Conditions / metabolism. Receptors, G-Protein-Coupled / metabolism. Risk. Time Factors. Trans-Activators / metabolism

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15688412.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Carcinogens; 0 / Coloring Agents; 0 / Homeodomain Proteins; 0 / Receptor, Cholecystokinin B; 0 / Receptors, G-Protein-Coupled; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein; 87299V3Q9W / Azaserine; G34N38R2N1 / Bromodeoxyuridine
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45. Khalili M, Wax BN, Reed WP, Schuss A, Drexler S, Weston SR, Katz DS: Radiology-pathology conference. Acinar cell carcinoma of the pancreas. Clin Imaging; 2006 Sep-Oct;30(5):343-6
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  • [Title] Radiology-pathology conference. Acinar cell carcinoma of the pancreas.
  • Acinar cell carcinoma (ACC) is a rare tumor that constitutes 1% of pancreatic neoplasms.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Intestinal Obstruction / diagnosis. Pancreatic Neoplasms / diagnosis. Retroperitoneal Neoplasms / diagnosis

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  • (PMID = 16919557.001).
  • [ISSN] 0899-7071
  • [Journal-full-title] Clinical imaging
  • [ISO-abbreviation] Clin Imaging
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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46. Sanchez D, Mueller CM, Zenilman ME: Pancreatic regenerating gene I and acinar cell differentiation: influence on cellular lineage. Pancreas; 2009 Jul;38(5):572-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic regenerating gene I and acinar cell differentiation: influence on cellular lineage.
  • Acinar cells can transdifferentiate into other pancreatic-derived cells, and we postulated that changes in intracellular levels of reg I would affect the state of differentiation.
  • CONCLUSIONS: These data demonstrate that in acinar cells, reg I overexpression is linked to acinar cell differentiation, whereas inhibition of reg I leads to beta cell and possibly ductal phenotype.
  • Reg I expression in acinar cells is important in maintaining pancreatic cell lineage, and when decreased, cells can dedifferentiate and move toward becoming other pancreatic cells.

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  • (PMID = 19557902.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK054511; United States / NIDDK NIH HHS / DK / DK054511-03; United States / NIDDK NIH HHS / DK / R01 DK054511-04; United States / NIDDK NIH HHS / DK / DK054511-04; United States / NIDDK NIH HHS / DK / R01 DK054511-03; United States / NIDDK NIH HHS / DK / Z01 DK054511
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Homeodomain Proteins; 0 / Insulin; 0 / Lithostathine; 0 / RNA, Messenger; 0 / Reg1 protein, rat; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein; EC 3.2.1.- / Amylases
  • [Other-IDs] NLM/ NIHMS100566; NLM/ PMC2702698
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47. Svrcek M, Lesurtel M, Lewin M, Afchain P, Fabre M, Scoazec JY, Parc R, Fléjou JF: [Acinar cell carcinoma of the pancreas with predominant intraductal growth: report of a case]. Gastroenterol Clin Biol; 2007 May;31(5):543-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acinar cell carcinoma of the pancreas with predominant intraductal growth: report of a case].
  • [Transliterated title] Carcinome à cellules acineuses du pancréas, de développement essentiellement intracanalaire: à propos d'un cas.
  • Acinar cell carcinoma (ACC) of the pancreas accounts for approximately 1% of all exocrine pancreatic tumours.
  • This tumour was revealed by epigastric pain and weight loss.
  • There was a marked dilatation of the main pancreatic duct upstream, with tumour spreading within this duct.
  • On the pancreaticoduodenectomy specimen, the dilated main pancreatic duct (2.5 cm in diameter) was filled by an exophytic tumour.
  • These rare forms of ACC can be confused with intraductal papillary-mucinous neoplasms.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Ducts / pathology. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Aged. Biopsy, Fine-Needle. Endosonography. Humans. Male. Neoplasm Invasiveness. Pancreaticoduodenectomy. Radiography, Abdominal. Tomography, X-Ray Computed. Ultrasonography, Interventional

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  • (PMID = 17541347.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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48. Kuroda N, Katto K, Tamura M, Shiotsu T, Nakamura S, Ohtsuki Y, Hes O, Michal M, Inoue K, Ohara M, Mizuno K, Lee GH: Immunohistochemical application of D2-40 as basal cell marker in evaluating atypical small acinar proliferation of initial routine prostatic needle biopsy materials. Med Mol Morphol; 2010 Sep;43(3):165-9
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  • [Title] Immunohistochemical application of D2-40 as basal cell marker in evaluating atypical small acinar proliferation of initial routine prostatic needle biopsy materials.
  • D2-40 has been recently discovered as a lymphatic endothelial cell marker, and some investigators have found that D2-40 is also expressed in myoepithelial cells of salivary gland or breast.
  • In this study, we evaluated D2-40 expression of basal cells and applied D2-40 immunohistochemistry in the combination of P504S, cytokeratin 5, and p63 for ten lesions with atypical small acinar proliferation (ASAP) in initial prostatic needle biopsy.
  • D2-40 was comparable to cytokeratin 5 and p63 as a basal cell marker, and there were no lesions that failed to provide an accurate final diagnosis using only D2-40 immunohistochemistry without cytokeratin 5 or p63.
  • [MeSH-major] Antibodies, Monoclonal / analysis. Biomarkers, Tumor / analysis. Carcinoma, Acinar Cell / diagnosis. Prostatic Neoplasms / diagnosis

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  • (PMID = 20857265.001).
  • [ISSN] 1860-1499
  • [Journal-full-title] Medical molecular morphology
  • [ISO-abbreviation] Med Mol Morphol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Keratin-5; 0 / Membrane Proteins; 0 / monoclonal antibody D2-40; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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49. Seki Y, Okusaka T, Ikeda M, Morizane C, Ueno H: Four cases of pancreatic acinar cell carcinoma treated with gemcitabine or S-1 as a single agent. Jpn J Clin Oncol; 2009 Nov;39(11):751-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Four cases of pancreatic acinar cell carcinoma treated with gemcitabine or S-1 as a single agent.
  • Pancreatic acinar cell carcinoma (ACC) is a comparatively rare tumor and account for approximately 1% of all cases of pancreatic cancer.
  • Disease control without obvious tumor shrinkage was observed in one patient.
  • On the other hand, fluoropyrimidine-based chemotherapy may have some activity against this tumor, because one of the three patients who received S-1 as second-line chemotherapy showed a partial response.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Deoxycytidine / analogs & derivatives. Oxonic Acid / therapeutic use. Pancreatic Neoplasms / drug therapy. Tegafur / therapeutic use

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  • (PMID = 19666905.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 0W860991D6 / Deoxycytidine; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; B76N6SBZ8R / gemcitabine
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50. Guzzo M, Ferrari A, Marcon I, Collini P, Gandola L, Pizzi N, Casanova M, Mattavelli F, Scaramellini G: Salivary gland neoplasms in children: the experience of the Istituto Nazionale Tumori of Milan. Pediatr Blood Cancer; 2006 Nov;47(6):806-10
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  • [Title] Salivary gland neoplasms in children: the experience of the Istituto Nazionale Tumori of Milan.
  • These results are presented in conjunction with a literature review of salivary tumors with a view to providing an up-to-date overview of the clinical course, prognosis, and treatment options for this rare tumor.
  • PROCEDURE: Fifty-two cases of epithelial salivary tumors were reviewed and the clinical-pathological information concerning tumor characteristics, therapy, and follow-up were collected.
  • RESULTS: The major salivary glands were the main site of tumor occurrence (79% of cases arose in parotid glands); 37 patients had benign tumors (pleomorphic adenoma), 15 had malignant tumors (12 mucoepidermoid carcinoma, 9 low grade).
  • When tumor enucleation was performed, recurrences occurred in 50% of benign neoplasms.
  • At the time of the report, all patients with benign tumors were alive, 35(95%) without evidence of disease; only one patient with malignant tumor died of disease.
  • CONCLUSIONS: Epithelial salivary glands tumor in children had different characteristics compared with their adult counterpart with respect to the frequency of histotypes and site of occurrence, but their prognosis seems to be similar.
  • [MeSH-major] Adenoma, Pleomorphic / surgery. Carcinoma, Acinar Cell / surgery. Carcinoma, Adenoid Cystic / surgery. Carcinoma, Mucoepidermoid / surgery. Neoplasm Recurrence, Local / surgery. Salivary Gland Neoplasms / surgery

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16425245.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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51. Morishima K, Hyodo M, Nihei Y, Sata N, Yasuda Y: [A case of acinar cell carcinoma of pancreas with liver metastases treated effectively by S-1]. Gan To Kagaku Ryoho; 2010 Jan;37(1):127-9
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  • [Title] [A case of acinar cell carcinoma of pancreas with liver metastases treated effectively by S-1].
  • A 65-year-old man underwent a total gastrectomy and distal pancreatectomy for acinar cell carcinoma of the pancreas.
  • Acinar cell carcinoma of the pancreas is a rare and highly malignant tumor, and there are few reports regarding treatment with chemotherapy.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / therapy. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Oxonic Acid / therapeutic use. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / therapy. Tegafur / therapeutic use

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  • (PMID = 20087046.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid
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52. De La O JP, Emerson LL, Goodman JL, Froebe SC, Illum BE, Curtis AB, Murtaugh LC: Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia. Proc Natl Acad Sci U S A; 2008 Dec 2;105(48):18907-12
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  • [Title] Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia.
  • Efforts to model pancreatic cancer in mice have focused on mimicking genetic changes found in the human disease, particularly the activating KRAS mutations that occur in pancreatic tumors and their putative precursors, pancreatic intraepithelial neoplasia (PanIN).
  • The basis for this selective response is unknown, and it is similarly unknown what cell types in the mature pancreas actually contribute to PanINs.
  • We hypothesize that Notch, which inhibits differentiation in the embryonic pancreas, contributes to PanIN formation by abrogating the normal differentiation program of tumor-initiating cells.
  • Furthermore, we find that Kras activation in mature acinar cells induces PanIN lesions identical to those seen upon ubiquitous Kras activation, and that Notch promotes both initiation and dysplastic progression of these acinar-derived PanINs, albeit short of invasive adenocarcinoma.
  • At the cellular level, Notch/Kras coactivation promotes rapid reprogramming of acinar cells to a duct-like phenotype, providing an explanation for how a characteristically ductal tumor can arise from nonductal acinar cells.

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  • (PMID = 19028876.001).
  • [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 / R21-CA123066; United States / NCI NIH HHS / CA / P30-CA042014; United States / NICHD NIH HHS / HD / 5T32-HD07491; United States / NCI NIH HHS / CA / CA123066-02; United States / NCI NIH HHS / CA / R21 CA123066; United States / NCI NIH HHS / CA / R21 CA123066-02; United States / NICHD NIH HHS / HD / T32 HD007491; United States / NCI NIH HHS / CA / P30 CA042014
  • [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 / Estrogen Antagonists; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, Notch; 094ZI81Y45 / Tamoxifen; EC 3.6.5.2 / ras Proteins
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53. Esposito I, Seiler C, Bergmann F, Kleeff J, Friess H, Schirmacher P: Hypothetical progression model of pancreatic cancer with origin in the centroacinar-acinar compartment. Pancreas; 2007 Oct;35(3):212-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypothetical progression model of pancreatic cancer with origin in the centroacinar-acinar compartment.
  • OBJECTIVES: Based mainly on animal models, 2 lesions have been suggested as possible precursors of pancreatic ductal adenocarcinoma (PDAC): pancreatic intraepithelial neoplasia (PanIN) and tubular complexes (TCs).
  • In 50% to 70% of the cases with TC and associated PanIN, a transitional zone of acinar-ductular transformation with mucinous differentiation of the ductular epithelium was identified.
  • Expression of acinar and centroacinar markers was detected in TC, in the ductular structures of the transitional zones, as well as within the epithelium of mature PanINs.
  • A progression model that originates in the centroacinar-acinar compartment and ends with the development of PanIN lesions is suggested.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / pathology. Pancreatic Diseases / pathology. Pancreatic Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Animals. Carcinoma in Situ / pathology. Cell Differentiation. Cell Transformation, Neoplastic. Cystadenoma, Serous / pathology. Disease Progression. Humans. Mice. Mice, Transgenic. Models, Animal. Models, Biological. Pancreatitis, Chronic / pathology. Rats. Species Specificity


54. Gamal G, Nagashima T, Kawashima O, Sugano M, Sakurai S, Sano T, Nakajima T: Unique case of pulmonary bronchial gland type tumor with broad spectrum of cell differentiation from the terminal duct-acinar unit to excretory duct. Pathol Int; 2006 Apr;56(4):217-21
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  • [Title] Unique case of pulmonary bronchial gland type tumor with broad spectrum of cell differentiation from the terminal duct-acinar unit to excretory duct.
  • In the lung, acinic cell carcinoma (ACC) is a rare form of tumor.
  • Reported herein is a unique bronchial gland-type tumor diagnosed as well-differentiated ACC that developed in the B9 bronchus of the left lung.
  • Moreover, this tumor contained various sizes of mucous cysts lined by columnar mucous cells, which produced abundant mucin positive for Alcian blue, which is usually present in mucoepidermoid carcinoma.
  • Therefore, the present case is a unique tumor having a broad spectrum of cell differentiation from the terminal duct--acinar unit to the striated duct and excretory duct.
  • This is the first case of unique bronchial gland-type tumor with mixed histological features of ACC and mucoepidermoid carcinoma.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Carcinoma, Bronchogenic / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Cell Differentiation. Humans. Immunohistochemistry. Male. Middle Aged. Thoracoscopy

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  • (PMID = 16634968.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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55. Hervieu V, Lombard-Bohas C, Dumortier J, Boillot O, Scoazec JY: Primary acinar cell carcinoma of the liver. Virchows Arch; 2008 Mar;452(3):337-41
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  • [Title] Primary acinar cell carcinoma of the liver.
  • We report a case of acinar cell carcinoma primary to the liver.
  • The tumor was diagnosed in a 35-year-old woman complaining of abdominal pain and asthenia; serum alpha-fetoprotein (AFP) levels were increased at 6,000 IU/mL; imaging studies showed a hypervascular mass located in the left lobe of the liver.
  • The tumor had a heterogeneous appearance.
  • In well-differentiated areas, tumor cells formed acinar structures, had a pyramidal shape and a highly eosinophilic, granular cytoplasm, PAS diastase resistant.
  • In less-differentiated areas, tumor cells were endocrinelike.
  • The immunohistochemical study showed that tumor cells expressed trypsin.
  • The final diagnosis, based on histological, immunohistochemical, and ultrastructural arguments, was extra-pancreatic acinar cell carcinoma, primary to the liver.
  • This unusual lesion is likely to be the result of an abnormal differentiation pathway involving a transformed multipotential progenitor cell.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Liver / pathology. Liver Neoplasms / pathology

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  • (PMID = 18193278.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / alpha 1-Antitrypsin; 0 / alpha-Fetoproteins
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56. Suzuki A, Sakaguchi T, Morita Y, Oishi K, Fukumoto K, Inaba K, Takehara Y, Baba S, Suzuki S, Konno H: Long-term survival after a repetitive surgical approach in a patient with acinar cell carcinoma of the pancreas and recurrent liver metastases: report of a case. Surg Today; 2010 Jul;40(7):679-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term survival after a repetitive surgical approach in a patient with acinar cell carcinoma of the pancreas and recurrent liver metastases: report of a case.
  • Acinar cell carcinoma is a relatively rare malignant neoplasm, which represents 1%-2% of all pancreatic exocrine tumors.
  • This report concerns a case of a long-term survivor of metastatic acinar cell carcinoma who was successfully treated with repetitive surgery.
  • A 62-year-old man underwent a distal pancreatectomy for a pancreatic tumor, which was histologically diagnosed as an acinar cell carcinoma.
  • The tumor recurred in the liver three times within 41 months.
  • Although no consensus has been reached on surgery for metastatic acinar cell carcinoma, the current case has important implications for establishing an appropriate treatment strategy.
  • [MeSH-major] Carcinoma, Acinar Cell / surgery. Hepatectomy. Liver Neoplasms / surgery. Neoplasm Recurrence, Local / surgery. Pancreatectomy. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Humans. Male. Middle Aged. Neoplasm Metastasis. Reoperation. Survivors

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  • (PMID = 20582524.001).
  • [ISSN] 1436-2813
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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57. Yamaguchi H, Shimizu M, Ban S, Koyama I, Hatori T, Fujita I, Yamamoto M, Kawamura S, Kobayashi M, Ishida K, Morikawa T, Motoi F, Unno M, Kanno A, Satoh K, Shimosegawa T, Orikasa H, Watanabe T, Nishimura K, Ebihara Y, Koike N, Furukawa T: Intraductal tubulopapillary neoplasms of the pancreas distinct from pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasms. Am J Surg Pathol; 2009 Aug;33(8):1164-72
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  • [Title] Intraductal tubulopapillary neoplasms of the pancreas distinct from pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasms.
  • We have encountered cases of unusual intraductal pancreatic neoplasms with predominant tubulopapillary growth.
  • We collected data on 10 similar cases of "intraductal tubulopapillary neoplasms (ITPNs)" and analyzed their clinicopathologic and molecular features.
  • Tumor specimens were obtained from 5 men and 5 women with a mean age of 58 years.
  • The tumor cells formed tubulopapillae and contained little cytoplasmic mucin.
  • All the features of ITPN were distinct from those of other known intraductal pancreatic neoplasms, including pancreatic intraepithelial neoplasia, intraductal papillary mucinous neoplasm, and the intraductal variant of acinar cell carcinoma.
  • In conclusion, ITPNs can be considered to represent a new disease entity encompassing intraductal tubular carcinoma as a morphologic variant.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. DNA Mutational Analysis. Female. Humans. Immunohistochemistry. Male. Middle Aged

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  • (PMID = 19440145.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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58. Yang TM, Han SC, Wu CJ, Mo LR: Acinar cell carcinomas with exophytic growth and intraductal pancreatic duct invasion: peculiar multislice computed tomographic picture. J Hepatobiliary Pancreat Surg; 2009;16(2):238-41
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  • [Title] Acinar cell carcinomas with exophytic growth and intraductal pancreatic duct invasion: peculiar multislice computed tomographic picture.
  • MSCT showed 8.4 cm well-enhancing exophytic tumor of the pancreatic head which also protruded into the duodenum.
  • The pathological diagnosis was acinar cell carcinoma (ACC) originating in the pancreatic head and directly invading through the duodenal wall and the main pancreatic duct, without any lymph node involvement.
  • [MeSH-major] Carcinoma, Acinar Cell / radiography. Pancreatic Neoplasms / radiography. Tomography, X-Ray Computed
  • [MeSH-minor] Aged. Female. Humans. Neoplasm Invasiveness. Pancreatic Ducts / pathology

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  • (PMID = 19183830.001).
  • [ISSN] 1436-0691
  • [Journal-full-title] Journal of hepato-biliary-pancreatic surgery
  • [ISO-abbreviation] J Hepatobiliary Pancreat Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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59. Kitagami H, Kondo S, Hirano S, Kawakami H, Egawa S, Tanaka M: Acinar cell carcinoma of the pancreas: clinical analysis of 115 patients from Pancreatic Cancer Registry of Japan Pancreas Society. Pancreas; 2007 Jul;35(1):42-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinar cell carcinoma of the pancreas: clinical analysis of 115 patients from Pancreatic Cancer Registry of Japan Pancreas Society.
  • OBJECTIVES: Acinar cell carcinoma (ACC) of the pancreas is a rare tumor, and many aspects remain unclear because no large-scale clinical studies have been conducted.
  • RESULTS: Although ACC has been associated with advanced stage and poor prognosis, this tumor was resectable in 76.5% of the patients, and the 5-year survival rate after resection was favorable, being 43.9%.
  • [MeSH-major] Carcinoma, Acinar Cell / mortality. Pancreatic Neoplasms / mortality. Registries / statistics & numerical data
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor. Female. Humans. Japan / epidemiology. Male. Middle Aged. Neoplasm Staging / statistics & numerical data. Prognosis. Survival Rate. Treatment Outcome

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  • (PMID = 17575544.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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60. Mulkeen AL, Yoo PS, Cha C: Less common neoplasms of the pancreas. World J Gastroenterol; 2006 May 28;12(20):3180-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Less common neoplasms of the pancreas.
  • Recently, there has been an increased recognition of neoplasms of the pancreas other than ductal adenocarcinoma.
  • These lesions include: endocrine neoplasms, cystic tumors, solid pseudopapillary tumors, acinar cell carcinoma, squamous cell carcinoma, primary lymphoma of the pancreas, and metastatic lesions to the pancreas.
  • These less common neoplasms are being diagnosed more frequently as the number and sensitivity of diagnostic imaging studies increase.
  • This review article discusses the clinical course, diagnosis, and treatment of these less common, but quite relevant, neoplasms of the pancreas.
  • [MeSH-major] Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Adenocarcinoma, Mucinous / diagnosis. Adenocarcinoma, Mucinous / therapy. Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / therapy. Carcinoma, Papillary / diagnosis. Carcinoma, Papillary / therapy. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / therapy. Cystadenoma, Mucinous / diagnosis. Cystadenoma, Mucinous / therapy. Cystadenoma, Serous / diagnosis. Cystadenoma, Serous / therapy. Endocrine Gland Neoplasms / diagnosis. Endocrine Gland Neoplasms / therapy. Humans. Lymphoma / diagnosis. Lymphoma / therapy

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  • (PMID = 16718837.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Number-of-references] 51
  • [Other-IDs] NLM/ PMC4087960
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61. Diegel CR, Cho KR, El-Naggar AK, Williams BO, Lindvall C: Mammalian target of rapamycin-dependent acinar cell neoplasia after inactivation of Apc and Pten in the mouse salivary gland: implications for human acinic cell carcinoma. Cancer Res; 2010 Nov 15;70(22):9143-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mammalian target of rapamycin-dependent acinar cell neoplasia after inactivation of Apc and Pten in the mouse salivary gland: implications for human acinic cell carcinoma.
  • Cross-talk between the canonical Wnt and mammalian target of rapamycin (mTOR) signaling pathways occurs at multiple levels in the cell and likely contributes to the oncogenic effects of these pathways in human cancer.
  • To gain more insight into the interplay between Wnt and mTOR signaling in salivary gland tumorigenesis, we developed a mouse model in which both pathways are constitutively activated by the conditional inactivation of the Apc and Pten tumor suppressor genes.
  • Loss of either Apc or Pten alone did not cause tumor development.
  • However, deletion of both genes resulted in the formation of salivary gland tumors with 100% penetrance and short latency that showed a remarkable morphologic similarity to human acinic cell carcinoma.
  • Treatment of tumor-bearing mice using the mTOR inhibitor rapamycin led to complete regression of tumors, indicating that tumor growth was dependent on continued mTOR signaling.
  • Importantly, we found that human salivary gland acinic cell carcinomas also express markers of activated mTOR signaling.
  • Together, these results suggest that aberrant activation of mTOR signaling plays a pivotal role in acinar cell neoplasia of the salivary gland.
  • Because rapamycin analogues are approved for treating other types of human malignancies, our findings suggest that rapamycin therapy should be evaluated for treating patients with salivary gland acinic cell carcinoma.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / deficiency. Carcinoma, Acinar Cell / metabolism. PTEN Phosphohydrolase / deficiency. Salivary Glands / metabolism. TOR Serine-Threonine Kinases / metabolism
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Female. Flow Cytometry. Humans. Immunohistochemistry. Male. Mice. Mice, 129 Strain. Mice, Knockout. Salivary Gland Neoplasms / genetics. Salivary Gland Neoplasms / metabolism. Salivary Gland Neoplasms / pathology. Signal Transduction / drug effects. Sirolimus / pharmacology. Tumor Burden / drug effects


62. Tanaka H, Fukamachi K, Futakuchi M, Alexander DB, Long N, Tamamushi S, Minami K, Seino S, Ohara H, Joh T, Tsuda H: Mature acinar cells are refractory to carcinoma development by targeted activation of Ras oncogene in adult rats. Cancer Sci; 2010 Feb;101(2):341-6
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  • [Title] Mature acinar cells are refractory to carcinoma development by targeted activation of Ras oncogene in adult rats.
  • When adenovirus with Cre recombinase under the control of the CMV enhancer/chicken beta-actin (CAG) promoter (Ad-CAG-Cre) is injected into the pancreatic duct of these animals, pancreatic neoplasias develop.
  • Pathologically, the origin of these lesions is duct, intercalated duct, and centroacinar cells, but not acinar cells.
  • The present study was undertaken to test the effect of acinar cell-specific oncogenic ras expression.
  • Adult transgenic rats were injected with adenovirus with Cre recombinase under the control of the acinar cell-specific promoters amylase (Ad-Amy-Cre) and elastase-1 (Ad-Ela-Cre) or under the control of the non-specific CAG promoter.
  • Injection of either Ad-Amy-Cre or Ad-Ela-Cre into the pancreatic ducts of transgenic animals in which oncogenic Kras is tagged with hemagglutinin (HA), HA-Kras(G12V) rats resulted in expression of oncogenic ras in acinar cells but not in duct, intercalated duct, or centroacinar cells.
  • These results indicate that adult acinar cells are refractory to Ras oncogene activation and do not develop neoplasia in this model.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / etiology. Genes, ras. Pancreas, Exocrine / pathology. Pancreatic Neoplasms / etiology

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  • (PMID = 19917056.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
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63. Poelman SM, Nguyen K: Pancreatic panniculitis associated with acinar cell pancreatic carcinoma. J Cutan Med Surg; 2008 Jan-Feb;12(1):38-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic panniculitis associated with acinar cell pancreatic carcinoma.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Diseases / diagnosis. Pancreatic Neoplasms / diagnosis. Panniculitis / diagnosis

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  • (PMID = 18258147.001).
  • [ISSN] 1203-4754
  • [Journal-full-title] Journal of cutaneous medicine and surgery
  • [ISO-abbreviation] J Cutan Med Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 31
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64. Wargo JA, Warshaw AL: Surgical approach to pancreatic exocrine neoplasms. Minerva Chir; 2005 Dec;60(6):445-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surgical approach to pancreatic exocrine neoplasms.
  • Pancreatic exocrine neoplasms represent a wide spectrum of pathophysiologic entities that challenge us as surgeons.
  • In this review, we will explore the contemporary clinical management of pancreatic adenocarcinoma, acinar cell carcinoma, and cystic neoplasms of the pancreas.
  • [MeSH-major] Pancreas, Exocrine / surgery. Pancreatectomy. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adenocarcinoma / surgery. Algorithms. Carcinoma, Acinar Cell / surgery. Chemotherapy, Adjuvant. Cystadenocarcinoma / surgery. Cystadenoma / surgery. Decision Trees. Humans. Magnetic Resonance Imaging. Neoadjuvant Therapy / methods. Neoplasm Staging. Radiotherapy, Adjuvant. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 16401999.001).
  • [ISSN] 0026-4733
  • [Journal-full-title] Minerva chirurgica
  • [ISO-abbreviation] Minerva Chir
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 181
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65. Ban D, Shimada K, Sekine S, Sakamoto Y, Kosuge T, Kanai Y, Hiraoka N: Pancreatic ducts as an important route of tumor extension for acinar cell carcinoma of the pancreas. Am J Surg Pathol; 2010 Jul;34(7):1025-36
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  • [Title] Pancreatic ducts as an important route of tumor extension for acinar cell carcinoma of the pancreas.
  • Acinar cell carcinoma (ACC) of the pancreas is very rare, which usually grows expansively.
  • We reviewed the detailed gross and histologic features of 13 cases of ACC, of which 7 (54%) showed intraductal polypoid growth (IPG) of the tumor in the large pancreatic ducts with a mean IPG length of 24.8 mm.
  • Comparison of the clinicopathologic characteristics showed that ACC with IPG had less infiltrative features including lymphatic, venous, and neural invasion, formation of tumor thrombus in the portal vein, nodal metastasis, and invasion beyond the pancreas to the surrounding organs; death in only 1 case (14%) of ACC with IPG was the result of ACC itself.
  • In contrast, ACC without IPG frequently showed more infiltrative growth, and was the cause of death in 50% of patients with this type of tumor.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Female. Humans. Japan / epidemiology. Male. Middle Aged. Neoplasm Invasiveness. Survival Rate

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  • (PMID = 20534994.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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66. Mancuso PA, Chabert C, Chin P, Kovac P, Skyring T, Watt WH, Napaki S: Prostate cancer detection in men with an initial diagnosis of atypical small acinar proliferation. BJU Int; 2007 Jan;99(1):49-52
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  • [Title] Prostate cancer detection in men with an initial diagnosis of atypical small acinar proliferation.
  • OBJECTIVE: To determine the subsequent prostatic adenocarcinoma detection rate amongst men with an initial diagnosis of atypical small acinar proliferation (ASAP).
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biopsy, Needle. Cell Proliferation. Cohort Studies. Humans. Immunohistochemistry. Male. Middle Aged. Predictive Value of Tests. Prostate-Specific Antigen / blood. Retrospective Studies

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  • (PMID = 17227491.001).
  • [ISSN] 1464-4096
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen
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67. Takanami K, Abe K, Mitamura A, Miyazaki S, Abe K, Ishida K, Yamada S, Takahashi S: Two cases of 18 F-FDG PET/CT findings in acinar cell carcinoma of the pancreas. Clin Nucl Med; 2009 Apr;34(4):209-12
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  • [Title] Two cases of 18 F-FDG PET/CT findings in acinar cell carcinoma of the pancreas.
  • They underwent F-18 FDG PET/CT and subsequently a pancreaticoduodenectomy and acinar cell carcinoma in the pancreas was proven histopathologically.
  • In one case, the tumor consisted of a solid component presenting intense FDG uptake and necrotic tissue.
  • In another case, the tumor consisted of cystic and papillary components presenting with weak FDG uptake.
  • This report thus documents 2 cases of acinar cell carcinoma that showed contrasting histopathologic and F-18 FDG PET/CT findings.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / radionuclide imaging. Fluorodeoxyglucose F18 / pharmacology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / radionuclide imaging. Positron-Emission Tomography / methods. Tomography, X-Ray Computed / methods

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  • (PMID = 19300048.001).
  • [ISSN] 1536-0229
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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68. Shi G, Zhu L, Sun Y, Bettencourt R, Damsz B, Hruban RH, Konieczny SF: Loss of the acinar-restricted transcription factor Mist1 accelerates Kras-induced pancreatic intraepithelial neoplasia. Gastroenterology; 2009 Apr;136(4):1368-78
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  • [Title] Loss of the acinar-restricted transcription factor Mist1 accelerates Kras-induced pancreatic intraepithelial neoplasia.
  • BACKGROUND & AIMS: Invasive pancreatic ductal adenocarcinoma is thought to originate from duct-like lesions called pancreatic intraepithelial neoplasia (PanIN).
  • METHODS: In this study, we examined the importance of the acinar-restricted transcription factor Mist1 to KrasG12D-induced mouse PanIN (mPanIN) formation in 3 different mouse models of pancreatic cancer.
  • RESULTS: In the absence of Mist1 (Mist1KO), KrasG12D-expressing mice exhibited severe exocrine pancreatic defects that were rescued by ectopic expression of Mist1 in acinar cells. mPanIN development was greatly accelerated in Mist1KO/KrasG12D/+ pancreata, and in vitro assays revealed that Mist1KO acinar cells were predisposed to convert to a ductal phenotype and activate epidermal growth factor receptor (EGFR) and Notch-signaling pathways.
  • CONCLUSIONS: We propose that convergence of EGFR, Notch, and Kras pathways in acinar cells lacking Mist1 leads to enhanced mPanIN formation.

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  • (PMID = 19249398.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK055489-10; United States / NCI NIH HHS / CA / P50CA62924; United States / NCI NIH HHS / CA / R01 CA124586-02; United States / NCI NIH HHS / CA / P50 CA062924; United States / NIDDK NIH HHS / DK / DK055489-10; United States / NCI NIH HHS / CA / CA124586-02; United States / NIDDK NIH HHS / DK / DK55489; United States / NIDDK NIH HHS / DK / R01 DK055489; United States / NCI NIH HHS / CA / R01 CA124586; United States / NCI NIH HHS / CA / CA124586
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Mist1 protein, mouse; 0 / Receptors, Notch; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ NIHMS182460; NLM/ PMC2845927
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69. Blaine SA, Ray KC, Anunobi R, Gannon MA, Washington MK, Means AL: Adult pancreatic acinar cells give rise to ducts but not endocrine cells in response to growth factor signaling. Development; 2010 Jul;137(14):2289-96
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  • [Title] Adult pancreatic acinar cells give rise to ducts but not endocrine cells in response to growth factor signaling.
  • Studies in both humans and rodents have found that insulin(+) cells appear within or near ducts of the adult pancreas, particularly following damage or disease, suggesting that these insulin(+) cells arise de novo from ductal epithelium.
  • Therefore, we tested the hypothesis that both hyperplastic ductal cells and their associated insulin(+) cells arise from the same cell of origin.
  • Using a mouse model that develops insulin(+) cell-containing hyperplastic ducts in response to the growth factor TGFalpha, we performed genetic lineage tracing experiments to determine which cells gave rise to both hyperplastic ductal cells and duct-associated insulin(+) cells.
  • We found that hyperplastic ductal cells arose largely from acinar cells that changed their cell fate, or transdifferentiated, into ductal cells.
  • However, insulin(+) cells adjacent to acinar-derived ductal cells arose from pre-existing insulin(+) cells, suggesting that islet endocrine cells can intercalate into hyperplastic ducts as they develop.
  • We conclude that apparent pancreatic plasticity can result both from the ability of acinar cells to change fate and of endocrine cells to reorganize in association with duct structures.

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  • (PMID = 20534672.001).
  • [ISSN] 1477-9129
  • [Journal-full-title] Development (Cambridge, England)
  • [ISO-abbreviation] Development
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P60 DK020593; United States / NIDDK NIH HHS / DK / NIH P30DK058404; United States / NIDDK NIH HHS / DK / DK58404; United States / NIDDK NIH HHS / DK / P30 DK058404; United States / NICHD NIH HHS / HD / P30 HD015052; United States / NCI NIH HHS / CA / NIH CA68485; United States / NEI NIH HHS / EY / EY08126; United States / NEI NIH HHS / EY / P30 EY008126; United States / NIDDK NIH HHS / DK / DK59637; United States / NIDDK NIH HHS / DK / P30 DK020593; United States / NCI NIH HHS / CA / P30 CA068485; United States / NICHD NIH HHS / HD / HD15052; United States / NIDDK NIH HHS / DK / DK20593; United States / NIDDK NIH HHS / DK / U24 DK059637
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Insulin; 0 / Intercellular Signaling Peptides and Proteins
  • [Other-IDs] NLM/ PMC2889602
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70. Du YC, Klimstra DS, Varmus H: Activation of PyMT in beta cells induces irreversible hyperplasia, but oncogene-dependent acinar cell carcinomas when activated in pancreatic progenitors. PLoS One; 2009 Sep 07;4(9):e6932
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activation of PyMT in beta cells induces irreversible hyperplasia, but oncogene-dependent acinar cell carcinomas when activated in pancreatic progenitors.
  • It is unclear whether the cellular origin of various forms of pancreatic cancer involves transformation or transdifferentiation of different target cells or whether tumors arise from common precursors, with tumor types determined by the specific genetic alterations.
  • To ask whether PyMT transforms and transdifferentiates endocrine cells toward exocrine tumor phenotypes, we generated transgenic mice that carry tetracycline-inducible PyMT and a linked luciferase reporter.
  • Induction of PyMT in beta cells causes beta-cell hyperplastic lesions that do not progress to malignant neoplasms.
  • When PyMT is de-induced, beta cell proliferation and growth cease; however, regression does not occur, suggesting that continued production of PyMT is not required to maintain the viable expanded beta cell population.
  • In contrast, induction of PyMT in early pancreatic progenitor cells under the control of Pdx1 produces acinar cell carcinomas and beta-cell hyperplasia.
  • The survival of acinar tumor cells is dependent on continued expression of PyMT.
  • Our findings indicate that PyMT can induce exocrine tumors from pancreatic progenitor cells, but cells in the beta cell lineage are not transdifferentiated toward exocrine cell types by PyMT; instead, they undergo oncogene-dependent hyperplastic growth, but do not require PyMT for survival.

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  • (PMID = 19812721.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA105492; United States / NCI NIH HHS / CA / P30 CA08748; United States / NCI NIH HHS / CA / P01 CA94060; United States / NCI NIH HHS / CA / P30 CA008748; United States / NCI NIH HHS / CA / P30-CA 08748; United States / NCI NIH HHS / CA / P01 CA094060; United States / NCI NIH HHS / CA / R24 CA83084; United States / NCI NIH HHS / CA / 5U01CA105492; United States / NCI NIH HHS / CA / R24 CA083084
  • [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 / Antigens, Polyomavirus Transforming; EC 1.13.12.- / Luciferases; F8VB5M810T / Tetracycline
  • [Other-IDs] NLM/ PMC2758666
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71. Rossetti S, Hoogeveen AT, Esposito J, Sacchi N: Loss of MTG16a (CBFA2T3), a novel rDNA repressor, leads to increased ribogenesis and disruption of breast acinar morphogenesis. J Cell Mol Med; 2010 Jun;14(6A):1358-70
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  • [Title] Loss of MTG16a (CBFA2T3), a novel rDNA repressor, leads to increased ribogenesis and disruption of breast acinar morphogenesis.
  • We also show that either knocking down MTG16a by RNA interference, or sequestering MTG16a outside the nucleolus of human breast epithelial cells, hampers acinar morphogenesis concomitant with up-regulation of rRNA synthesis and increased ribogenesis.
  • [MeSH-major] Breast / embryology. Breast / metabolism. DNA, Ribosomal / metabolism. Morphogenesis. Repressor Proteins / deficiency. Ribosomes / metabolism. Tumor Suppressor Proteins / deficiency
  • [MeSH-minor] Breast Neoplasms / genetics. Breast Neoplasms / pathology. Cell Nucleolus / metabolism. Down-Regulation / genetics. Epithelial Cells / metabolism. Female. Fibroblasts / metabolism. Gene Expression Regulation, Neoplastic. Gene Knockdown Techniques. HeLa Cells. Humans. Models, Biological. Nucleolus Organizer Region / genetics. Protein Transport. Proto-Oncogene Proteins c-myc / metabolism. Up-Regulation / genetics

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  • [ErratumIn] J Cell Mol Med. 2010 Aug;14(8):2186
  • (PMID = 19961547.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CBFA2T3 protein, human; 0 / DNA, Ribosomal; 0 / Proto-Oncogene Proteins c-myc; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC3828852
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72. Imamura M, Kimura Y, Ito H, Nobuoka T, Koito K, Sasaki A, Hirata K: Acinar cell carcinoma of the pancreas with intraductal growth: report of a case. Surg Today; 2009;39(11):1006-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinar cell carcinoma of the pancreas with intraductal growth: report of a case.
  • Acinar cell carcinomas (ACCs) of the pancreas are rare neoplasms, accounting for approximately 1% of all exocrine pancreatic tumors.
  • This type of tumor is known to be aggressive, although the survival rates are somewhat better than they are for ductal carcinoma.
  • The tumor tends to present nonspecific symptoms.
  • [MeSH-major] Carcinoma, Acinar Cell / surgery. Neoplasm Invasiveness. Pancreatectomy / methods. Pancreatic Ducts / pathology. Pancreatic Neoplasms / surgery

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  • (PMID = 19882327.001).
  • [ISSN] 1436-2813
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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73. Kim H: DNA repair Ku proteins in gastric cancer cells and pancreatic acinar cells. Amino Acids; 2008 Feb;34(2):195-202
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA repair Ku proteins in gastric cancer cells and pancreatic acinar cells.
  • In this review, the role of Ku on cell proliferation and apoptosis will be discussed.
  • Both Ku70 and Ku80 expressions are mediated by constitutively activated NF-kappaB and constitutively expressed cyclooxygenase-2 in gastric cancer cells, which may be related to gastric cell proliferation and carcinogenesis.
  • In addition, nuclear loss of Ku may underlie the mechanism of apoptosis in pancreatic acinar cells after oxidative stress.
  • [MeSH-major] Antigens, Nuclear / metabolism. DNA Helicases / metabolism. DNA Repair. DNA-Binding Proteins / metabolism. Pancreas / physiology. Stomach Neoplasms / physiopathology
  • [MeSH-minor] Animals. Apoptosis. Cell Proliferation. Dimerization. Humans. Immunoglobulin J Recombination Signal Sequence-Binding Protein / metabolism. NF-kappa B p50 Subunit / metabolism. Oxidative Stress / physiology. Prostaglandin-Endoperoxide Synthases / physiology. Stomach / cytology

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  • (PMID = 17031478.001).
  • [ISSN] 1438-2199
  • [Journal-full-title] Amino acids
  • [ISO-abbreviation] Amino Acids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / DNA-Binding Proteins; 0 / Immunoglobulin J Recombination Signal Sequence-Binding Protein; 0 / Ku autoantigen; 0 / NF-kappa B p50 Subunit; 0 / XRCC5 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 3.6.4.- / DNA Helicases
  • [Number-of-references] 69
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74. Rodríguez-Patrón Rodríguez R, Mayayo Dehesa T, Burgos Revilla FJ, Sanz Mayayo E, García González R: [Prognostic significance of PIN and Atypical Small Acinar Proliferation on transrectal ultrasound-guided prostate biopsy]. Actas Urol Esp; 2006 Apr;30(4):359-66
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  • [Title] [Prognostic significance of PIN and Atypical Small Acinar Proliferation on transrectal ultrasound-guided prostate biopsy].
  • [Transliterated title] Significación pronóstica del PIN y la atípia glandular focal en la Biopsia Transrectal Ecodirigida de Próstata.
  • OBJECTIVE: To review the incidence of PIN and Atypical Small Acinar Proliferation (ASAP) on first biopsy, the risk to find cancer on following biopsies and what is the importance given to this findings, analizing how frequently and how long after the initial finding this patients are rebiopsied.
  • [MeSH-major] Adenocarcinoma / pathology. Biopsy, Needle / methods. Prostate / pathology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology. Surgery, Computer-Assisted. Ultrasonography, Interventional
  • [MeSH-minor] Adult. Cell Division. Humans. Male. Reoperation / utilization. Retrospective Studies. Time Factors

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  • (PMID = 16838607.001).
  • [ISSN] 0210-4806
  • [Journal-full-title] Actas urologicas españolas
  • [ISO-abbreviation] Actas Urol Esp
  • [Language] spa
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] Spain
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75. Chung WJ, Byun JH, Lee SS, Lee MG: Imaging findings in a case of mixed acinar-endocrine carcinoma of the pancreas. Korean J Radiol; 2010 May-Jun;11(3):378-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imaging findings in a case of mixed acinar-endocrine carcinoma of the pancreas.
  • Mixed acinar-endocrine carcinoma (MAEC) of the pancreas is extremely uncommon.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / radiography. Endocrine Gland Neoplasms / pathology. Endocrine Gland Neoplasms / radiography. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / radiography

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  • [Cites] AJR Am J Roentgenol. 2000 Mar;174(3):671-5 [10701607.001]
  • [Cites] Eur J Radiol. 2008 Aug;67(2):321-8 [17766075.001]
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  • (PMID = 20461195.001).
  • [ISSN] 2005-8330
  • [Journal-full-title] Korean journal of radiology
  • [ISO-abbreviation] Korean J Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2864868
  • [Keywords] NOTNLM ; Endocrine / Exocrine / Mixed acinar-endocrine carcinoma / Pancreas
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76. Comper F, Antonello D, Beghelli S, Gobbo S, Montagna L, Pederzoli P, Chilosi M, Scarpa A: Expression pattern of claudins 5 and 7 distinguishes solid-pseudopapillary from pancreatoblastoma, acinar cell and endocrine tumors of the pancreas. Am J Surg Pathol; 2009 May;33(5):768-74
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  • [Title] Expression pattern of claudins 5 and 7 distinguishes solid-pseudopapillary from pancreatoblastoma, acinar cell and endocrine tumors of the pancreas.
  • Solid-pseudopapillary tumor (SPT) of the pancreas is characterized by a discohesive appearance of the neoplastic cells.
  • This latter includes pancreatic endocrine tumor (PET) as SPT may show neuroendocrine differentiation, and pancreatic acinar cell carcinoma (ACC) and pancreatoblastoma (PB) that may often show nuclear beta-catenin staining.
  • However, the role of additional cell-cell adhesion systems remains to be elucidated in SPT, particularly that of claudins that are essential components of tight junctions showing modulated expression in diverse tumor types.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Acinar Cell / chemistry. Membrane Proteins / analysis. Pancreas / chemistry. Pancreatic Neoplasms / chemistry. Tight Junctions / chemistry

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  • (PMID = 19194274.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDH1 protein, human; 0 / CLDN5 protein, human; 0 / CLDN7 protein, human; 0 / CTNNB1 protein, human; 0 / Cadherins; 0 / Claudin-5; 0 / Claudins; 0 / Membrane Proteins; 0 / beta Catenin
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77. Rembao-Bojórquez D, Vega R, Bermúdez-Maldonado L, Gutiérrez R, Salinas C, Tena-Suck M: Choroid plexus acinar adenoma: a case report. J Neurooncol; 2007 Jun;83(2):191-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Choroid plexus acinar adenoma: a case report.
  • Mucus-secreting adenomas or acinar adenoma of the choroid plexus are very rare.
  • He was admitted to the hospital with significant tumor expansion and clinical deterioration.
  • Pathological findings were consistent with an acinar choroid plexus adenoma.
  • The tumor was attached to the ependymal lining and was strongly adhered to the walls and floor of the IV ventricle.
  • Post-operative bleeding complicated partial removal of this tumor.
  • [MeSH-major] Adenoma / pathology. Carcinoma, Acinar Cell / pathology. Cerebral Ventricle Neoplasms / pathology. Choroid Plexus Neoplasms / pathology

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  • (PMID = 17406790.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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78. Tatli S, Mortele KJ, Levy AD, Glickman JN, Ros PR, Banks PA, Silverman SG: CT and MRI features of pure acinar cell carcinoma of the pancreas in adults. AJR Am J Roentgenol; 2005 Feb;184(2):511-9
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  • [Title] CT and MRI features of pure acinar cell carcinoma of the pancreas in adults.
  • OBJECTIVE: We sought to describe the CT and MRI features of pure acinar cell carcinoma of the pancreas in adults.
  • MATERIALS AND METHODS: Eleven patients (six women and five men; mean age, 64 years) with acinar cell carcinoma, documented by pathologic examination of resected specimens, underwent CT (n=9) or MRI (n=2) examinations.
  • Two radiologists evaluated imaging studies and determined, by consensus, the following data for each tumor: size, location, margination, internal density or signal intensity, and contrast enhancement pattern.
  • CONCLUSION: Pure acinar cell carcinoma of the pancreas is usually an exophytic, oval or round, well-marginated, and hypovascular mass on CT and MRI.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Magnetic Resonance Imaging. Pancreatic Neoplasms / pathology. Tomography, X-Ray Computed

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  • (PMID = 15671372.001).
  • [ISSN] 0361-803X
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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79. Fitzgerald TL, Hickner ZJ, Schmitz M, Kort EJ: Changing incidence of pancreatic neoplasms: a 16-year review of statewide tumor registry. Pancreas; 2008 Aug;37(2):134-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Changing incidence of pancreatic neoplasms: a 16-year review of statewide tumor registry.
  • OBJECTIVES: Although most pancreatic neoplasms are adenocarcinoma, there are many other histological types, some of which may be increasing in frequency.
  • To better define these trends, we reviewed 16 years of data from a statewide tumor registry.
  • METHODS: Using the State of Michigan tumor registry, all patients with primary pancreatic cancers from 1986 to 2002 were identified, and patients were excluded if there were insufficient data or the histological subtype was not clearly defined in the literature.
  • RESULTS: There were 17,610 pancreatic neoplasms identified, and 2425 were excluded, leaving a final population of 15,185.
  • Twenty-five types of primary pancreatic neoplasms were identified.
  • The most common were adenocarcinoma, mucinous cystadenocarcinoma, nonfunctional neuroendocrine, adenosquamous, anaplastic, intraductal papillary mucinous, and acinar cell (8.37, 0.43, 0.18, 0.05, 0.04, 0.04, and 0.02 per 100,000 per year, respectively).
  • The mean age at presentation was similar for tumor types, 69.2 years old, with the exception of endocrine neoplasms occurring at a younger age, 58.5 years old (P < 0.0005).
  • There was a significant change in the incidence of nonfunctional neuroendocrine neoplasms, greater than 2-fold increase (P = 0.0003).
  • CONCLUSIONS: The incidence of most pancreatic neoplasms has changed a little; however, nonfunctional neuroendocrine neoplasms increased greater than 2-fold.
  • [MeSH-major] Pancreatic Neoplasms / epidemiology
  • [MeSH-minor] Adenocarcinoma / epidemiology. Aged. Carcinoma, Acinar Cell / epidemiology. Carcinoma, Adenosquamous / epidemiology. Carcinoma, Pancreatic Ductal / epidemiology. Cystadenocarcinoma, Mucinous / epidemiology. Female. Humans. Male. Michigan / epidemiology. Middle Aged. Neuroendocrine Tumors / epidemiology. Registries. Time Factors

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  • (PMID = 18665072.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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80. Dimri M, Naramura M, Duan L, Chen J, Ortega-Cava C, Chen G, Goswami R, Fernandes N, Gao Q, Dimri GP, Band V, Band H: Modeling breast cancer-associated c-Src and EGFR overexpression in human MECs: c-Src and EGFR cooperatively promote aberrant three-dimensional acinar structure and invasive behavior. Cancer Res; 2007 May 1;67(9):4164-72
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  • [Title] Modeling breast cancer-associated c-Src and EGFR overexpression in human MECs: c-Src and EGFR cooperatively promote aberrant three-dimensional acinar structure and invasive behavior.
  • Using a combination of morphologic analysis and confocal imaging of polarity markers in three-dimensional Matrigel culture together with functional analyses of early oncogenic traits, we show for the first time that EGFR and c-Src co-overexpression but not EGFR or c-Src overexpression alone unleashes an oncogenic signaling program that leads to hyperproliferation and loss of polarity in three-dimensional acinar cultures, marked enhancement of migratory and invasive behavior, and anchorage-independent growth.

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  • (PMID = 17483327.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096986-01A1; United States / NCI NIH HHS / CA / R01 CA095221-02; United States / NCI NIH HHS / CA / CA096986-01A1; United States / NCI NIH HHS / CA / R01 CA095221-01A1; United States / NCI NIH HHS / CA / R01 CA096986-04; United States / NCI NIH HHS / CA / R01 CA095221-05; United States / NCI NIH HHS / CA / CA 94143; United States / NCI NIH HHS / CA / R01 CA096986-05; United States / NCI NIH HHS / CA / CA095221-01A1; United States / NCI NIH HHS / CA / R01 CA096986-02; United States / NCI NIH HHS / CA / CA 87986; United States / NCI NIH HHS / CA / CA 81076; United States / NCI NIH HHS / CA / CA 99163; United States / NCI NIH HHS / CA / 1U54 CA 119341-01; United States / NCI NIH HHS / CA / CA 96844; United States / NCI NIH HHS / CA / CA 76118; United States / NCI NIH HHS / CA / CA 99900; United States / NCI NIH HHS / CA / R01 CA095221-03; United States / NCI NIH HHS / CA / R01 CA096986-03; United States / NCI NIH HHS / CA / R01 CA095221-04
  • [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 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 119978-18-6 / matrigel; 9007-34-5 / Collagen; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / src-Family Kinases
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81. Machado MC, Machado MA, Perini MV, Herman P, Jukemura J, Leite KR, Bacchella T: Acinar cell carcinoma of the pancreas: is the absence of neuroendocrine component related to a more malignant behavior? Hepatogastroenterology; 2008 Mar-Apr;55(82-83):708-10
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  • [Title] Acinar cell carcinoma of the pancreas: is the absence of neuroendocrine component related to a more malignant behavior?
  • BACKGROUND/AIMS: Acinar cell carcinomas are uncommon malignant tumors of the pancreas, accounting for 1-2% of all the cases of exocrine pancreatic tumor.
  • Some authors have estimated acinar cell tumors to be as aggressive as ductal adenocarcinoma of the pancreas whereas other series showed acinar cell tumors to have a favorable clinical outcome.
  • This discrepancy in prognosis may be related to the cellular components of the tumor.
  • METHODOLOGY: With the aim to evaluate the possible relationship between the presence of neuroendocrine differentiation and behavior of these tumors, the authors reviewed all patients presenting acinar cell carcinoma of the pancreas in the last 5 years with emphasis in the immunohistochemical evaluation.
  • This data suggests that this tumor is less aggressive than ductal adenocarcinoma and even with nodal involvement, long-term survival after complete resection can be achieved.
  • Due to the rarity of this pancreatic tumor, this relationship remains to be confirmed with a multicentric study including a larger number of patients.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18613439.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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82. Schmidt CM, Matos JM, Bentrem DJ, Talamonti MS, Lillemoe KD, Bilimoria KY: Acinar cell carcinoma of the pancreas in the United States: prognostic factors and comparison to ductal adenocarcinoma. J Gastrointest Surg; 2008 Dec;12(12):2078-86
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  • [Title] Acinar cell carcinoma of the pancreas in the United States: prognostic factors and comparison to ductal adenocarcinoma.
  • INTRODUCTION: Pancreatic acinar cell carcinoma (ACC) is a rare tumor with poorly defined prognosis.
  • OBJECTIVE: Our objective was to compare a large population of patients with ACC to pancreatic ductal cell adenocarcinoma (DCC) in order to determine distinguishing characteristics and to assess survival.
  • RESULTS: Median tumor size was 6.9 cm (vs. 4.6 cm DCC); 32.1% had nodal metastases (vs. 48.0% DCC); and 47% had high-grade tumors (vs. 37.3% DCC).
  • Patients with ACC were more likely to be male, white, and have larger tumor size, no nodal involvement, or pancreatic tail tumors.
  • [MeSH-major] Carcinoma, Acinar Cell / epidemiology. Carcinoma, Acinar Cell / surgery. Pancreatic Neoplasms / epidemiology. Pancreatic Neoplasms / surgery

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  • (PMID = 18836784.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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83. Iczkowski KA: Current prostate biopsy interpretation: criteria for cancer, atypical small acinar proliferation, high-grade prostatic intraepithelial neoplasia, and use of immunostains. Arch Pathol Lab Med; 2006 Jun;130(6):835-43
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  • [Title] Current prostate biopsy interpretation: criteria for cancer, atypical small acinar proliferation, high-grade prostatic intraepithelial neoplasia, and use of immunostains.
  • CONCLUSIONS: Diagnosis begins by evaluating a focus of atypical single-cell layer lined acini according to the 3 minimal diagnostic criteria for cancer: an infiltrative pattern, nuclear enlargement and hyperchromasia, and prominent nucleoli.
  • Atypical small acinar proliferation suspicious for malignancy designates foci that have either qualitative or quantitative limitations in atypia precluding a definite cancer diagnosis.
  • Isolated high-grade prostatic intraepithelial neoplasia has a 3% to 14% incidence and predicts cancer on repeat biopsy in 23% of cases.
  • Immunostaining for a marker of benign prostate (cytoplasmic keratin 34betaE12 or nuclear p63) and a marker of cancer (alpha-methylacyl coA racemase, clone P504S) may or may not resolve atypical small acinar proliferation diagnoses.
  • Performance of 34betaE12 and P504S immunostains resolved 76% of atypical small acinar proliferation diagnoses per consensus of 3 urologic pathologists studied; a technical limitation is preservation of the focus in question on the levels used for immunostaining.
  • [MeSH-major] Immunohistochemistry / methods. Precancerous Conditions / pathology. Prostate / pathology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Biopsy, Needle. Cell Nucleus / pathology. Cell Proliferation. Humans. Male

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  • (PMID = 16740037.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 58
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84. Azúa-Romeo J, Sánchez-Garnica JC, Azúa-Blanco J, Tovar-Lázaro M: DNA quantification as prognostic factor in a case of acinar cell carcinoma of the parotid gland, diagnosed by FNA. Med Oral Patol Oral Cir Bucal; 2005 Aug-Oct;10(4):289-93

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  • [Title] DNA quantification as prognostic factor in a case of acinar cell carcinoma of the parotid gland, diagnosed by FNA.
  • Fine needle aspiration cytology was performed, diagnosing of compatible with acinar cell carcinoma, thus DNA quantification by image cytometry was carried out.
  • [MeSH-major] Carcinoma, Acinar Cell / genetics. Parotid Neoplasms / genetics
  • [MeSH-minor] Adult. Aneuploidy. Biopsy, Fine-Needle. DNA Replication. DNA, Neoplasm / analysis. Humans. Image Cytometry. Male. Neoplasm Invasiveness. Prognosis

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  • (PMID = 16056182.001).
  • [ISSN] 1698-6946
  • [Journal-full-title] Medicina oral, patología oral y cirugía bucal
  • [ISO-abbreviation] Med Oral Patol Oral Cir Bucal
  • [Language] eng; spa
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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85. Ambrosini-Spaltro A, Potì O, De Palma M, Filotico M: Pancreatic-type acinar cell carcinoma of the stomach beneath a focus of pancreatic metaplasia of the gastric mucosa. Hum Pathol; 2009 May;40(5):746-9
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  • [Title] Pancreatic-type acinar cell carcinoma of the stomach beneath a focus of pancreatic metaplasia of the gastric mucosa.
  • Acinar cell carcinoma is an uncommon type of carcinoma of the pancreas that can exceptionally arise in ectopic pancreatic tissue.
  • Herein, we report a case of a 52-year-old man with pancreatic-type acinar cell carcinoma of the stomach and concomitant pancreatic metaplasia of the adjacent nonneoplastic gastric mucosa.
  • There was neither clinical nor radiographic evidence of a tumor in the pancreas itself.
  • Macroscopically, an ulcerated tumor, measuring 4 x 1.7 cm, was found in the distal antrum.
  • Microscopically, the biopsy and the surgical specimen revealed a neoplasm with a predominantly trabecular architecture composed of moderately atypical cells with finely dispersed chromatin and indistinct nucleoli.
  • The neoplastic cells and those of the adjacent metaplastic mucosa were both strongly immunoreactive for alpha-1-antitrypsin, consistent with pancreatic acinar cell differentiation.
  • Ectopic pancreatic-type acinar cell carcinoma is an extremely rare condition, having been previously reported only in 5 occasions, none of them in association with pancreatic acinar cell metaplasia of the gastric mucosa.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Gastric Mucosa / pathology. Pancreas / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Cell Differentiation. Humans. Male. Metaplasia / pathology. Middle Aged. alpha 1-Antitrypsin / biosynthesis

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  • (PMID = 19144387.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / SERPINA1 protein, human; 0 / alpha 1-Antitrypsin
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86. Hsu MY, Pan KT, Chu SY, Hung CF, Wu RC, Tseng JH: CT and MRI features of acinar cell carcinoma of the pancreas with pathological correlations. Clin Radiol; 2010 Mar;65(3):223-9
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  • [Title] CT and MRI features of acinar cell carcinoma of the pancreas with pathological correlations.
  • AIM: To document the computed tomography (CT) and magnetic resonance imaging (MRI) features of acinar cell carcinoma of the pancreas and to correlate them with pathological findings to determine the unique imaging manifestations of this rare subtype tumour of the pancreas.
  • MATERIALS AND METHODS: From January 1986 to August 2008, six patients (five men and one woman, mean age 61.3 years) with histologically proven acinar cell carcinoma of the pancreas underwent CT (n=6) and MRI (n=4) examinations.
  • The imaging features of each tumour were documented and compared with pathological findings.
  • Two tumours (33%) exhibited intratumoural haemorrhage, and one tumour (17%) had amorphous intratumoural calcification.
  • CONCLUSION: Acinar cell carcinoma of the pancreas has distinct imaging features, and both CT and MRI are useful and complementary imaging methods.
  • [MeSH-major] Carcinoma, Acinar Cell. Magnetic Resonance Imaging. Pancreatic Neoplasms. Tomography, X-Ray Computed

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  • [Copyright] Copyright (c) 2010 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.
  • (PMID = 20152279.001).
  • [ISSN] 1365-229X
  • [Journal-full-title] Clinical radiology
  • [ISO-abbreviation] Clin Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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87. Wisnoski NC, Townsend CM Jr, Nealon WH, Freeman JL, Riall TS: 672 patients with acinar cell carcinoma of the pancreas: a population-based comparison to pancreatic adenocarcinoma. Surgery; 2008 Aug;144(2):141-8
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  • [Title] 672 patients with acinar cell carcinoma of the pancreas: a population-based comparison to pancreatic adenocarcinoma.
  • BACKGROUND: Acinar cell carcinoma (ACC) is a rare cancer of the pancreas accounting for approximately 1% of nonendocrine tumors.
  • The demographic factors, tumor characteristics, resection status, and long-term survival were compared between the 2 groups.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18656619.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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88. Kobayashi S, Asakura T, Ohike N, Enomoto T, Sakurai J, Koizumi S, Watanabe T, Nakano H, Otsubo T: Mixed acinar-endocrine carcinoma of the pancreas with intraductal growth into the main pancreatic duct: Report of a case. Surg Today; 2010 Apr;40(4):380-4
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  • [Title] Mixed acinar-endocrine carcinoma of the pancreas with intraductal growth into the main pancreatic duct: Report of a case.
  • The patient was a 75-year-old asymptomatic man, in whom a tumor mass in the pancreatic tail had been found 6 months earlier.
  • Computed tomography revealed a mass 7 cm in diameter, and an enhancement with contrast medium was observed at the periphery and partially inside the mass, but not in most parts of the tumor.
  • A distal pancreatectomy was performed because of the possibility of a malignant tumor.
  • The tumor consisted of a lobular invasive growth component and a component with intraductal growth into the main pancreatic duct, and histologically the tumor cells had solid acinar to partially trabecular/tubular patterns.
  • Trypsin (an acinic cell marker) expression was widely observed, followed by the expression of chromogranin A (an endocrine cell marker) in about 30% of the tumor cells.
  • The tumor was diagnosed as mixed acinar-endocrine carcinoma according to the WHO classification.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Endocrine Gland Neoplasms / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 20339996.001).
  • [ISSN] 1436-2813
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Chromogranin A
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89. Fujii M, Sato H, Ogasawara T, Ando T, Tsujii S, Nagahori J, Komatsu Y, Matsuoka A: [A case of liver metastasis of pancreatic acinar cell carcinoma treated with S-1 and intra-arterial CDDP combination therapy]. Gan To Kagaku Ryoho; 2010 Oct;37(10):1987-90
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  • [Title] [A case of liver metastasis of pancreatic acinar cell carcinoma treated with S-1 and intra-arterial CDDP combination therapy].
  • A 55-year-old man underwent a pylorus-preserving pancreatoduodenectomy in August 2006 because of acinar cell carcinoma of the head of the pancreas.
  • At the beginning of this treatment, it seemed to be a stable disease, but CT revealed tumor progression in January 2007.
  • We suggest that combination chemotherapy with oral S-1 and intra-arterial CDDP can be effective treatments for pancreatic acinar cell carcinoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Cisplatin / therapeutic use. Liver Neoplasms / drug therapy. Oxonic Acid / therapeutic use. Pancreatic Neoplasms / drug therapy. Tegafur / therapeutic use

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  • (PMID = 20948270.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; Q20Q21Q62J / Cisplatin
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90. Flury SC, Galgano MT, Mills SE, Smolkin ME, Theodorescu D: Atypical small acinar proliferation: biopsy artefact or distinct pathological entity? BJU Int; 2007 Apr;99(4):780-5
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  • [Title] Atypical small acinar proliferation: biopsy artefact or distinct pathological entity?
  • OBJECTIVE: To determine if atypical small acinar proliferation (ASAP) represents minimally sampled prostate cancer not fully evaluated on a biopsy or a distinct pathological entity, by examining prostates removed at radical cystectomy, as a finding of ASAP of the prostate on needle-core biopsy is closely associated with the detection of cancer on subsequent biopsy.
  • The presence of high-grade prostatic intraepithelial neoplasia (HGPIN), ASAP, and adenocarcinoma was recorded.
  • The remaining eight foci all lacked CK903 stain, indicating disruption of the basal cell layer.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Acinar Cell / pathology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy, Needle. Cell Proliferation. Cystectomy / methods. Humans. Immunohistochemistry. Male. Middle Aged. Predictive Value of Tests. Prostate / pathology. Prostatectomy / methods

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  • (PMID = 17378841.001).
  • [ISSN] 1464-4096
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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91. Herawi M, Epstein JI: Immunohistochemical antibody cocktail staining (p63/HMWCK/AMACR) of ductal adenocarcinoma and Gleason pattern 4 cribriform and noncribriform acinar adenocarcinomas of the prostate. Am J Surg Pathol; 2007 Jun;31(6):889-94
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  • [Title] Immunohistochemical antibody cocktail staining (p63/HMWCK/AMACR) of ductal adenocarcinoma and Gleason pattern 4 cribriform and noncribriform acinar adenocarcinomas of the prostate.
  • Overexpression of alpha-methylacyl coenzyme A racemase (AMACR) in combination with absence of basal cell markers [ie, p63 and high molecular weight cytokeratin (HMWCK)] is typical of classic acinar prostatic adenocarcinoma.
  • We studied the expression and diagnostic utility of p63/HMWCK/AMACR immunohistochemical cocktail staining in ductal adenocarcinoma and cribriform Gleason pattern 4 acinar prostate cancer and compared it to noncribriform Gleason pattern 4 acinar prostate cancer.
  • One to 4 representative formalin-fixed paraffin-embedded archival tissue blocks from 62 radical prostatectomy specimens harboring prostate cancer of ductal (n=51), cribriform Gleason pattern 4 acinar (n=27), and noncribriform Gleason pattern 4 acinar adenocarcinoma (n=48) were included in this study.
  • Seventy-seven percent of ductal prostatic adenocarcinoma, 67% of cribriform acinar prostatic carcinoma, and 81% of noncribriform acinar prostatic carcinoma showed positive staining for AMACR.
  • There was no statistically significant difference between AMACR staining among the 3 histologic types, although there was a trend for noncribriform acinar prostatic carcinoma to have greater expression of AMACR than cribriform acinar prostatic carcinoma (P=0.07).
  • Basal cells were detectable by p63 and HMWCK in a patchy fashion in 31.4% (16/51) of ductal and 29.6% (8/27) of cribriform acinar carcinomas compared with 2.1% (1/48) of noncribriform acinar carcinomas. In summary:.
  • (1) the majority of prostatic ductal and cribriform acinar carcinomas strongly expressed AMACR, however, subpopulations of these prostatic carcinoma were either completely negative or only weakly positive;.
  • (2) AMACR staining was often heterogeneous in intensity in the same histologic type of tumor, even within the same case;.
  • (3) patchy basal cell staining in noncribriform acinar prostatic carcinoma is rare.
  • In contrast, remnants of basal cells identified by p63/HMWCK were seen in a patchy fashion in a significant minority of both ductal and cribriform acinar prostatic adenocarcinoma, which most likely represents intraductal spread of tumor.
  • [MeSH-major] Adenocarcinoma / diagnosis. Biomarkers, Tumor / analysis. Keratins / metabolism. Membrane Proteins / metabolism. Prostatic Neoplasms / diagnosis. Racemases and Epimerases / metabolism

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  • (PMID = 17527076.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Membrane Proteins; 68238-35-7 / Keratins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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92. Seo JY, Masamune A, Shimosegawa T, Kim H: Protective effect of lycopene on oxidative stress-induced cell death of pancreatic acinar cells. Ann N Y Acad Sci; 2009 Aug;1171:570-5
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  • [Title] Protective effect of lycopene on oxidative stress-induced cell death of pancreatic acinar cells.
  • In the present study, we aim to investigate whether lycopene protects oxidative stress-induced cell death of pancreatic acinar AR42J cells by preventing the loss of Ku70 in the nucleus.
  • Viable cell numbers, the levels of H(2)O(2) in the medium, level of Ku70 protein, and Ku-DNA-binding activity were determined.
  • As a result, glucose/glucose oxidase induced the decrease in cell viability, increase in H(2)O(2) production, decrease in Ku70 levels in whole-cell extracts and nuclear extracts, and decrease in Ku-DNA-binding activity of AR42J cells.
  • Lycopene inhibited glucose/glucose oxidase-induced cell death by preventing nuclear loss of Ku70 and a decrease in Ku-DNA-binding activity of AR42J cells.
  • In conclusion, lycopene may be beneficial for the treatment of oxidative stress-induced cell death by preventing loss of DNA repair protein Ku70.
  • [MeSH-minor] Animals. Antigens, Nuclear / metabolism. Antioxidants / pharmacology. Cell Line, Tumor. Cell Survival / drug effects. DNA-Binding Proteins / metabolism. Hydrogen Peroxide / metabolism. Oligonucleotides / genetics. Oligonucleotides / metabolism. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Protein Binding / drug effects. Rats. Time Factors

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  • [ErratumIn] Ann N Y Acad Sci. 2009 Oct;1178:319
  • (PMID = 19723106.001).
  • [ISSN] 1749-6632
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Antioxidants; 0 / DNA-Binding Proteins; 0 / Ku autoantigen; 0 / Oligonucleotides; 0 / Protective Agents; 36-88-4 / Carotenoids; BBX060AN9V / Hydrogen Peroxide; SB0N2N0WV6 / lycopene
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93. Seth AK, Argani P, Campbell KA, Cameron JL, Pawlik TM, Schulick RD, Choti MA, Wolfgang CL: Acinar cell carcinoma of the pancreas: an institutional series of resected patients and review of the current literature. J Gastrointest Surg; 2008 Jun;12(6):1061-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinar cell carcinoma of the pancreas: an institutional series of resected patients and review of the current literature.
  • INTRODUCTION: Acinar cell carcinoma (ACC) is a rare, malignant neoplasm with a generally poor prognosis.
  • MATERIALS AND METHODS: The Johns Hopkins pathology prospective database was reviewed from 1988 to 2006 to identify patients with pancreatic neoplasms possessing features of acinar cell differentiation.
  • Median tumor size was 3.9 cm with 12 patients found to have stage IIB disease or worse.
  • CONCLUSION: Acinar cell carcinomas are rare, aggressive neoplasms that are difficult to diagnose and treat.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatectomy / methods. Pancreatic Neoplasms / pathology. Pancreaticoduodenectomy / methods
  • [MeSH-minor] Adult. Aged. Disease-Free Survival. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Survival Rate / trends. Treatment Outcome. United States / epidemiology

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  • (PMID = 17957440.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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94. Mearini L, Costantini E, Bellezza G, Cavaliere A, Zucchi A, Bini V, Porena M: Is there any clinical parameter able to predict prostate cancer after initial diagnosis of atypical small acinar proliferation? Urol Int; 2008;81(1):29-35
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  • [Title] Is there any clinical parameter able to predict prostate cancer after initial diagnosis of atypical small acinar proliferation?
  • INTRODUCTION: Tissue samples from prostate biopsy may contain atypical small acinar proliferation (ASAP): present guidelines recommend a repeat biopsy policy.
  • [MeSH-major] Cell Proliferation. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / pathology

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18645268.001).
  • [ISSN] 1423-0399
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] EC 3.4.21.77 / Prostate-Specific Antigen
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95. Borowicz J, Morrison M, Hogan D, Miller R: Subcutaneous fat necrosis/panniculitis and polyarthritis associated with acinar cell carcinoma of the pancreas: a rare presentation of pancreatitis, panniculitis and polyarthritis syndrome. J Drugs Dermatol; 2010 Sep;9(9):1145-50
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  • [Title] Subcutaneous fat necrosis/panniculitis and polyarthritis associated with acinar cell carcinoma of the pancreas: a rare presentation of pancreatitis, panniculitis and polyarthritis syndrome.
  • He was under the care of hospice for end-stage acinar cell carcinoma of the pancreas.
  • [MeSH-major] Arthritis / pathology. Carcinoma, Acinar Cell / complications. Pancreatic Neoplasms / complications. Pancreatitis / complications. Panniculitis / pathology. Skin / pathology. Subcutaneous Fat / pathology


96. Lee JH, Lee KG, Park HK, Lee KS: [Acinar cell carcinoma of the pancreas in Korea--clinicopathologic analysis of 27 patients from korean literature and 2 cases from our hospital--]. Korean J Gastroenterol; 2010 Apr;55(4):245-51
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  • [Title] [Acinar cell carcinoma of the pancreas in Korea--clinicopathologic analysis of 27 patients from korean literature and 2 cases from our hospital--].
  • BACKGROUND/AIMS: Acinar cell carcinoma (ACC) of the pancreas is a rare malignancy.
  • The mean tumor size was 7.0 cm, and most common location was tail.
  • CONCLUSIONS: In Korea, the clinical features of ACC include young age, large size, tail location, and nonspecific tumor markers.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Age Factors. Aged. Biomarkers, Tumor / analysis. Female. Humans. Male. Middle Aged. Prognosis. Republic of Korea. Survival Analysis

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  • (PMID = 20389178.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 22
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97. Lim JW, Song JY, Seo JY, Kim H, Kim KH: Role of pancreatitis-associated protein 1 on oxidative stress-induced cell death of pancreatic acinar cells. Ann N Y Acad Sci; 2009 Aug;1171:545-8
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  • [Title] Role of pancreatitis-associated protein 1 on oxidative stress-induced cell death of pancreatic acinar cells.
  • Previously we showed that oxidative stress induces apoptosis of pancreatic acinar cells with nuclear loss of DNA repair proteins.
  • In this study, we investigated the role of PAP-1 on oxidative stress-induced cell death of pancreatic acinar AR42J cells.
  • PAP-1 mRNA expression and cell viability were determined.
  • Cell viability decreased with the concentration of glucose oxides delivered to the cells that had received glucose.
  • Cell death caused by oxidative stress was inhibited in the cells transfected with PAP-1 S cDNA, but it increased in the cells transfected with PAP-1 AS cDNA.
  • These results indicate that PAP-1 may be a defensive gene for oxidative stress-induced cell death of pancreatic acinar cells.
  • [MeSH-major] Antigens, Neoplasm / physiology. Apoptosis / physiology. Biomarkers, Tumor / physiology. Lectins, C-Type / physiology. Oxidative Stress / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / physiology. DNA, Antisense / genetics. DNA, Complementary / genetics. Gene Expression Regulation, Neoplastic. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 19723102.001).
  • [ISSN] 1749-6632
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA, Antisense; 0 / DNA, Complementary; 0 / Lectins, C-Type; 0 / RNA, Messenger; 0 / pancreatitis-associated protein
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98. Jang SH, Choi SY, Min JH, Kim TW, Lee JA, Byun SJ, Lee JW: [A case of acinar cell carcinoma of pancreas, manifested by subcutaneous nodule as initial clinical symptom]. Korean J Gastroenterol; 2010 Feb;55(2):139-43
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  • [Title] [A case of acinar cell carcinoma of pancreas, manifested by subcutaneous nodule as initial clinical symptom].
  • Pancreas acinar cell carcinoma (ACC) accounts for only 1-2% of pancreatic exocrine malignant tumor.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Neoplasms / diagnosis. Subcutaneous Fat / pathology

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  • (PMID = 20168061.001).
  • [ISSN] 2233-6869
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Synaptophysin; 68238-35-7 / Keratins
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99. Tapia B, Ahrens W, Kenney B, Touloukian R, Reyes-Múgica M: Acinar cell carcinoma versus solid pseudopapillary tumor of the pancreas in children: a comparison of two rare and overlapping entities with review of the literature. Pediatr Dev Pathol; 2008 Sep-Oct;11(5):384-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinar cell carcinoma versus solid pseudopapillary tumor of the pancreas in children: a comparison of two rare and overlapping entities with review of the literature.
  • Primary epithelial tumors of the pancreas are extremely uncommon in children, and among these, acinar cell carcinoma (ACC) is the most rare.
  • We also provide a comparison with an example of solid pseudopapillary tumor, another relatively infrequent epithelial tumor of the pancreas in the young.
  • We review the relevant literature addressing the clinical and pathologic features of ACC and its distinction from other pancreatic neoplasms.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / pathology. Pancreatic Cyst / pathology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / pathology

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  • (PMID = 19006424.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / SERPINA1 protein, human; 0 / alpha 1-Antitrypsin
  • [Number-of-references] 37
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100. Luebke AM, Schlomm T, Gunawan B, Bonkhoff H, Füzesi L, Erbersdobler A: Simultaneous tumour-like, atypical basal cell hyperplasia and acinar adenocarcinoma of the prostate: a comparative morphological and genetic approach. Virchows Arch; 2005 Mar;446(3):338-41
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  • [Title] Simultaneous tumour-like, atypical basal cell hyperplasia and acinar adenocarcinoma of the prostate: a comparative morphological and genetic approach.
  • Basal cell tumours of the prostatic gland are rare, and the classification is difficult.
  • In the present case report, a large, tumour-like proliferation of atypical basaloid cells was found incidentally in a prostatectomy specimen that otherwise contained a conventional acinar adenocarcinoma.
  • However, there were no definite criteria for a malignant behaviour of the basal cell tumour.
  • Comparative genomic hybridisation from microdissected tumour cells yielded losses at the short arms of chromosomes 8 and 12 in the conventional adenocarcinoma and a normal karyotype in the basal cell tumour.
  • The pathological findings favoured the diagnosis of an atypical basal cell hyperplasia.
  • [MeSH-major] Carcinoma, Acinar Cell / complications. Carcinoma, Acinar Cell / pathology. Prostatic Hyperplasia / complications. Prostatic Hyperplasia / pathology. Prostatic Neoplasms / complications. Prostatic Neoplasms / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasms, Basal Cell / genetics. Neoplasms, Basal Cell / pathology. Nucleic Acid Hybridization

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  • (PMID = 15726402.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Germany
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