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1. 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.
  • 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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2. Marrache F, Tu SP, Bhagat G, Pendyala S, Osterreicher CH, Gordon S, Ramanathan V, Penz-Osterreicher M, Betz KS, Song Z, Wang TC: Overexpression of interleukin-1beta in the murine pancreas results in chronic pancreatitis. Gastroenterology; 2008 Oct;135(4):1277-87
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  • [Title] Overexpression of interleukin-1beta in the murine pancreas results in chronic pancreatitis.
  • BACKGROUND & AIMS: Chronic pancreatitis is a significant cause of morbidity and a known risk factor for pancreatic adenocarcinoma.
  • Interleukin-1beta is a proinflammatory cytokine involved in pancreatic inflammation.
  • We sought to determine whether targeted overexpression of interleukin-1beta in the pancreas could elicit localized inflammatory responses and chronic pancreatitis.
  • RESULTS: Three transgenic lines were generated, and in each line the pancreas was atrophic and occasionally showed dilation of pancreatic and biliary ducts secondary to proximal fibrotic stenosis.
  • Pancreatic histology showed typical features of chronic pancreatitis.
  • There was evidence for increased acinar proliferation and apoptosis, along with prominent expression of tumor necrosis factor-alpha; chemokine (C-X-C motif) ligand 1; stromal cell-derived factor 1; transforming growth factor-beta1; matrix metallopeptidase 2, 7, and 9; inhibitor of metalloproteinase 1; and cyclooxygenase 2.
  • Older mice displayed acinar-ductal metaplasia but did not develop mouse pancreatic intraepithelial neoplasia or tumors.
  • Elastase sshIL-1beta*p53(R172H/+) mice had increased frequency of tubular complexes, some of which were acinar-ductal metaplasia.
  • CONCLUSIONS: Overexpression of interleukin-1beta in the murine pancreas induces chronic pancreatitis.
  • Elastase sshIL-1beta mice consistently develop severe chronic pancreatitis and constitute a promising model for studying chronic pancreatitis and its relationship with pancreatic adenocarcinoma.

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  • (PMID = 18789941.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA093405; United States / NCI NIH HHS / CA / R01 CA120979-03; United States / NCI NIH HHS / CA / U54 CA126513; United States / NCI NIH HHS / CA / R01 CA093405-07A1; United States / NCI NIH HHS / CA / CA093405-07A1; United States / NCI NIH HHS / CA / CA120979-03; United States / NCI NIH HHS / CA / U54 CA126513-03; United States / NCI NIH HHS / CA / CA126513-03; United States / NCI NIH HHS / CA / R01 CA120979
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-1beta; EC 3.4.21.36 / Pancreatic Elastase
  • [Other-IDs] NLM/ NIHMS73579; NLM/ PMC2707078
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3. Vakiani E, Young RH, Carcangiu ML, Klimstra DS: Acinar cell carcinoma of the pancreas metastatic to the ovary: a report of 4 cases. Am J Surg Pathol; 2008 Oct;32(10):1540-5
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  • [Title] Acinar cell carcinoma of the pancreas metastatic to the ovary: a report of 4 cases.
  • We report 4 cases of acinar cell carcinoma of the pancreas, 3 presenting as metastases in the ovary, the first report of this circumstance, which may pose a broad differential diagnosis and caused significant diagnostic difficulty in all the cases.
  • In 3 cases, the ovarian tumors were detected before the pancreatic tumor; in 1 case, a large abdominal mass and ovarian tumors were discovered synchronously.
  • Two cases had a predominant acinar growth pattern of cells with brightly eosinophilic, granular cytoplasm.
  • The main differential diagnostic consideration was well-differentiated neuroendocrine neoplasm (carcinoid tumor); positive immunostaining with antibodies against chymotrypsin and trypsin and negative immunostaining with antibodies against synaptophysin and chromogranin helped exclude this diagnosis.
  • We observed focal alpha-inhibin immunostaining in 2 cases, which may represent a potential diagnostic pitfall, as a Sertoli cell tumor or unusual granulosa cell tumor may also enter the differential diagnosis.
  • Inclusion of antibodies against the pancreatic enzymes chymotrypsin and trypsin in the immunohistochemical panel is critical in establishing the correct diagnosis and should be considered when evaluating ovarian tumors with architectural (mainly acinar) and cytologic (granular eosinophilic cytoplasm) characteristics that should bring a metastatic acinar cell carcinoma into consideration.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Ovarian Neoplasms / secondary. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Middle Aged

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  • (PMID = 18724247.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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4. 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.
  • At the time of diagnosis only 50% of the tumors appear to be resectable.
  • 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.
  • 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

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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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5. Radhi J, Tse F, Marcaccio M: Papillocystic variant of acinar cell pancreatic carcinoma. J Oncol; 2010;2010:242016
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  • [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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6. 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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  • [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 patient has remained disease-free for 22 months since the last surgery and has survived 65 months since the initial diagnosis.
  • 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

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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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7. Ozaki N, Ohmuraya M, Hirota M, Ida S, Wang J, Takamori H, Higashiyama S, Baba H, Yamamura K: Serine protease inhibitor Kazal type 1 promotes proliferation of pancreatic cancer cells through the epidermal growth factor receptor. Mol Cancer Res; 2009 Sep;7(9):1572-81
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  • [Title] Serine protease inhibitor Kazal type 1 promotes proliferation of pancreatic cancer cells through the epidermal growth factor receptor.
  • Serine protease inhibitor, Kazal type 1 (SPINK1) is expressed not only in normal human pancreatic acinar cells but also in a variety of pancreatic ductal neoplasms.
  • We first showed that SPINK1 induced proliferation of NIH 3T3 cells and pancreatic cancer cell lines.
  • To determine which pathway is the most important for cell growth, we further analyzed the effect of inhibitors.
  • To further analyze the clinical importance of SPINK1 in the development of pancreatic cancer, we examined the expression of SPINK1 and EGFR in pancreatic tubular adenocarcinomas and pancreatic intraepithelial neoplasm.
  • Both SPNK1 and EGFR were coexpressed not only in the early stage of cancer, PanIN-1A, but also in advanced stages.
  • Taken together, these results suggest that SPINK1 stimulates the proliferation of pancreatic cancer cells through the EGFR/mitogen-activated protein kinase cascade.
  • [MeSH-major] Carrier Proteins / pharmacology. Pancreatic Neoplasms / pathology. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Animals. Carcinoma in Situ / metabolism. Carcinoma in Situ / pathology. Cell Growth Processes / drug effects. Cell Line, Tumor. Fibroblasts / drug effects. Humans. Immunohistochemistry. MAP Kinase Signaling System / drug effects. Mice. NIH 3T3 Cells. Phosphorylation / drug effects


8. 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.
  • This report presents a case of ACC of the pancreas with intraductal papillary growth and lymph node metastasis.
  • [MeSH-major] Carcinoma, Acinar Cell / surgery. Neoplasm Invasiveness. Pancreatectomy / methods. Pancreatic Ducts / pathology. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Aged. Cholangiopancreatography, Endoscopic Retrograde. Diagnosis, Differential. Endosonography. Female. Humans

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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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9. Martínez-Romero C, Rooman I, Skoudy A, Guerra C, Molero X, González A, Iglesias M, Lobato T, Bosch A, Barbacid M, Real FX, Hernández-Muñoz I: The epigenetic regulators Bmi1 and Ring1B are differentially regulated in pancreatitis and pancreatic ductal adenocarcinoma. J Pathol; 2009 Oct;219(2):205-13
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  • [Title] The epigenetic regulators Bmi1 and Ring1B are differentially regulated in pancreatitis and pancreatic ductal adenocarcinoma.
  • Chronic pancreatitis and pancreatic ductal adenocarcinoma (PDAC) are associated with major changes in cell differentiation.
  • Polycomb proteins are epigenetic silencers expressed in adult stem cells; up-regulation of Polycomb proteins has been reported to occur in a variety of solid tumours such as colon and breast cancer.
  • We hypothesized that Polycomb might play a role in preneoplastic states in the pancreas and in tumour development/progression.
  • To test these ideas, we determined the expression of PRC1 complex proteins (Bmi1 and Ring1b) during pancreatic development and in pancreatic tissue from mouse models of disease: acute and chronic pancreatic injury, duct ligation, and in K-Ras(G12V) conditional knock-in and caerulein-treated K-Ras(G12V) mice.
  • The study was extended to human pancreatic tissue samples.
  • To obtain mechanistic insights, Bmi1 expression in cells undergoing in vitro exocrine cell metaplasia and the effects of Bmi1 depletion in an acinar cancer cell line were studied.
  • We found that Bmi1 and Ring1B are expressed in pancreatic exocrine precursor cells during early development and in ductal and islet cells-but not acinar cells-in the adult pancreas.
  • Bmi1 expression was induced in acinar cells during acute injury, in acinar-ductal metaplastic lesions, as well as in pancreatic intraepithelial neoplasia (PanIN) and PDAC.
  • Bmi1 knockdown in cultured acinar tumour cells led to changes in the expression of various digestive enzymes.
  • Our results suggest that Bmi1 and Ring1B are modulated in pancreatic diseases and could contribute differently to tumour development.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Nuclear Proteins / metabolism. Pancreatic Neoplasms / metabolism. Pancreatitis, Chronic / metabolism. Proto-Oncogene Proteins / metabolism. Repressor Proteins / metabolism
  • [MeSH-minor] Acute Disease. Animals. Cells, Cultured. Disease Models, Animal. Humans. Male. Metaplasia / metabolism. Mice. Mice, Inbred C57BL. Pancreas / metabolism. Pancreas, Exocrine / metabolism. Pancreas, Exocrine / pathology. Pancreatitis / metabolism. Polycomb Repressive Complex 1. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Rats. Rats, Wistar. Transcription Factors / metabolism

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  • [Copyright] 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 19585519.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BMI1 protein, human; 0 / Bmi1 protein, mouse; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / transcription factor PTF1; EC 6.3.2.19 / Polycomb Repressive Complex 1
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10. Michl J, Scharf B, Schmidt A, Huynh C, Hannan R, von Gizycki H, Friedman FK, Brandt-Rauf P, Fine RL, Pincus MR: PNC-28, a p53-derived peptide that is cytotoxic to cancer cells, blocks pancreatic cancer cell growth in vivo. Int J Cancer; 2006 Oct 1;119(7):1577-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PNC-28, a p53-derived peptide that is cytotoxic to cancer cells, blocks pancreatic cancer cell growth in vivo.
  • PNC-28 is a p53 peptide from its mdm-2-binding domain (residues 17-26), which contains the penetratin sequence enabling cell penetration on its carboxyl terminal end.
  • We have found that this peptide induces necrosis, but not apoptosis, of a variety of human tumor cell lines, including several with homozygous deletion of p53, and a ras-transformed rat acinar pancreatic carcinoma cell line, BMRPA1. Tuc3.
  • On the other hand, PNC-28 has no effect on untransformed cells, such as rat pancreatic acinar cells, BMRPA1, and human breast epithelial cells and no effect on the differentiation of human stem cells.
  • When delivered concurrently with tumor explantation at a remote site, PNC-28 causes a complete blockade of any tumor growth during its 2-week period of administration and 2 weeks posttreatment, followed by weak tumor growth that plateaus at low tumor sizes compared with tumor growth in the presence of a control peptide.
  • [MeSH-major] Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / pathology. Peptide Fragments / toxicity. Tumor Suppressor Protein p53 / toxicity
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Humans. Mice. Mice, Nude. Rats. Xenograft Model Antitumor Assays

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16688716.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA42500
  • [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 / PNC-28; 0 / Peptide Fragments; 0 / Tumor Suppressor Protein p53
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11. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

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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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12. Wang W, Reiser-Erkan C, Michalski CW, Raggi MC, Quan L, Yupei Z, Friess H, Erkan M, Kleeff J: Hypoxia inducible BHLHB2 is a novel and independent prognostic marker in pancreatic ductal adenocarcinoma. Biochem Biophys Res Commun; 2010 Oct 22;401(3):422-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypoxia inducible BHLHB2 is a novel and independent prognostic marker in pancreatic ductal adenocarcinoma.
  • In the present study, the expression, regulation, functions and prognostic impact of BHLHB2 in pancreatic cancer were investigated.
  • METHODS: Expression analyses were carried out in tissues of the normal pancreas (n=10) and pancreatic ductal adenocarcinoma (n=77) as well as in eight pancreatic cancer cell lines using quantitative RT-PCR, semiquantitative immunohistochemistry, and immunoblot analyses.
  • RESULTS: BHLHB2 mRNA and protein expressions were strongly induced by hypoxia and by serum starvation in pancreatic cancer cell lines.
  • Ex vivo, the weak/absent nuclear staining in normal pancreatic ducts and acinar cells was replaced by moderate to strong nuclear/cytoplasmic staining in PanIN lesions and pancreatic cancer cells.
  • CONCLUSIONS: Hypoxia-inducible BHLHB2 expression is a novel independent prognostic marker in pancreatic cancer patients and indicates increased chemosensitivity towards gemcitabine.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Basic Helix-Loop-Helix Transcription Factors / metabolism. Biomarkers, Tumor / metabolism. Carcinoma, Pancreatic Ductal / mortality. Deoxycytidine / analogs & derivatives. Drug Resistance, Neoplasm. Homeodomain Proteins / metabolism. Pancreatic Neoplasms / mortality
  • [MeSH-minor] Aged. Cell Hypoxia. Female. Humans. Male. Pancreas / metabolism. Pancreas / pathology. Prognosis. RNA Interference

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20863812.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / BHLHE40 protein, human; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / Homeodomain Proteins; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
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13. 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.
  • An examination of a biopsy specimen was inconclusive.
  • 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.
  • Intraoperatively, the mass in the pylorus invaded the pancreatic head, and the lymph node in the hepatoduodenal ligament was swollen.
  • We performed a pancreaticoduodenectomy as a radical excision.
  • Histopathologically, the tumor was identified as pancreatic ACC with lymph node metastasis.
  • Because of the tumor location, we considered the tumor to have originated from the ectopic pancreatic tissue in the stomach.
  • This is only the second case of ACC originating from an ectopic pancreas reported in the literature.
  • [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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14. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • Available evidence suggests that VREP have different risk factors and prognoses from those of adenocarcinoma of the pancreas.
  • 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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15. 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.
  • Although not as well studied or characterized as pancreatic adenocarcinoma there are many distinct lesions which exhibit diverse biological behaviors and varying degrees of malignancy.
  • 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.
  • 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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16. Yoshida T, Shiraki N, Baba H, Goto M, Fujiwara S, Kume K, Kume S: Expression patterns of epiplakin1 in pancreas, pancreatic cancer and regenerating pancreas. Genes Cells; 2008 Jul;13(7):667-78
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression patterns of epiplakin1 in pancreas, pancreatic cancer and regenerating pancreas.
  • Here we analyzed the expression patterns of Eppk1 in the developing and adult pancreas in the mice.
  • In the embryonic pancreas, Eppk1+/Pdx1+ and Eppk1+/Sox9+ pancreatic progenitor cells were observed in early pancreatic epithelium.
  • In the adult pancreas, Eppk1 is expressed in centroacinar cells (CACs) and in duct cells.
  • Eppk1 is observed in pancreatic intraepithelial neoplasia (PanIN), previously identified as pancreatic ductal adenocarcinoma (PDAC) precursor lesions.
  • In addition, the expansion of Eppk1-positive cells occurs in a caerulein-induced acute pancreatitis, an acinar cell regeneration model.
  • These results suggest that Eppk1 serves as a useful marker for detecting pancreatic progenitor cells in developing and regenerating pancreas.
  • [MeSH-major] Autoantigens / biosynthesis. Autoantigens / genetics. Gene Expression Regulation / physiology. Pancreas / metabolism. Pancreatic Neoplasms / metabolism. Regeneration / physiology
  • [MeSH-minor] Animals. Biomarkers / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Pancreatic Ductal / pathology. Gene Expression Regulation, Neoplastic / physiology. Mice. Mice, Knockout. Mice, Transgenic. Stem Cells / cytology. Stem Cells / metabolism


17. Jiang X, Zhang W, Kayed H, Zheng P, Giese NA, Friess H, Kleeff J: Loss of ONECUT1 expression in human pancreatic cancer cells. Oncol Rep; 2008 Jan;19(1):157-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of ONECUT1 expression in human pancreatic cancer cells.
  • ONECUT1 (HNF-6) is the prototype of a new class of homeodomain transcription factors, that controls the development of pancreatic ducts during mouse development.
  • In the present study, the role of ONECUT1 and its targeted genes TCF2, PKHD1 and CYS1 was analyzed in human pancreatic ductal adenocarcinoma (PDAC).
  • mRNA levels of ONECUT1, TCF2, PKHD1 and CYS1 were measured in pancreatic tissues and pancreatic cancer cell lines by quantitative reverse-transcriptase polymerase chain reaction (QRT-PCR).
  • Protein expression of ONECUT1 and TCF2 was assessed in pancreatic tissues by immunohistochemistry.
  • ONECUT1 was transfected into Panc-1 and T3M4 pancreatic cancer cells and its effects on anchorage-dependent and -independent growth as well as invasion and adhesion were analyzed.
  • ONECUT1 protein was expressed in normal acinar and ductal cells, but neither in the cancer cells of PDAC tissues nor in 7 of 8 cultured pancreatic cancer cell lines.
  • Transfection of ONECUT1 into pancreatic cancer cells resulted in up-regulation of the target gene TCF2, a reduction in invasiveness, but no change in adhesion or growth.
  • In conclusion, ONECUT1 expression is lost in pancreatic cancer cells, suggesting a tumor suppressor function in this malignancy.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Hepatocyte Nuclear Factor 6 / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Movement / physiology. Gene Expression. Hepatocyte Nuclear Factor 1-beta / metabolism. Humans. Immunoblotting. Immunohistochemistry. Lasers. Membrane Proteins / metabolism. Microdissection. Oligonucleotide Array Sequence Analysis. RNA, Messenger / analysis. Receptors, Cell Surface / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 18097590.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / CYS1 protein, human; 0 / HNF1B protein, human; 0 / Hepatocyte Nuclear Factor 6; 0 / Membrane Proteins; 0 / ONECUT1 protein, human; 0 / PKHD1 protein, human; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 138674-15-4 / Hepatocyte Nuclear Factor 1-beta
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18. Stelow EB, Adams RB, Moskaluk CA: The prevalence of pancreatic intraepithelial neoplasia in pancreata with uncommon types of primary neoplasms. Am J Surg Pathol; 2006 Jan;30(1):36-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The prevalence of pancreatic intraepithelial neoplasia in pancreata with uncommon types of primary neoplasms.
  • Pancreatic ductal adenocarcinoma is thought to develop through a series of genetic events through its purported precursor lesion, pancreatic intraepithelial neoplasia (PanIN).
  • Little, however, is known regarding the role of possible precursor lesions in the development of other primary neoplasms of the pancreas.
  • All pancreata resected at the University of Virginia from June 1, 1991 to March 1, 2005 for neoplasia not diagnosed as conventional ductal adenocarcinoma were reviewed and classified according to the World Health Organization's classification schema for tumors of the exocrine and endocrine pancreas.
  • Three acinar cell carcinomas (ACCs), 18 mucinous cystic neoplasms (MCNs), 24 pancreatic endocrine tumors (PETs), 12 serous cystadenomas (SCs), and 3 solid-pseudopapillary tumors (SPTs) were identified.
  • Although the high prevalence of PanIN in pancreata concomitantly harboring certain uncommon neoplasms of the pancreas could signify its role as a precursor lesion for those neoplasms, its high prevalence throughout our series may simply be the result of a coincidental, prevalent finding seen in all pancreata, especially with aging.
  • Because of the ubiquitous nature of PanIN, it should not be used histologically to assist in the diagnosis and subclassification of pancreatic neoplasia.
  • [MeSH-major] Carcinoma in Situ / pathology. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Age Factors. Aged. Cystadenocarcinoma, Mucinous / pathology. Cystadenocarcinoma, Serous / pathology. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Prevalence

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  • (PMID = 16330940.001).
  • [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
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19. 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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20. Bockman DE: Transition to pancreatic cancer in response to carcinogen. Langenbecks Arch Surg; 2008 Jul;393(4):557-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transition to pancreatic cancer in response to carcinogen.
  • BACKGROUND: It has become obvious that the traditional assumptions about the transition from normal pancreas to pancreatic cancer are incomplete.
  • Experimental studies reveal that the earliest changes during transition to pancreatic adenocarcinoma involve premalignant lesions that are derived from acinar, islet, and ductal cells.
  • As part of redifferentiation and transformation to adenocarcinoma, cells regain the characteristics of developing pancreas.
  • Elements significant in identifying precursor cell types include Pdx1, hedgehog signaling, notch signaling, and nestin, an intermediate filament expressed by precursor cell types.
  • CONCLUSIONS: Thus pancreatic carcinogenesis is not simply a matter of transition of ductal cells to cancer cells months after insult by the carcinogen; ductal cells are not the sole source transitioning to cancer, and PanINs are not the sole route to adenocarcinoma.
  • Tubular complexes, derived from multiple cell sources, are included in routes to pancreatic cancer.
  • Markers characteristic of developing pancreas are consistent with this transition.
  • [MeSH-major] Carcinogens. Cell Transformation, Neoplastic / chemically induced. Pancreatic Neoplasms / chemically induced. Precancerous Conditions / chemically induced
  • [MeSH-minor] Animals. Carcinoma, Pancreatic Ductal / genetics. Carcinoma, Pancreatic Ductal / pathology. Gene Expression Regulation, Neoplastic / genetics. Hedgehog Proteins / genetics. Homeodomain Proteins / genetics. Humans. Intermediate Filament Proteins / genetics. Nerve Tissue Proteins / genetics. Nestin. Receptors, Notch / genetics. Signal Transduction / drug effects. Signal Transduction / genetics. Smoking / adverse effects. Stem Cells / drug effects. Stem Cells / pathology. Trans-Activators / genetics

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  • (PMID = 18189145.001).
  • [ISSN] 1435-2451
  • [Journal-full-title] Langenbeck's archives of surgery
  • [ISO-abbreviation] Langenbecks Arch Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Hedgehog Proteins; 0 / Homeodomain Proteins; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / Receptors, Notch; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein
  • [Number-of-references] 35
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21. Seretis EC, Gavriil AN, Golematis VC, Voloudakis-Baltatzis IE: Immunoelectron study of pancreatic carcinomas using antibodies to gastrointestinal hormones. Ultrastruct Pathol; 2007 Jul-Aug;31(4):303-14
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  • [Title] Immunoelectron study of pancreatic carcinomas using antibodies to gastrointestinal hormones.
  • The aim of this study was to investigate the ultrastructural appearance of pancreatic adenocarcinoma combined with glucagon and gastrin/cholecystokinin (CCK) expression.
  • The authors investigated the ultrastructure and the immunocytochemistry of 12 human pancreatic cancer specimens and used 3 chronic pancreatitis samples and 6 adjacent histological normal pancreatic tissues (away from the tumor) as controls.
  • Glucagon appeared to be located not only in islet alpha cells but also in intermediate alpha acinar cells.
  • The changes were more significant in adenocarcinoma cases.
  • Abnormality in the immunoreaction of the peptides was indicated not only in the tumor area but also in the islets near the cancer.
  • Cells immunoreactive with antibodies were found in all 12 adenocarcinoma cases.
  • Abnormal co-location of both hormones in the same type of endocrine cell was also found.
  • Increased and ectopic gastrin/CCK expression was correlated with pancreatic adenocarcinomas exhibiting poor histological grade and neoplastic endocrine cells, providing a potential marker for pancreatic adenocarcinomas with aggressive behavior.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / ultrastructure. Antibodies, Monoclonal. Gastrointestinal Hormones / biosynthesis. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / ultrastructure

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  • (PMID = 17786831.001).
  • [ISSN] 1521-0758
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Gastrointestinal Hormones; 9007-92-5 / Glucagon; 9011-97-6 / Cholecystokinin
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22. 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.
  • The nuclear localization of beta-catenin is also a feature of SPT that helps in differential diagnosis.
  • 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.
  • We studied 20 SPT, 20 nonfunctioning PET, 7 ACC, 2 PB, and their matched normal pancreas for the immunohistochemical expression of claudin family members 1, 2, 3, 4, 5, and 7, beta-catenin and E-cadherin.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Acinar Cell / chemistry. Membrane Proteins / analysis. Pancreas / chemistry. Pancreatic Neoplasms / chemistry. Tight Junctions / chemistry
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cadherins / analysis. Child. Claudin-5. Claudins. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Predictive Value of Tests. Young Adult. beta Catenin / analysis

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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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23. Stelow EB, Woon C, Pambuccian SE, Thrall M, Stanley MW, Lai R, Mallery S, Gulbahce HE: Fine-needle aspiration cytology of pancreatic somatostatinoma: the importance of immunohistochemistry for the cytologic diagnosis of pancreatic endocrine neoplasms. Diagn Cytopathol; 2005 Aug;33(2):100-5
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  • [Title] Fine-needle aspiration cytology of pancreatic somatostatinoma: the importance of immunohistochemistry for the cytologic diagnosis of pancreatic endocrine neoplasms.
  • Pancreatic somatostatinoma is a rare pancreatic endocrine neoplasm representing as little as 1% of pancreatic endocrine neoplasms (PENs).
  • The histologic features of this tumor are like those of other PENs, except that it commonly forms acinar structures and often has cells with abundant, granular cytoplasm.
  • We discuss the cytologic and immunohistochemical findings of these two cases and the cytologic similarities these neoplasms share with pancreatic acinar-cell carcinoma (PACC).
  • We review the cytologic features of PEN and PACC and discuss the importance of cell block immunohistochemistry in the diagnosis of pancreatic neoplasia sampled by EUS-guided FNA.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16007666.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Antoine M, Khitrik-Palchuk M, Saif MW: Long-term survival in a patient with acinar cell carcinoma of pancreas. A case report and review of literature. JOP; 2007;8(6):783-9
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  • [Title] Long-term survival in a patient with acinar cell carcinoma of pancreas. A case report and review of literature.
  • CONTEXT: Acinar cell carcinoma of the pancreas is a rare malignancy that may have acinar and endocrine differentiation.
  • Clinical practice guidelines exist for pancreatic ductal adenocarcinoma.
  • However, treatment protocols for acinar cell carcinoma of the pancreas have not been standardized.
  • CASE REPORT: We describe a case of a 44-year-old woman presenting with low grade fever and mid-abdominal tenderness secondary to a pancreatic mass with acinar and endocrine differentiation metastatic to the liver.
  • The patient developed Clostridium difficile colitis and septic shock resulting in death 37 months after the diagnosis of acinar cell carcinoma of the pancreas.
  • CONCLUSION: This is a case of acinar cell carcinoma of the pancreas with an endocrine component, treated with multiple chemotherapeutic agents, in which the patient survived 37 months after diagnosis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Pancreatic Neoplasms / drug therapy

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  • (PMID = 17993731.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 28
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25. 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.
  • FISH abnormalities of all other cancer genes studied were observed in all forms of pancreatic tumors in this investigation.
  • 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.


26. Hashimoto M, Miki K, Beck Y, Kokudo N, Makuuchi M, Tanaka H: Femoral neck fracture as a complication of lipase-secreting pancreatic acinar cell carcinoma. Surgery; 2007 Nov;142(5):779-80
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  • [Title] Femoral neck fracture as a complication of lipase-secreting pancreatic acinar cell carcinoma.
  • [MeSH-major] Carcinoma, Acinar Cell / complications. Femoral Neck Fractures / etiology. Pancreatic Neoplasms / complications

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  • (PMID = 17981202.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.1.1.3 / Lipase
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27. 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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  • [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.
  • METHODS: The present study investigated the clinical characteristics, treatment, and therapeutic outcomes of 115 patients registered in the Pancreatic Cancer Registry of the Japan Pancreas Society, and therapeutic plans were reviewed.
  • CONCLUSIONS: Confirming the diagnosis of ACC preoperatively is difficult, but this diagnosis should be kept in mind while planning surgery for ordinary pancreatic cancer.
  • Once the diagnosis has been confirmed, a possibility of surgical resection should be pursued to achieve better prognosis.
  • [MeSH-major] Carcinoma, Acinar Cell / mortality. Pancreatic Neoplasms / mortality. Registries / statistics & numerical data

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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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28. Torrisani J, Bournet B, du Rieu MC, Bouisson M, Souque A, Escourrou J, Buscail L, Cordelier P: let-7 MicroRNA transfer in pancreatic cancer-derived cells inhibits in vitro cell proliferation but fails to alter tumor progression. Hum Gene Ther; 2009 Aug;20(8):831-44
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  • [Title] let-7 MicroRNA transfer in pancreatic cancer-derived cells inhibits in vitro cell proliferation but fails to alter tumor progression.
  • Pancreatic ductal adenocarcinoma (PDAC) is still the fourth leading cause of cancer-related deaths in Western countries, with increasing incidence.
  • Neither effective prognostic markers nor therapies exist for this cancer.
  • Because let-7 microRNA targets the K-ras oncogene, we aimed to characterize let-7 expression and function in PDAC in vitro and in vivo.
  • Let-7 is present in normal acinar pancreatic cells, and lost in poorly differentiated cancer samples.
  • Restoring let-7 levels in cancer-derived cell lines strongly inhibits cell proliferation, K-ras expression, and mitogen-activated protein kinase activation, but fails to impede tumor growth progression after intratumoral gene transfer or after implantation of Capan-1 cells stably overexpressing let-7 microRNA.
  • In addition, this study provides the initial steps for a microRNA replacement therapy for this cancer.
  • [MeSH-major] MicroRNAs / genetics. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Animals. Biopsy, Fine-Needle. Cell Line, Tumor. Cell Proliferation. Disease Progression. Enzyme Activation. Female. Gene Expression Regulation, Neoplastic. Genes, ras. Humans. Male. Mice. Middle Aged. Mitogen-Activated Protein Kinases / metabolism. Transfection

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  • (PMID = 19323605.001).
  • [ISSN] 1557-7422
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / mirnlet7 microRNA, human; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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29. Dall'igna P, Cecchetto G, Bisogno G, Conte M, Chiesa PL, D'Angelo P, De Leonardis F, De Salvo G, Favini F, Ferrari A, TREP Group: Pancreatic tumors in children and adolescents: the Italian TREP project experience. Pediatr Blood Cancer; 2010 May;54(5):675-80
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  • [Title] Pancreatic tumors in children and adolescents: the Italian TREP project experience.
  • INTRODUCTION: Malignant pancreatic tumors are exceedingly rare in pediatric age and their clinical features and treatment usually go unappreciated by most pediatric oncologists and surgeons.
  • METHODS: From January 2000 to July 2009, 21 patients <18 years old with pancreatic tumors were prospectively registered in the Italian cooperative TREP project dedicated to very rare pediatric tumors.
  • RESULTS: Tumor types were 4 pancreatoblastomas, 2 pancreatic carcinomas, 3 neoplasms of the endocrine pancreas, and 12 solid pseudopapillary tumors.
  • Three of the four patients with pancreatoblastoma had advanced disease at diagnosis and were given chemotherapy; at the time of this report, three patients were alive in first remission, while one died due to treatment toxicity.
  • Both the cases of pancreatic carcinoma had the acinar cell subtype and successfully underwent pancreaticoduodenectomy with complete tumor resection, remaining without evidence of disease at the time of this analysis.
  • The histological diagnoses of the three endocrine tumors were a malignant islet cell tumor, a gastrinoma, and a well-differentiated tumor.
  • All 12 patients with solid pseudopapillary tumors underwent complete tumor resection and were given no adjuvant treatment; 11 were alive in first remission, while one experienced a local and distant relapse 5 years after diagnosis.
  • CONCLUSIONS: Surgery remains the keystone of treatment for pancreatic tumors in pediatric age as in adults.
  • The TREP project shows that prospective cooperative studies are feasible even for such very rare tumors as these and may serve as a model for developing international cooperative schemes.
  • [MeSH-major] Pancreatic Neoplasms / epidemiology. Rare Diseases / epidemiology

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  • [CommentIn] Pediatr Blood Cancer. 2010 May;54(5):659-60 [20063425.001]
  • (PMID = 19998473.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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30. Fu XM, Dai X, Ding J, Zhu BT: Pancreas-specific protein disulfide isomerase has a cell type-specific expression in various mouse tissues and is absent in human pancreatic adenocarcinoma cells: implications for its functions. J Mol Histol; 2009 Jun;40(3):189-99
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  • [Title] Pancreas-specific protein disulfide isomerase has a cell type-specific expression in various mouse tissues and is absent in human pancreatic adenocarcinoma cells: implications for its functions.
  • However, the pancreas-specific PDI homolog was previously suggested to be exclusively expressed in the pancreas (thus commonly referred to as PDIp).
  • Notably, in the digestive organs, such as the stomach and pancreas, very high levels of PDIp were selectively expressed in the digestive enzyme-secreting cells (e.g., gastric chief cells and pancreatic acinar cells).
  • This observation suggests that PDIp may function as a protein-folding catalyst for secretory digestive enzymes.
  • In addition, high levels of PDIp expression were also detected in normal human pancreas, but its expression was mostly absent in human pancreatic duct adenocarcinoma and pancreatic cancer cell lines.
  • The absence of PDIp expression in pancreatic adenocarcinoma may serve as an additional biomarker for pancreatic cancer.
  • [MeSH-major] Adenocarcinoma / enzymology. Pancreas / enzymology. Pancreatic Neoplasms / enzymology. Protein Disulfide-Isomerases / metabolism
  • [MeSH-minor] Animals. Blotting, Western. COS Cells. Carcinoma, Pancreatic Ductal / enzymology. Carcinoma, Pancreatic Ductal / pathology. Cell Line, Tumor. Cercopithecus aethiops. Humans. Mice. Organ Specificity. Protein Transport. Subcellular Fractions / enzymology

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  • (PMID = 19821078.001).
  • [ISSN] 1567-2387
  • [Journal-full-title] Journal of molecular histology
  • [ISO-abbreviation] J. Mol. Histol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA097109; United States / NCI NIH HHS / CA / CA97109; United States / NCRR NIH HHS / RR / P20RR021940
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 5.3.4.1 / Protein Disulfide-Isomerases
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31. 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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  • [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.
  • Overall median survival and disease-free survival were 33 and 25 months, respectively, as compared to a median survival of 18 months for pancreatic adenocarcinoma.
  • CONCLUSION: Acinar cell carcinomas are rare, aggressive neoplasms that are difficult to diagnose and treat.
  • These lesions have a better prognosis than the more common pancreatic adenocarcinomas.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatectomy / methods. Pancreatic Neoplasms / pathology. Pancreaticoduodenectomy / methods

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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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32. Guerra C, Schuhmacher AJ, Cañamero M, Grippo PJ, Verdaguer L, Pérez-Gallego L, Dubus P, Sandgren EP, Barbacid M: Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice. Cancer Cell; 2007 Mar;11(3):291-302
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  • [Title] Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice.
  • Pancreatic ductal adenocarcinoma (PDA), one of the deadliest human cancers, often involves somatic activation of K-Ras oncogenes.
  • We report that selective expression of an endogenous K-Ras(G12V) oncogene in embryonic cells of acinar/centroacinar lineage results in pancreatic intraepithelial neoplasias (PanINs) and invasive PDA, suggesting that PDA originates by differentiation of acinar/centroacinar cells or their precursors into ductal-like cells.
  • [MeSH-major] Carcinoma in Situ / pathology. Carcinoma, Pancreatic Ductal / pathology. Genes, ras. Pancreatic Neoplasms / pathology. Pancreatitis, Chronic / pathology
  • [MeSH-minor] Animals. Cell Lineage. Cell Transformation, Neoplastic. Ceruletide. Doxycycline / pharmacology. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Mice. Mice, Mutant Strains. Mutation. Neoplasm Invasiveness. Pancreas / pathology. Signal Transduction


33. 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.
  • In addition, they assessed the presence of calcification, pancreatic or bile duct dilation, and metastases.
  • RESULTS: Masses were distributed throughout the pancreas (head, n=5; body, n=2; and tail, n=4).
  • All masses enhanced less than the surrounding pancreas.
  • Common bile and pancreatic duct dilatation was present in two and three patients, respectively.
  • 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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34. Wargo JA, Warshaw AL: Surgical approach to pancreatic exocrine neoplasms. Minerva Chir; 2005 Dec;60(6):445-68
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  • [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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35. Wang Y, Xie SL, Wang CF, Liu SM, Shan Y, Zhao DB, Liu Q, Luo W, Zhao P: [Clinical and pathological analysis of 114 cases with non-ductal pancreatic adenocarcinoma occupying lesions]. Zhonghua Yi Xue Za Zhi; 2010 Apr 27;90(16):1089-92
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  • [Title] [Clinical and pathological analysis of 114 cases with non-ductal pancreatic adenocarcinoma occupying lesions].
  • OBJECTIVE: To improve the diagnosis and treatment of non-ductal pancreatic adenocarcinoma-occupying lesions.
  • METHODS: A retrospective analysis was made for 114 cases of pancreatic non-ductal adenocarcinoma-occupying pathologically confirmed lesions. RESULTS:.
  • (4) pancreaticoduodenectomy was performed in 26 patients, distal pancreatectomy in 53, tumor enucleation in 15, segmental pancreatectomy in 9, partial resection in 3, duodenum-preserving pancreatic head resection in 1 and palliative surgery (either cholecystojejunostomy anastomosis or gastrojejunostomy) in 7;.
  • (5) pathologic analysis revealed 35 solid pseudopapillary neoplasm of pancreas, 28 pancreatic endocrine tumors, 18 focal chronic pancreatitis, 11 serous cystic neoplasms, 9 mucinous cystic neoplasms, 4 pancreatic cysts, 3 acinar cell carcinomas, 2 pancreatic cavernous hemangiomas, 1 sarcoma of pancreas, 1 sarcomatoid carcinoma of pancreas, 1 pancreatic schwannoma and 1 pancreatic neuroblastoma.
  • CONCLUSION: The non-ductal pancreatic adenocarcinoma-occupying lesions have no specific clinical presentation or serum tumor marker.
  • [MeSH-major] Pancreatic Neoplasms / pathology

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  • (PMID = 20646423.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen
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36. Jorgenson TC, Williams BR, Wendland A, Bilger A, Sandgren EP, Drinkwater NR: Identification of susceptibility loci in a mouse model of KRASG12D-driven pancreatic cancer. Cancer Res; 2010 Nov 1;70(21):8398-406
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  • [Title] Identification of susceptibility loci in a mouse model of KRASG12D-driven pancreatic cancer.
  • Genetic background affects susceptibility to pancreatic ductal adenocarcinoma in the Ela-KRAS(G12D) mouse model.
  • In this model, KRAS oncogene expression is driven by an elastase promoter in acinar cells of the pancreas on an FVB/NTac (FVB) background [FVB-Tg(Ela-KRAS(G12D))] with the transgene carried on the Y chromosome.
  • Markers on chromosome 2 segregated with high tumor multiplicity in all three strains; these loci were designated Prsq1-3 (pancreatic ras susceptibility quantitative trait loci 1-3; combined F2 and N2 LOD(W), 6.0, 4.1, and 2.7, respectively).
  • Our findings provide evidence that regions of chromosomes 2, 4, and 12 influence the development and progression of pancreatic neoplasms initiated by an oncogenic allele of KRAS in mice.

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  • [Copyright] ©2010 AACR.
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  • (PMID = 20959479.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA076361; United States / NCI NIH HHS / CA / P01 CA022484; United States / NCI NIH HHS / CA / P01CA022484; United States / NCI NIH HHS / CA / R01CA076361; United States / NCI NIH HHS / CA / T32 CA009135
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS305961; NLM/ PMC3141286
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37. 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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38. 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).
  • Abdominal computed tomography scan revealed a large pancreatic mass with infiltration of the splenic artery.
  • [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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39. Haas M, Laubender RP, Stieber P, Holdenrieder S, Bruns CJ, Wilkowski R, Mansmann U, Heinemann V, Boeck S: Prognostic relevance of CA 19-9, CEA, CRP, and LDH kinetics in patients treated with palliative second-line therapy for advanced pancreatic cancer. Tumour Biol; 2010 Aug;31(4):351-7
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  • [Title] Prognostic relevance of CA 19-9, CEA, CRP, and LDH kinetics in patients treated with palliative second-line therapy for advanced pancreatic cancer.
  • The objective of this study was to define prognostic serum biomarkers that could serve as surrogate survival endpoints during second-line treatment for advanced pancreatic cancer.
  • This retrospective single-center study included patients treated with second-line therapy for advanced exocrine pancreatic cancer.
  • A cutoff of a >20% increase from baseline during treatment was defined in order to form groups with suspected different outcomes.
  • Serum biomarker kinetics might serve as useful prognostic tools during second-line chemotherapy in advanced pancreatic cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. C-Reactive Protein / metabolism. CA-19-9 Antigen / blood. Carcinoembryonic Antigen / blood. L-Lactate Dehydrogenase / blood. Palliative Care. Pancreatic Neoplasms / blood
  • [MeSH-minor] Adenocarcinoma / blood. Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adult. Aged. Biomarkers, Tumor / blood. Bone Neoplasms / blood. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Carcinoma, Acinar Cell / blood. Carcinoma, Acinar Cell / drug therapy. Carcinoma, Acinar Cell / pathology. Female. Humans. Kinetics. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lung Neoplasms / blood. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Male. Middle Aged. Neoplasm Staging. Peritoneal Neoplasms / blood. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / secondary. Prognosis. Retrospective Studies. Survival Rate

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  • (PMID = 20480409.001).
  • [ISSN] 1423-0380
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen; 0 / Carcinoembryonic Antigen; 9007-41-4 / C-Reactive Protein; EC 1.1.1.27 / L-Lactate Dehydrogenase
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40. Heller A, Zörnig I, Müller T, Giorgadze K, Frei C, Giese T, Bergmann F, Schmidt J, Werner J, Buchler MW, Jaeger D, Giese NA: Immunogenicity of SEREX-identified antigens and disease outcome in pancreatic cancer. Cancer Immunol Immunother; 2010 Sep;59(9):1389-400
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  • [Title] Immunogenicity of SEREX-identified antigens and disease outcome in pancreatic cancer.
  • Despite spontaneous or vaccination-induced immune responses, pancreatic cancer remains one of the most deadly immunotherapy-resistant malignancies.
  • We sought to comprehend the spectrum of pancreatic tumor-associated antigens (pTAAs) and to assess the clinical relevance of their immunogenicity.
  • An autologous SEREX-based screening of a cDNA library constructed from a pancreatic T3N0M0/GIII specimen belonging to a long-term survivor (36 months) revealed 18 immunogenic pTAA.
  • PNLIPRP2 and MIA demonstrated the most distinct pancreatic cancer-specific patterns.
  • ELISA-based screening of sera for corresponding autoantibodies revealed that although significantly increased, the immunogenicity of these molecules was not a common feature in pancreatic cancer.
  • QRT-PCR and immunohistochemistry characterized PNLIPRP2 as a robust acinar cell-specific marker whose decreased expression mirrored the disappearance of parenchyma in the diseased organ, but was not related to the presence of PNLIPRP2 autoantibodies.
  • The observed pTAA spectrum comprised molecules associated with acinar, stromal and malignant structures, thus presenting novel targets for tumor cell-specific therapies as well as for approaches based on the bystander effects.
  • Applying the concept of cancer immunoediting to interpret relationships between gene expression, antitumor immune responses, and clinical outcome might better discriminate between past and ongoing immune responses, consequently enabling prognostic stratification of patients and individual adjustment of immunotherapy.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / immunology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / immunology
  • [MeSH-minor] Aged. Antigens, Tumor-Associated, Carbohydrate / genetics. Antigens, Tumor-Associated, Carbohydrate / immunology. Antigens, Tumor-Associated, Carbohydrate / metabolism. Autoantibodies / blood. Cloning, Molecular. Enzyme-Linked Immunosorbent Assay. Female. Gene Library. Humans. Immunochemistry. Lipase / genetics. Lipase / immunology. Lipase / metabolism. Male. Middle Aged. Neoplasm Staging. Pancreas / metabolism. Pancreas / pathology. Prognosis

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  • (PMID = 20514540.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Tumor-Associated, Carbohydrate; 0 / Autoantibodies; 0 / MIA antigen, human; EC 3.1.1.- / pancreatic lipase related protein 2; EC 3.1.1.3 / Lipase
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41. Lin J, Jing X: Fine-needle aspiration of intrapancreatic accessory spleen, mimic of pancreatic neoplasms. Arch Pathol Lab Med; 2010 Oct;134(10):1474-8
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  • [Title] Fine-needle aspiration of intrapancreatic accessory spleen, mimic of pancreatic neoplasms.
  • Distinguishing IPAS from pancreatic neoplasm/malignancy is extremely important from a treatment perspective.
  • We report the case of a 67-year-old asymptomatic man who had a 1.3-cm, incidentally detected, pancreatic tail mass.
  • The image findings were highly suggestive of a pancreatic endocrine neoplasm.
  • Hematoxylin-eosin–stained cell block sections showed conspicuous thin-walled blood vessels in addition to inflammatory cells.
  • By correlating the cytologic findings with the result of immunostaining, we rendered the diagnosis of IPAS.
  • Our experience supports the view that endoscopic ultrasound-guided fine-needle aspiration may enable a reliable, preoperative diagnosis of IPAS and thus prevent unnecessary surgery.
  • [MeSH-major] Biopsy, Fine-Needle / methods. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology. Spleen / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / ultrasonography. Aged. Animals. Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / ultrasonography. Coloring Agents. Diagnosis, Differential. Humans. Inflammation / pathology. Inflammation / ultrasonography. Lymphocytes / pathology. Lymphocytes / ultrasonography. Male. Pancreas / anatomy & histology. Pancreas / ultrasonography

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  • (PMID = 20923303.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Coloring Agents
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42. 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.
  • A 69-year-old man was found to have a mass lesion measuring approximately 4 cm in diameter in the pancreatic head on ultrasound, abdominal dynamic CT, and percutaneous transhepatic cholangiography.
  • 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.
  • A 55-year-old man with upper abdominal pain and nausea, had a cystic lesion approximately 3 cm in size in the pancreatic tail on CT.
  • The tumor cells resembled acinar cells in solid growths.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Common Bile Duct / pathology. Common Bile Duct Neoplasms / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / 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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43. Hruban RH, Maitra A, Goggins M: Update on pancreatic intraepithelial neoplasia. Int J Clin Exp Pathol; 2008;1(4):306-16
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  • [Title] Update on pancreatic intraepithelial neoplasia.
  • Pancreatic intraepithelial neoplasia (PanIN) is a histologically well-defined precursor to invasive ductal adenocarcinoma of the pancreas.
  • Molecular studies have helped establish the progression of PanIN to invasive cancer, and recently genetically engineered mouse models have been generated that recapitulate the entire spectrum of lesions from precursor to invasive pancreatic cancer.
  • Some PanIN lesions produce lobulocentric atrophy of the pancreatic parenchyma, and, when multifocal, this lobulocentric atrophy may be detectable using currently available imaging techniques such as endoscopic ultrasound.
  • The association of acinar-ductal metaplasia with PanIN lesions has led some to hypothesize that PanINs develop from acinar cells that undergo acinar-ductal metaplasia.

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  • (PMID = 18787611.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2480542
  • [Keywords] NOTNLM ; Pancreatic cancer / epigenetics / genetics / intraepithelial neoplasm / metaplasia
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44. Khanna AK, Yadav SK, Dixit VK, Kumar M: AgNOR count and subjective AgNOR pattern assessment (SAPA) score in carcinoma of the pancreatic head including periampullary tumors. JOP; 2005 Nov;6(6):575-80
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  • [Title] AgNOR count and subjective AgNOR pattern assessment (SAPA) score in carcinoma of the pancreatic head including periampullary tumors.
  • CONTEXT: Only a few studies are available in the literature regarding the AgNOR (argyrophilic nucleolar organizer region) count in pancreatic adenocarcinoma but studies on the SAPA (subjective AgNOR pattern assessment) score are completely lacking.
  • OBJECTIVE: We attempted to estimate the AgNOR count and the SAPA score in carcinoma of the pancreatic head including periampullary tumors and to correlate them with other various clinico-histological parameters.
  • SETTING: Patients undergoing pancreatic resection at the University Hospital, Banaras Hindu University, Varanasi, India.
  • PATIENTS: Twenty-four cases of carcinoma of the pancreatic head including periampullary tumors.
  • In addition, on the resected specimen of the pancreas, the area which was normal was chosen and, in that normal tissue, the AgNOR was also studied.
  • RESULTS: The values of the AgNOR count and the SAPA score were significantly higher in cases of pancreatic cancer than in the healthy pancreas.
  • The AgNOR count was 1.6+/-0.1 in the healthy pancreas while it was 2.8+/-0.5 in cases of pancreatic carcinoma (P<0.001).
  • The SAPA score was 5.6+/-0.2 in the healthy pancreas while it was 8.0+/-1.4 in pancreatic carcinoma (P<0.001).
  • Periampullary tumors had a significantly lower (P<0.001) AgNOR count (2.7+/-0.06) and SAPA score (7.8+/-0.2) as compared to carcinoma of the head of the pancreas (AgNOR count 3.3+/-0.03 and SAPA score 9.2+/-0.7).
  • Well-differentiated carcinomas had significantly lower AgNOR counts as compared to other tumors except acinar cell carcinomas since acinar cell carcinomas are also well-differentiated tumors.
  • The SAPA score was also higher in moderately-differentiated tumors and the difference between moderately-differentiated tumor and other types of tumors was significant although there was no significant difference between cystadenocarcinomas and unclassified tumors, and between acinar cell carcinomas and well-differentiated tumors on SAPA scoring.
  • [MeSH-major] Antigens, Nuclear. Nuclear Proteins. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Cell Count. Female. Humans. Male. Middle Aged. Pancreatectomy

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  • (PMID = 16286708.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Nuclear Proteins; 0 / nucleolar organizer region associated proteins
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45. De La O JP, Murtaugh LC: Notch and Kras in pancreatic cancer: at the crossroads of mutation, differentiation and signaling. Cell Cycle; 2009 Jun 15;8(12):1860-4
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  • [Title] Notch and Kras in pancreatic cancer: at the crossroads of mutation, differentiation and signaling.
  • Activating mutations in the KRAS proto-oncogene occur almost ubiquitously in pancreatic ductal adenocarcinoma (PDAC) and in its putative precursor lesions, pancreatic intraepithelial neoplasia (PanIN).
  • Conditional expression of an activated Kras allele in the mouse pancreas produces a model that faithfully recapitulates PanIN formation and progression to PDAC.
  • Importantly, although nearly every cell in the pancreata of these mice express activated Kras, only a very small minority of cells give rise to PanINs.
  • How the transforming activity of Kras is constrained in the pancreas remains unknown, and the cell types from which PanINs and PDAC arise are similarly unknown.
  • Here, we describe our recent results demonstrating that acinar cells are competent to form Kras-induced PanINs, and that active Notch signaling can synergize with Kras in PanIN initiation and progression.
  • Further efforts to understand how Notch and Kras synergize, as well as experiments to determine how other pancreatic cell types contribute to PDAC development, should aid in the development of new therapies and early detection techniques that are desperately needed for this cancer.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins p21(ras) / metabolism. Receptors, Notch / metabolism
  • [MeSH-minor] Animals. Cell Differentiation. Disease Models, Animal. Humans. Mice. Mice, Transgenic. Mutation / genetics. Mutation / physiology. Signal Transduction / physiology

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  • (PMID = 19440048.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R21-CA123066; United States / NCI NIH HHS / CA / R21 CA123066-02; United States / NICHD NIH HHS / HD / 5T32-HD07491; United States / NCI NIH HHS / CA / R21 CA123066; United States / NICHD NIH HHS / HD / T32 HD007491
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [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/ NIHMS118588; NLM/ PMC2719432
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46. 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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  • [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.
  • There are no established treatments for unresectable pancreatic ACC.
  • Prospective clinical trials are necessary to confirm the effectiveness of fluoropyrimidine for the treatment of pancreatic ACC.
  • [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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47. Li W, Nakagawa T, Koyama N, Wang X, Jin J, Mizuno-Horikawa Y, Gu J, Miyoshi E, Kato I, Honke K, Taniguchi N, Kondo A: Down-regulation of trypsinogen expression is associated with growth retardation in alpha1,6-fucosyltransferase-deficient mice: attenuation of proteinase-activated receptor 2 activity. Glycobiology; 2006 Oct;16(10):1007-19
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  • Consistently, the expression of trypsinogen proteins was found to be lower in Fut8-/- mice in the duodenum, small intestine, and pancreas.
  • Trypsin, an active form of trypsinogen, regulates cell growth through a G-protein-coupled receptor, the proteinase-activated receptor 2 (PAR-2).
  • In a cell culture system, a Fut8 knockdown mouse pancreatic acinar cell carcinoma, TGP49-Fut8-KDs, showed decreased growth rate, similar to that seen in Fut8-/- mice, and the decreased growth rate was rescued by the application of the PAR-2-activating peptide (SLIGRL-NH2).
  • Again, the EGF-induced up-regulation of c-fos and c-jun mRNA expression was significantly blocked by the protein kinase C (PKC) inhibitor.
  • Our findings clearly demonstrate a relationship between Fut8 and the regulation of EGF receptor (EGFR)-trypsin-PAR-2 pathway in controlling cell growth and that the EGFR-trypsin-PAR-2 pathway is suppressed in TGP49-Fut8-KDs as well as in Fut8-/- mice.
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Down-Regulation. Embryo, Mammalian / metabolism. Male. Mice. Mice, Knockout. Oligopeptides / pharmacology. Phosphorylation. Receptor, Epidermal Growth Factor / metabolism. Tumor Cells, Cultured

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  • (PMID = 16861703.001).
  • [ISSN] 0959-6658
  • [Journal-full-title] Glycobiology
  • [ISO-abbreviation] Glycobiology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oligopeptides; 0 / Receptor, PAR-2; 0 / seryl-leucyl-isoleucyl-glycyl--arginyl-leucinamide; 9002-08-8 / Trypsinogen; EC 2.4.1.- / Fucosyltransferases; EC 2.4.1.68 / Glycoprotein 6-alpha-L-fucosyltransferase; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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48. 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.
  • METHODS: Patients were identified from the National Cancer Database.
  • Patients with ACC were more likely to be male, white, and have larger tumor size, no nodal involvement, or pancreatic tail tumors.
  • Aggressive surgical resection with negative margins is associated with long-term survival in these more favorable pancreatic cancers.
  • [MeSH-major] Carcinoma, Acinar Cell / epidemiology. Carcinoma, Acinar Cell / surgery. Pancreatic Neoplasms / epidemiology. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Aged. Carcinoma, Pancreatic Ductal / epidemiology. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Pancreatic Ductal / surgery. Chi-Square Distribution. Female. Humans. Lymphatic Metastasis. Male. Middle Aged. Pancreatectomy. Prognosis. ROC Curve. Regression Analysis. Statistics, Nonparametric. Survival Rate. Treatment Outcome. United States / epidemiology

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  • [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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49. 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.
  • One clue comes from the fact that PanINs, unlike most cells in the adult pancreas, exhibit active Notch signaling.
  • 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.
  • Through conditional expression in the mouse pancreas, we find dramatic synergy between activated Notch and Kras in inducing PanIN formation.
  • 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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50. Bhatia P, Srinivasan R, Rajwanshi A, Nijhawan R, Khandelwal N, Wig J, Vasishtha RK: 5-year review and reappraisal of ultrasound-guided percutaneous transabdominal fine needle aspiration of pancreatic lesions. Acta Cytol; 2008 Sep-Oct;52(5):523-9
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  • [Title] 5-year review and reappraisal of ultrasound-guided percutaneous transabdominal fine needle aspiration of pancreatic lesions.
  • OBJECTIVE: To reevaluate the efficacy and safety offine needle aspiration cytology (FNAC) of pancreatic lesions performed by transabdominal approach.
  • STUDY DESIGN: Retrospective 5-year (2001-2006) audit of all pancreatic FNA samples.
  • Seven cases (2.6%) yielded insufficient material for diagnosis; 260 cases were classified as benign (n=118) and malignant (n=142) lesions.
  • Of the 142 malignant aspirates, the cytodiagnosis was adenocarcinoma in 126, neuroendocrine/carcinoid tumor in 7, papillary solid epithelial neoplasm in 2, mucinous cystadenocarcinoma in 2, acinar cell carcinoma in 1 and metastatic small cell carcinoma in lung in 4 cases.
  • CONCLUSION: A spectrum of pancreatic lesions can be accurately diagnosed by the technique.
  • [MeSH-major] Pancreatic Neoplasms / pathology

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  • [CommentIn] Acta Cytol. 2008 Sep-Oct;52(5):521-2 [18833811.001]
  • (PMID = 18833812.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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51. Qi T, Han J, Cui Y, Zong M, Liu X, Zhu B: Comparative proteomic analysis for the detection of biomarkers in pancreatic ductal adenocarcinomas. J Clin Pathol; 2008 Jan;61(1):49-58
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  • [Title] Comparative proteomic analysis for the detection of biomarkers in pancreatic ductal adenocarcinomas.
  • AIMS: To search for novel potential protein biomarkers for the early detection and better intervention of pancreatic ductal adenocarcinoma (PDAC).
  • METHODS: Eight pairs of matched PDAC and non-cancerous pancreas tissues were profiled with two-dimensional electrophoresis; differentially expressed proteins were identified by mass spectrometry.
  • Immunohistochemistry showed that TBX4 expression could be seen in both centroacinar cells and small ducts in normal pancreas and tumour cells in 5/5 (100%) well differentiated, 35/38 (92.1%) moderately differentiated, and 11/18 (61.1%) poorly differentiated PDAC tissues with different staining intensity.
  • However, in normal acinar cells and tumour cells in the other 3/38 (7.9%) moderately differentiated and 7/18 (38.9%) poorly differentiated PDAC tissues, there was no visible TBX4 expression.
  • Strong expression of HSP60 could be seen in both acinar cells and small ducts in normal pancreas tissues and tumour cells in PDAC tissues except for islets and tumour stoma; no correlation was found between HSP60 expression and differentiation of PDAC tissues.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Cell Differentiation. Female. HSP40 Heat-Shock Proteins / metabolism. Humans. Male. Middle Aged. Neoplasm Proteins / metabolism. Pancreas / metabolism. Proteomics. T-Box Domain Proteins / metabolism. Trypsin / metabolism

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  • (PMID = 17412869.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HSP40 Heat-Shock Proteins; 0 / Neoplasm Proteins; 0 / T-Box Domain Proteins; 0 / TBX4 protein, human; EC 3.4.21.4 / Trypsin
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52. Ikezoe M, Nishihara T, Yanagawa K, Kohro T, Yamai T, Ikezoe S, Yasunaga Y, Inui Y, Nishikawa M: A case of pancreatic acinar cell carcinoma metastatic to skin. Rare Tumors; 2010;2(4):e62
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  • [Title] A case of pancreatic acinar cell carcinoma metastatic to skin.
  • We report a rare case of pancreatic acinar cell carcinoma with widespread metastases in a 68-year-old woman who presented with subcutaneous nodules as the initial symptom.
  • Computed tomography showed a pancreatic mass with hepatic tumors and enlarged lymph nodes besides ring-enhanced subcutaneous nodules.
  • Histological analysis of a colonic polypoid lesion revealed carcinoma with endocrine and acinar differentiation compatible with pancreatic origin.
  • Regrettably, she died of a cerebral infarction without any treatment, and autopsy findings confirmed our diagnosis.

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  • (PMID = 21234254.001).
  • [ISSN] 2036-3613
  • [Journal-full-title] Rare tumors
  • [ISO-abbreviation] Rare Tumors
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC3019597
  • [Keywords] NOTNLM ; magnetic resonance diffusion-weighted imaging. / pancreatic acinar cell carcinoma / subcutaneous nodules / widespread metastases
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53. Kayed H, Bekasi S, Keleg S, Michalski CW, Giese T, Friess H, Kleeff J: BGLAP is expressed in pancreatic cancer cells and increases their growth and invasion. Mol Cancer; 2007;6:83
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  • [Title] BGLAP is expressed in pancreatic cancer cells and increases their growth and invasion.
  • In this study, we analyzed the expression and role of BGLAP in the normal human pancreas, chronic pancreatitis (CP), and pancreatic ductal adenocarcinoma (PDAC) using quantitative RT-PCR, immunohistochemistry, immunocytochemistry and enzyme immunoassays, as well as cell proliferation and invasion assays.
  • RESULTS: Compared to the normal pancreas, BGLAP mRNA and protein levels were not significantly different in CP and PDAC tissues.
  • BGLAP was faintly present in the cytoplasm of normal acinar cells but was strongly expressed in the cytoplasm and nuclei of tubular complexes and PanIN lesions of CP and PDAC tissues.
  • Furthermore, BGLAP expression was found in the cancer cells in PDAC tissues as well as in 4 cultured pancreatic cancer cell lines.
  • TNFalpha reduced BGLAP mRNA and protein expression levels in pancreatic cancer cell lines.
  • In addition, BGLAP silencing led to reduction of both cell growth and invasion in those cells.
  • CONCLUSION: BGLAP is expressed in pancreatic cancer cells, where it potentially increases pancreatic cancer cell growth and invasion through autocrine and/or paracrine mechanisms.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Pancreatic Ductal / genetics. Cell Proliferation. Gene Expression Regulation, Neoplastic / physiology. Osteocalcin / genetics. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Collagen / metabolism. Drug Combinations. Enzyme-Linked Immunosorbent Assay. Gene Silencing. Humans. Immunoenzyme Techniques. Laminin / metabolism. Middle Aged. Neoplasm Invasiveness. Pancreas / metabolism. Pancreas / pathology. Pancreatitis, Chronic / genetics. Pancreatitis, Chronic / pathology. Proteoglycans / metabolism. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18163903.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 104982-03-8 / Osteocalcin; 119978-18-6 / matrigel; 9007-34-5 / Collagen
  • [Other-IDs] NLM/ PMC2245975
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54. 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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  • [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).
  • The aim of the study was to find support for either of the 2 models through the analysis of a large panel of human pancreatic tissues.
  • 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


55. Békási S, Zalatnai A: Overexpression of glucocorticoid receptor in human pancreatic cancer and in xenografts. An immunohistochemical study. Pathol Oncol Res; 2009 Dec;15(4):561-6
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  • [Title] Overexpression of glucocorticoid receptor in human pancreatic cancer and in xenografts. An immunohistochemical study.
  • Glucocorticoid receptor overexpression has been reported in a variety of human solid tumors, but much less in known about its presence in pancreatic cancer.
  • Immunohistochemical analysis of paraffin-embedded tissue sections was performed in human normal pancreata and well differentiated pancreatic adenocarcinomas (monoclonal primary antibody, ABCAM, Cambridge, UK).
  • As positive control invasive ductal adenocarcinoma of the breast was used.
  • In the normal non-tumorous pancreas a strong positivity was detected in all acinar cells, typically in the cytoplasm.
  • The ductal pancreatic carcinoma cells also displayed a strong positivity.
  • Strong glucocorticoid receptor expression was also found in xenografted human pancreatic cancer showing a diffuse, mainly cytoplasmic positivity.
  • Our studies have shown that the human pancreatic carcinomas do overexpress a strong glucocorticoid receptor positivity, but its significance is not clear.
  • [MeSH-major] Adenocarcinoma / metabolism. Pancreas / metabolism. Pancreatic Neoplasms / metabolism. Receptors, Glucocorticoid / metabolism
  • [MeSH-minor] Animals. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / metabolism. Carcinoma, Ductal, Breast / pathology. Case-Control Studies. Humans. Mice. Mice, Inbred CBA. Transplantation, Heterologous

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  • (PMID = 19253003.001).
  • [ISSN] 1532-2807
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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56. Scoazec JY: [Case 8: Liver metastasis of pancreatic acinar cell carcinoma]. Ann Pathol; 2007 Apr;27(2):120-7
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  • [Title] [Case 8: Liver metastasis of pancreatic acinar cell carcinoma].
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Liver Neoplasms / secondary. Pancreatic Neoplasms / pathology

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  • (PMID = 17909469.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
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57. Treiber M, Schulz HU, Landt O, Drenth JP, Castellani C, Real FX, Akar N, Ammann RW, Bargetzi M, Bhatia E, Demaine AG, Battagia C, Kingsnorth A, O'Reilly D, Truninger K, Koudova M, Spicak J, Cerny M, Menzel HJ, Moral P, Pignatti PF, Romanelli MG, Rickards O, De Stefano GF, Zarnescu NO, Choudhuri G, Sikora SS, Jansen JB, Weiss FU, Pietschmann M, Teich N, Gress TM, Ockenga J, Schmidt H, Kage A, Halangk J, Rosendahl J, Groneberg DA, Nickel R, Witt H: Keratin 8 sequence variants in patients with pancreatitis and pancreatic cancer. J Mol Med (Berl); 2006 Dec;84(12):1015-22
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  • [Title] Keratin 8 sequence variants in patients with pancreatitis and pancreatic cancer.
  • Transgenic mice over-expressing human KRT8 display pancreatic mononuclear infiltration, interstitial fibrosis and dysplasia of acinar cells resulting in exocrine pancreatic insufficiency.
  • This prompted us to investigate KRT8 polymorphisms in patients with pancreatic disorders.
  • The KRT8 Y54H and G62C polymorphisms were assessed in a cohort of patients with acute and chronic pancreatitis of various aetiologies or pancreatic cancer originating from Austria (n=16), the Czech Republic (n=90), Germany (n=1698), Great Britain (n=36), India (n=60), Italy (n=143), the Netherlands (n=128), Romania (n=3), Spain (n=133), and Switzerland (n=129).
  • The frequency of G62C did not differ between patients with acute or chronic pancreatitis, pancreatic adenocarcinoma and control individuals.
  • Our data suggest that the KRT8 alterations, Y54H and G62C, do not predispose patients to the development of pancreatitis or pancreatic cancer.
  • [MeSH-major] Genetic Variation. Keratin-8 / genetics. Pancreatic Neoplasms / genetics. Pancreatitis / genetics. Pancreatitis, Alcoholic / genetics
  • [MeSH-minor] Acute Disease. Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adult. African Continental Ancestry Group / genetics. Aged. Alleles. Asian Continental Ancestry Group / genetics. Carcinoma, Pancreatic Ductal / genetics. Carcinoma, Pancreatic Ductal / pathology. Case-Control Studies. Chronic Disease. Cohort Studies. European Continental Ancestry Group / genetics. Female. Gene Frequency. Geography. Heterozygote. Humans. Male. Middle Aged. Polymorphism, Genetic. Retrospective Studies

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  • (PMID = 17039343.001).
  • [ISSN] 0946-2716
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / KRT8 protein, human; 0 / Keratin-8
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58. Xu X, Ehdaie B, Ohara N, Yoshino T, Deng CX: Synergistic action of Smad4 and Pten in suppressing pancreatic ductal adenocarcinoma formation in mice. Oncogene; 2010 Feb 4;29(5):674-86
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  • [Title] Synergistic action of Smad4 and Pten in suppressing pancreatic ductal adenocarcinoma formation in mice.
  • Mutations of SMAD4/DPC4 are found in about 60% of human invasive pancreatic ductal adenocarcinomas (PDACs); yet, the manner in which SMAD4 deficiency enhances tumorigenesis remains elusive.
  • Using a Cre-LoxP approach, we generated a mutant mouse carrying a targeted deletion of Smad4 in the pancreas.
  • We showed that the absence of Smad4 alone did not trigger pancreas tumor formation; however, it increased the expression of an inactivated form of Pten, suggesting a role of Pten in preventing Smad4-/- cells from undergoing malignancy.
  • The absence of Smad4 in a Pten-mutant background enhanced cell proliferation and triggered transdifferentiation from acinar, centroacinar and islet cells, accompanied by activation of Notch1 signaling.
  • We showed that all tumors developed in the Smad4/Pten-mutant pancreas exhibited high levels of pAKT and mTOR, and that about 50 and 83% of human pancreatic cancers examined showed increased pAKT and pmTOR, respectively.
  • Besides the similarity in gene expression, the pAKT and/or pmTOR-positive human PDACs and mouse pancreatic tumors also shared some histopathological similarities.
  • These observations indicate that Smad4/Pten-mutant mice mimic the tumor progression of human pancreatic cancers that are driven by activation of the AKT-mTOR pathway, and uncovered a synergistic action of Smad4 and Pten in repressing pancreatic tumorigenesis.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. PTEN Phosphohydrolase / metabolism. Pancreatic Neoplasms / metabolism. Signal Transduction / physiology. Smad4 Protein / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Cell Transdifferentiation / physiology. Gene Expression. Genotype. Humans. Immunohistochemistry. Intracellular Signaling Peptides and Proteins / metabolism. Mice. Mice, Knockout. Phenotype. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. TOR Serine-Threonine Kinases


59. Pujal J, Huch M, José A, Abasolo I, Rodolosse A, Duch A, Sánchez-Palazón L, Smith FJ, McLean WH, Fillat C, Real FX: Keratin 7 promoter selectively targets transgene expression to normal and neoplastic pancreatic ductal cells in vitro and in vivo. FASEB J; 2009 May;23(5):1366-75
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  • [Title] Keratin 7 promoter selectively targets transgene expression to normal and neoplastic pancreatic ductal cells in vitro and in vivo.
  • In the pancreas, it is present in ductal but not in acinar cells.
  • K7 mRNA is overexpressed in pancreatic cancers.
  • All elements required for appropriate cell and tissue specificity in reporter assays are present within the Krt7 -234 bp sequence.
  • This fragment appears more selective to pancreatic ductal cells than the Krt19 promoter.
  • Sequences located 1.5 or 0.25 kb upstream of the transcription initiation site drive reporter expression to ductal, but not acinar, cells in transgenic mice.
  • LacZ mRNA was detected in the pancreas as well as in additional epithelial tissues--such as the intestine and the lung--using both promoter constructs.
  • An AdK7Luc adenovirus was generated to assess targeting selectivity in vivo by intravenous injection to immunocompetent mice and in a xenograft model of pancreatic cancer.
  • The -0.25 kb region showed pancreatic selectivity, high activity in pancreatic cancers, and sustained transgene expression in xenografts.
  • In conclusion, the krt7 promoter is useful to target pancreatic ductal adenocarcinoma cells in vitro and in vivo.
  • [MeSH-major] Keratin-7 / genetics. Pancreatic Ducts / metabolism. Pancreatic Neoplasms / metabolism. Promoter Regions, Genetic. Transgenes
  • [MeSH-minor] Adenoviridae / genetics. Animals. Cell Line, Tumor. Female. Humans. Mice. Mice, Transgenic. Regulatory Sequences, Nucleic Acid / genetics. Sp1 Transcription Factor / metabolism

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  • (PMID = 19124560.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 104151; United Kingdom / Medical Research Council / / G0700314; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Keratin-7; 0 / Krt2-7 protein, mouse; 0 / Sp1 Transcription Factor
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60. Stelow EB, Bardales RH, Stanley MW: Pitfalls in endoscopic ultrasound-guided fine-needle aspiration and how to avoid them. Adv Anat Pathol; 2005 Mar;12(2):62-73
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  • Although a broad range of pancreatic, gastrointestinal, thoracic, and abdominal pathology may be sampled by endoscopic ultrasound (EUS)-guided fine-needle aspiration (FNA), certain difficulties tend to recur because of the frequency of certain sample types and because of the nature of their individual cytomorphologic profiles.
  • We discuss the diagnosis of pancreatic ductal adenocarcinoma and of other pancreatic epithelioid tumors including pancreatic endocrine neoplasms, solid pseudopapillary tumors, and acinar cell carcinomas.
  • We also discuss the diagnosis of pancreatic cystic neoplasia including intraductal papillary mucinous neoplasms and mucinous cystic neoplasms and the diagnosis of gastrointestinal mesenchymal neoplasia with particular attention to gastrointestinal stromal tumors.
  • [MeSH-major] Adenocarcinoma / pathology. Biopsy, Fine-Needle / methods. Diagnostic Errors / prevention & control. Endosonography. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans

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  • (PMID = 15731574.001).
  • [ISSN] 1072-4109
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 137
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61. Morris JP 4th, Cano DA, Sekine S, Wang SC, Hebrok M: Beta-catenin blocks Kras-dependent reprogramming of acini into pancreatic cancer precursor lesions in mice. J Clin Invest; 2010 Feb;120(2):508-20
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  • [Title] Beta-catenin blocks Kras-dependent reprogramming of acini into pancreatic cancer precursor lesions in mice.
  • WT mouse acinar cells rapidly regenerate following injury that mimics acute pancreatitis, a process characterized by transient reactivation of pathways involved in embryonic pancreatic development.
  • In contrast, such injury promotes the development of pancreatic ductal adenocarcinoma (PDA) precursor lesions in mice expressing a constitutively active form of the GTPase, Kras, in the exocrine pancreas.
  • The molecular environment that mediates acinar regeneration versus the development of PDA precursor lesions is poorly understood.
  • Here, we used genetically engineered mice to demonstrate that mutant Kras promotes acinar-to-ductal metaplasia (ADM) and pancreatic cancer precursor lesion formation by blocking acinar regeneration following acute pancreatitis.
  • Our results indicate that beta-catenin is required for efficient acinar regeneration.
  • In addition, canonical beta-catenin signaling, a pathway known to regulate embryonic acinar development, is activated following acute pancreatitis.
  • This regeneration-associated activation of beta-catenin signaling was not observed during the initiation of Kras-induced acinar-to-ductal reprogramming.
  • Therefore, these results suggest that beta-catenin signaling is a critical determinant of acinar plasticity and that it is inhibited during Kras-induced fate decisions that specify PDA precursors, highlighting the importance of temporal regulation of embryonic signaling pathways in the development of neoplastic cell fates.


62. Young RH: From Krukenberg to today: the ever present problems posed by metastatic tumors in the ovary. Part II. Adv Anat Pathol; 2007 May;14(3):149-77
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  • This is the second of a two-part consideration of metastatic tumors to the ovary.
  • The first tumor discussed is gastric carcinoma of intestinal-type whose ovarian manifestations have been the subject of a recent paper which emphasized its differences from the Krukenberg tumor.
  • Coverage of intestinal adenocarcinoma emphasizes the landmark 1987 paper of RH Lash and WR Hart.
  • The section on pancreatic neoplasms reemphasizes the problems caused by metastatic ductal carcinoma, considered primarily in Part I, and discusses less common issues such as spread of neuroendocrine and acinar cell carcinomas.
  • The limited information on spread of tumors of the gallbladder and extrahepatic bile ducts is then reviewed before more detailed consideration of hepatic neoplasms, prompted by recent contributions on hepatocellular carcinoma and intrahepatic cholangiocarcinoma, the latter based on significant experience with this problem in Thailand.
  • The section on appendiceal neoplasms highlights ovarian spread of diverse tumors ranging from typical intestinal-type adenocarcinoma to signet-ring cell carcinomas with various patterns which in the ovary may prompt diagnoses such as a goblet cell (mucinous) carcinoid tumor, but whose ovarian features place them in the category of a Krukenberg tumor.
  • The diverse problems in differential diagnosis of carcinoid tumor (provoked by nested, acinar, and other patterns, including folliclelike spaces) are then reviewed.
  • The section on breast cancer emphasizes that, although usually a manifestation of late stage disease and often not bulky in the ovaries, metastatic breast cancer may form large masses which can represent the clinical presentation.
  • That patients with breast cancer have an increased risk of primary ovarian cancer and that the latter is more common than secondary spread of breast cancer is noted.
  • The section on lung tumors largely reflects information in a recent paper that small cell carcinoma and adenocarcinoma are the lung cancers that spread to the ovary most commonly.
  • The extremely broad differential diagnosis posed by metastatic malignant melanoma ranging from that of an oxyphilic tumor, to a small cell tumor, to a follicle-forming neoplasm, is then considered.
  • The sections on renal cell carcinoma and other urinary tract neoplasms emphasize the differential diagnosis of metastatic clear cell carcinoma and primary clear cell carcinoma, an issue usually resolvable by an awareness of the various features of the ovarian variant, rarely or never seen in the renal variant.
  • The endometrial stromal tumors are problematic largely because the history of a primary tumor may be remote, in the ovaries the typical growth and vascular pattern of endometrial stromal neoplasms is not always conspicuous, and some endometrial stromal sarcomas in the ovary show sex cordlike patterns of growth.
  • The sections on ovarian spread of uterine carcinomas emphasize the problems owing to cervical adenocarcinomas, which have a greater tendency to involve the ovaries than squamous cell carcinomas and can simulate primary mucinous or endometrioid cancers.
  • The final neoplasms considered are malignant mesothelioma and the desmoplastic small round cell tumor.
  • The microscopic features of malignant mesothelioma are so different from those of primary ovarian carcinoma in most instances that the diagnosis should be readily established on routine microscopic evaluation.
  • The differential diagnosis of the desmoplastic small round cell tumor is more complex because of the greater overlap with the many other small cell malignant tumors that may involve the ovaries primarily or secondarily.
  • However, as pointed out in brief concluding remarks, despite the aid of that modality, as in surgical pathology overall, careful consideration of the clinical background, distribution of disease, gross characteristics and spectrum of routine microscopic findings, will lead to the correct diagnosis in the majority of cases and at the very least lead to formulation of a considered differential diagnosis such that use of special techniques may be judicious and those results placed in context of the time-honored clinical and pathologic features.
  • [MeSH-major] Carcinoma / secondary. Krukenberg Tumor / secondary. Ovarian Neoplasms / secondary
  • [MeSH-minor] Diagnosis, Differential. Female. History, 19th Century. History, 20th Century. Humans

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  • (PMID = 17452813.001).
  • [ISSN] 1072-4109
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 67
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63. 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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64. Chang F, Chandra A, Culora G, Mahadeva U, Meenan J, Herbert A: Cytologic diagnosis of pancreatic endocrine tumors by endoscopic ultrasound-guided fine-needle aspiration: a review. Diagn Cytopathol; 2006 Sep;34(9):649-58
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  • [Title] Cytologic diagnosis of pancreatic endocrine tumors by endoscopic ultrasound-guided fine-needle aspiration: a review.
  • Precise localization and diagnosis of pancreatic endocrine tumors (PETs) is important, because pancreatic PETs have different clinical and biological behavior and treatment modalities than do exocrine pancreatic tumors.
  • In contrast to the much more common exocrine adenocarcinomas, cytologic studies of PET are relatively rare and many cytopathologists lack experience with the cytomorphologic features of these tumors.During the last 10 yr, endoscopic ultrasound (EUS)-guided fine-needle aspiration (FNA) has matured into an accurate, highly sensitive, and cost-effective modality for the preoperative localization of pancreatic PETs.
  • This manuscript focuses on the cytomorphologic features most suggestive of pancreatic PETs, differential diagnosis, and diagnostic pitfalls of PETs.
  • The technical development of EUS-guided FNA and the ancillary studies for pancreatic PETs are also reviewed.
  • The data summarized in this review indicate that EUS-FNA is a valuable method in the recognition of pancreatic PETs and in most cases cytopathologists could reach a correct diagnosis of these tumors, including their hormone producing capability on aspirated cytologic material.
  • [MeSH-major] Biopsy, Fine-Needle / methods. Carcinoma, Islet Cell / pathology. Endoscopy, Digestive System / methods. Insulinoma / pathology. Pancreatic Neoplasms / pathology. Ultrasonography / methods
  • [MeSH-minor] Adenocarcinoma, Papillary / pathology. Biomarkers, Tumor / analysis. Carcinoma, Acinar Cell / pathology. Carcinoma, Pancreatic Ductal / pathology. Diagnosis, Differential. Gastrinoma / chemistry. Gastrinoma / pathology. Glucagonoma / chemistry. Glucagonoma / pathology. Humans. Immunohistochemistry. Lymphoma / pathology

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16900463.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 74
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65. Jena M, Shariff S, Jeyachandran P: Cystic variant of acinar cell carcinoma of the pancreas presenting as pseudo-pancreatic cyst. Indian J Pathol Microbiol; 2010 Jan-Mar;53(1):190-2
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  • [Title] Cystic variant of acinar cell carcinoma of the pancreas presenting as pseudo-pancreatic cyst.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / pathology. Pancreatic Pseudocyst / diagnosis. Pancreatic Pseudocyst / pathology
  • [MeSH-minor] Aged. Biopsy, Fine-Needle. Diagnosis, Differential. Histocytochemistry. Humans. Laparotomy. Male. Microscopy. Radiography, Abdominal

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  • (PMID = 20090274.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] India
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66. Cevasco M, Rodriguez JR, Fernandez-del Castillo C: Clinical challenges and images in GI: image 3. Pancreatic acinar cell carcinoma with subcutaneous fat necrosis. Gastroenterology; 2008 Oct;135(4):1054, 1433
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  • [Title] Clinical challenges and images in GI: image 3. Pancreatic acinar cell carcinoma with subcutaneous fat necrosis.
  • [MeSH-major] Carcinoma, Acinar Cell / radiography. Pancreas, Exocrine / radiography. Pancreatic Neoplasms / radiography. Subcutaneous Fat / pathology. Tomography, X-Ray Computed

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  • (PMID = 18789332.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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67. Chang SC, Liao JW, Lin YC, Liu CI, Wong ML: Pancreatic acinar cell carcinoma with intracranial metastasis in a dog. J Vet Med Sci; 2007 Jan;69(1):91-3
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  • [Title] Pancreatic acinar cell carcinoma with intracranial metastasis in a dog.
  • This report concerns a case of pancreatic carcinoma with widespread metastases to many organs including intracranial metastasis.
  • Based on gross and microscopic examination, the primary tumor cells were located in the left lobe of the pancreas and widespread metastasis was found into various organs, including the brain, lungs, liver, kidneys, tonsils, serosal surface of the esophagus, and submandibular, pulmonary hilar, mediastinal, and mesenteric lymph nodes.
  • This case indicates that pancreatic adenocarcinoma should be included in the differential diagnosis list when cervical neck masses are detected.

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  • (PMID = 17283409.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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68. 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.
  • ACC has been considered a cancer with poor prognosis due to frequent metastasis, a high recurrence rate, and low resectability.
  • RESULTS: ACC was more common in male, and age at diagnosis ranged from 25 to 68 years (median 54).
  • Liver was most common organ of metastasis at diagnosis and recurrence after operation.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Neoplasms / diagnosis

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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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69. 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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  • [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.
  • 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).
  • 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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70. 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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71. Sanlioglu AD, Dirice E, Elpek O, Korcum AF, Ozdogan M, Suleymanlar I, Balci MK, Griffith TS, Sanlioglu S: High TRAIL death receptor 4 and decoy receptor 2 expression correlates with significant cell death in pancreatic ductal adenocarcinoma patients. Pancreas; 2009 Mar;38(2):154-60
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  • [Title] High TRAIL death receptor 4 and decoy receptor 2 expression correlates with significant cell death in pancreatic ductal adenocarcinoma patients.
  • OBJECTIVES: The importance of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and TRAIL receptor expression in pancreatic carcinoma development is not known.
  • To reveal the putative connection of TRAIL and TRAIL receptor expression profile to this process, we analyzed and compared the expression profile of TRAIL and its receptors in pancreatic tissues of both noncancer patients and patients with pancreatic ductal adenocarcinoma (PDAC).
  • Annexin V binding revealed the apoptotic index in pancreas.
  • In addition, acinar cells from PDAC patients had higher DcR2 expression but lower death receptor 4 expression.
  • CONCLUSIONS: Differential alteration of TRAIL and TRAIL receptor expression profiles in PDAC patients suggest that the TRAIL/TRAIL receptor system may play a pivotal role during pancreatic carcinoma development.
  • [MeSH-major] Adenocarcinoma / pathology. Apoptosis. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / pathology. Receptors, Tumor Necrosis Factor / physiology. Tumor Necrosis Factor Decoy Receptors / physiology

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  • (PMID = 18981952.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF10A protein, human; 0 / TNFRSF10D protein, human; 0 / Tumor Necrosis Factor Decoy Receptors
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72. 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.
  • Histologically, tumour cells were organized in acinar structures resembling pancreatic acini and in solid nests and ribbons or diffusely infiltrated as poorly cohesive 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.
  • No immunoreactivity was observed for cytokeratin 7, MUC1, MUC5AC, pancreatic amylase or PDX1.
  • 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. CDX2 Transcription Factor. 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
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73. Cavallini A, Falconi M, Bortesi L, Crippa S, Barugola G, Butturini G: Pancreatoblastoma in adults: a review of the literature. Pancreatology; 2009;9(1-2):73-80
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  • METHODS: Adult patients with histologically proven pancreatoblastoma were identified from our prospective database of pancreatic resections.
  • RESULTS: At our Institution, 2 adult males, 26 and 69 years old, underwent successful pancreatic resection for pancreatoblastoma.
  • The diagnosis of pancreatoblastoma mainly depends on the pathological findings characterized by squamoid corpuscles at histopathology.
  • The differential diagnosis includes nonfunctional pancreatic endocrine tumor, acinar cell carcinoma, solid pseudopapillary tumor and adenocarcinoma.
  • [MeSH-major] Carcinoma, Neuroendocrine. Pancreatic Neoplasms
  • [MeSH-minor] Adult. Aged. Child. Child, Preschool. Diagnosis, Differential. Humans. Male. Pancreaticoduodenectomy

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  • [Copyright] Copyright 2008 S. Karger AG, Basel and IAP.
  • (PMID = 19077457.001).
  • [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; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 36
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74. Ji B, Tsou L, Wang H, Gaiser S, Chang DZ, Daniluk J, Bi Y, Grote T, Longnecker DS, Logsdon CD: Ras activity levels control the development of pancreatic diseases. Gastroenterology; 2009 Sep;137(3):1072-82, 1082.e1-6
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  • [Title] Ras activity levels control the development of pancreatic diseases.
  • BACKGROUND & AIMS: Differentiated pancreatic acinar cells expressing endogenous levels of mutant K-Ras do not spontaneously develop pancreatic ductal adenocarcinoma (PDAC).
  • However, we hypothesized that acinar cells would develop PDAC in the presence of Ras activity levels mimicking those of human tumor cells.
  • We compared the effects of acinar cell expression of mutant K-Ras at endogenous and elevated levels on Ras activity and on the development of PDAC.
  • Expression of endogenous levels of mutant K-Ras in differentiated acinar cells resulted in moderately elevated Ras activity and in sparse murine pancreatic intraepithelial neoplasias (mPanINs) that did not spontaneously advance to PDAC unless the tumor suppressor p53 was simultaneously deleted.
  • High Ras activity mimicking levels in PDAC led to acinar cell senescence and generated inflammation and fibrosis resembling the histologic features of chronic pancreatitis.
  • With higher Ras activity in acinar cells, abundant mPanINs formed and spontaneously progressed to both cystic papillary carcinoma and metastatic PDAC.
  • Sufficient Ras activity in pancreatic acinar induces several important pancreatic disease manifestations not previously reported and supports a potential direct linkage between chronic pancreatitis, cystic papillary carcinoma, and PDAC.

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  • (PMID = 19501586.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK052067-11; United States / NCI NIH HHS / CA / P30 CA016672; United States / NIDDK NIH HHS / DK / R21 DK068414; United States / NCI NIH HHS / CA / CA16672; United States / NIDDK NIH HHS / DK / R01 DK052067; United States / NIDDK NIH HHS / DK / R01 DK052067-11; United States / NIDDK NIH HHS / DK / 5R21DK068414; United States / NCI NIH HHS / CA / P20 CA101936; United States / NIAAA NIH HHS / AA / R01 AA020822; United States / NIDDK NIH HHS / DK / R01 DK052067-10; United States / NIDDK NIH HHS / DK / DK052067; United States / NIDDK NIH HHS / DK / DK052067-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS122586; NLM/ PMC2789008
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75. Frankel WL: Update on pancreatic endocrine tumors. Arch Pathol Lab Med; 2006 Jul;130(7):963-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Update on pancreatic endocrine tumors.
  • Endocrine tumors of the pancreas represent 1% to 2% of all pancreatic neoplasms.
  • The morphologic spectrum of these tumors can be variable, and the differential diagnosis includes chronic pancreatitis with neuroendocrine hyperplasia, ductal adenocarcinoma, solid pseudopapillary tumor, acinar cell carcinoma, and pancreatoblastoma.
  • It is important to be aware that unusual morphologic variants of pancreatic endocrine tumors are common, and immunohistochemical stains can help avoid misdiagnosis.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Pancreatic Ductal / diagnosis. Carcinoma, Papillary / diagnosis. Diagnosis, Differential. Humans. Islets of Langerhans / pathology. Neoplasms, Germ Cell and Embryonal / diagnosis. Pancreatitis, Chronic / diagnosis. Prognosis

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  • (PMID = 16831051.001).
  • [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] 26
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76. Igarashi H, Shinozaki S, Mukada T: A case of acinar cell carcinoma of the pancreas that formed extensive tumor thrombus of the portal vein. Clin J Gastroenterol; 2009 Apr;2(2):96-102
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  • [Title] A case of acinar cell carcinoma of the pancreas that formed extensive tumor thrombus of the portal vein.
  • Abdominal ultrasonography and computed tomography revealed a large mass in the body and tail of the pancreas, which directly invaded the stomach and the spleen.
  • The specimens obtained from portal tumor thrombus were histologically compatible with acinar cell carcinoma.
  • Portal tumor thrombus is a rare condition in pancreatic tumors; however, it seems to be important to differentiate tumor thrombus from blood thrombus of the portal vein in order to know the true clinical stage and provide a suitable treatment.

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  • (PMID = 26192173.001).
  • [ISSN] 1865-7257
  • [Journal-full-title] Clinical journal of gastroenterology
  • [ISO-abbreviation] Clin J Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Keywords] NOTNLM ; Acinar cell carcinoma / Pancreas / Portal vein / Tumor thrombus
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77. 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.
  • The patients consisted of a 60-year-old woman and a 72-year-old man with no significant symptoms, who were both referred to the hospital due to the presence of large pancreatic tumors.
  • 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.
  • 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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78. Grapin-Botton A: Ductal cells of the pancreas. Int J Biochem Cell Biol; 2005 Mar;37(3):504-10
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  • [Title] Ductal cells of the pancreas.
  • Ductal cells of the pancreas form the epithelial lining of the branched tubes that deliver enzymes produced by pancreatic acinar cells into the duodenum.
  • All endocrine, acinar and ductal cells arise from common precursors in this epithelial structure.
  • Based on challenged pancreas regeneration experiments, the adult ductal cells have been proposed to be pancreatic stem cells but their role in normal endocrine cell turnover has recently been challenged.
  • In addition, in the main form of pancreatic cancer, pancreas adenocarcinoma, tumor cells share similarities with ductal cells.
  • The secrets of an appropriate therapy for this deadly cancer may thus reside in the biology of ductal cells.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Pancreas / cytology. Pancreas / physiology. Pancreatic Ducts / metabolism. Pancreatic Neoplasms / metabolism. Stem Cells / cytology
  • [MeSH-minor] Animals. Cell Differentiation. Humans. Models, Biological

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  • (PMID = 15618005.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 34
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79. Kitoh H, Ryozawa S, Harada T, Kondoh S, Furuya T, Kawauchi S, Oga A, Okita K, Sasaki K: Comparative genomic hybridization analysis for pancreatic cancer specimens obtained by endoscopic ultrasonography-guided fine-needle aspiration. J Gastroenterol; 2005 May;40(5):511-7
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  • [Title] Comparative genomic hybridization analysis for pancreatic cancer specimens obtained by endoscopic ultrasonography-guided fine-needle aspiration.
  • BACKGROUND: Comparative genomic hybridization (CGH) analysis of pancreatic cancer has been done exclusively for surgical and autopsy specimens, because of the difficulty of tissue sampling without surgery.
  • METHODS: In the present study, we performed EUS-FNA for 17 patients with pancreatic cancer before surgery.
  • RESULTS: In the 15 patients with tubular adenocarcinoma, the most common loci of gains (including amplification) were 5p, 8q, and 20q (60% of the patients); and 1q, 7p, and 12p (27%).
  • Both of the patients with acinar cell carcinoma showed gains of 2q and 5p, and losses of 1p, 9p, 9q, 11p, 11q, 14q, 17p, 17q, and 18q.
  • This analytical strategy will enable us to evaluate the biological characteristics of pancreatic cancer before treatment.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / ultrasonography. Biopsy, Fine-Needle / methods. Nucleic Acid Hybridization. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / ultrasonography

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  • (PMID = 15942717.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
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80. Yamada Y, Hiraoka N: A case of acinar cell adenocarcinoma in the pancreatic tail. Jpn J Clin Oncol; 2006 Jul;36(7):473
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  • [Title] A case of acinar cell adenocarcinoma in the pancreatic tail.
  • [MeSH-major] Carcinoma, Acinar Cell / radiography. Pancreatic Neoplasms / radiography. Tomography, X-Ray Computed

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  • (PMID = 16887840.001).
  • [ISSN] 0368-2811
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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81. Kaifi JT, Heidtmann S, Schurr PG, Reichelt U, Mann O, Yekebas EF, Wachowiak R, Strate T, Schachner M, Izbicki JR: Absence of L1 in pancreatic masses distinguishes adenocarcinomas from poorly differentiated neuroendocrine carcinomas. Anticancer Res; 2006 Mar-Apr;26(2A):1167-70
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  • [Title] Absence of L1 in pancreatic masses distinguishes adenocarcinomas from poorly differentiated neuroendocrine carcinomas.
  • BACKGROUND: Pancreatic adenocarcinoma is a tumor with fatal outcome.
  • Cell adhesion molecules, such as L1 (CD171), have an essential function in tumor progression.
  • L1 has been shown to be specifically expressed in poorly differentiated neuroendocrine carcinomas of the pancreas.
  • The aim of this study was to determine the expression of L1 in pancreatic adenocarcinomas to evaluate whether L1 might differentiate between pancreatic carcinomas of neuroendocrine and ductal origin.
  • MATERIALS AND METHODS: L1 expression was retrospectively analyzed in 111 cases of pancreatic adenocarcinomas by immunohistochemistry on paraffin sections of primary tumors.
  • RESULTS: The focal expression of L1 was detected in 2 (2%) out of 111 pancreatic carcinomas only, the remaining 109 (98%) being L1-negative.
  • No expression was found in acinar or ductal cells of normal pancreatic tissue.
  • CONCLUSION: Our data suggest that L1 is expressed in few cases of pancreatic ductal adenocarcinoma.
  • Since L1 was previously found to be expressed specifically in neuroendocrine pancreatic carcinomas, its absence in unclear pancreatic masses might hint at a ductal origin for a malignant pancreatic tumor.
  • [MeSH-major] Adenocarcinoma / immunology. Adenocarcinoma / pathology. Carcinoma, Neuroendocrine / immunology. Carcinoma, Neuroendocrine / pathology. Leukocyte L1 Antigen Complex / biosynthesis. Pancreatic Neoplasms / immunology. Pancreatic Neoplasms / pathology

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  • (PMID = 16619519.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Leukocyte L1 Antigen Complex
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82. Kosmahl M, Pauser U, Anlauf M, Sipos B, Peters K, Lüttges J, Klöppel G: [Cystic pancreas tumors and their classification: features old and new]. Pathologe; 2005 Feb;26(1):22-30
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  • [Title] [Cystic pancreas tumors and their classification: features old and new].
  • Cystic tumors and tumor-like lesions of the pancreas are rare, but have attracted a great deal of attention because they are easily recognized with new imaging methods and, in contrast to ductal adenocarcinoma, they can usually be cured surgically.
  • The increasing resection rate in recent years has also increased our knowledge of cystic pancreatic tumors by conspicuously enlarging their morphological spectrum.
  • Known entities have been better characterized (i.e. solid pseudopapillary neoplasm, intraductal papillary mucinous neoplasm) and new ones described (serous oligocystic adenoma, mucinous non-neoplastic cyst, acinar cell cystadenoma and cystic hamartoma).
  • This review discusses the most important cystic tumors and tumor-like lesions, presents a new classification, and summarizes the immunohistochemical differential diagnosis.
  • [MeSH-major] Pancreatic Cyst / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 15624092.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 58
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83. 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.
  • 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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84. Peng HQ, Darwin P, Papadimitriou JC, Drachenberg CB: Liver metastases of pancreatic acinar cell carcinoma with marked nuclear atypia and pleomorphism diagnosed by EUS FNA cytology: a case report with emphasis on FNA cytological findings. Cytojournal; 2006;3:29
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  • [Title] Liver metastases of pancreatic acinar cell carcinoma with marked nuclear atypia and pleomorphism diagnosed by EUS FNA cytology: a case report with emphasis on FNA cytological findings.
  • BACKGROUND: Acinar cell carcinoma of the pancreas is a rare neoplasm.
  • Unlike ductal adenocarcinomas, endocrine tumors, and solid pseudopapillary tumors of the pancreas with their characteristic FNA cytological features, acinar cell carcinomas pose a particular diagnostic challenge by sharing many cytomorphologic features with endocrine tumors of the pancreas.
  • Computed tomography revealed a 7.8 x 7.3 cm irregular, partially cystic mass in the body and tail of the pancreas, and two lesions in the liver compatible with metastases.
  • FNA cytology revealed abundant, loosely cohesive clusters of malignant epithelial cells with vaguely acinar and trabecular formations.
  • A pancreatic endocrine tumor was suspected initially, but acinar cell carcinoma of the pancreas was confirmed by immunohistochemistry, cytochemical and ultrastructural studies.
  • CONCLUSION: We describe a case of pancreatic acinar cell carcinoma with unusual cytomorphologic features mimicking an endocrine tumor of pancreas, encountered in endoscopic ultrasound-guided fine needle aspiration of a metastatic liver mass and discuss the diagnostic approach for this unusual pancreatic tumor in fine needle aspiration cytology.

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  • (PMID = 17196112.001).
  • [ISSN] 1742-6413
  • [Journal-full-title] CytoJournal
  • [ISO-abbreviation] Cytojournal
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1779360
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85. Chen Y, Yu G, Ma D, Ni C, Zhu M: Microadenocarcinoma of the pancreas. Eur J Gastroenterol Hepatol; 2009 Dec;21(12):1373-8
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  • [Title] Microadenocarcinoma of the pancreas.
  • BACKGROUND: Microadenocarcinoma (MA) of the pancreas is a rare kind of neoplasm, whose status as an independent tumor entity is still a matter of controversy.
  • Cells of MA were morphologically uniform and were less pleomorphic than those of the ductal adenocarcinoma.
  • Immunohistochemistry revealed that MA, though with a certain extent of epithelial differentiation, possesses a different immunological phenotype from those of ductal carcinoma, acinar cell carcinoma, and endocrine tumors.
  • Genetic analysis showed no abnormality of p53, K-ras, and beta-catenin, which were usually mutated in pancreatic ductal adenocarcinoma.
  • CONCLUSION: Therefore, we suggest that MA should be taken as an independent tumor entity rather than a kind of growth pattern, but a final decision should be reached after cautious differential diagnosis of other kinds of pancreatic neoplasms.
  • [MeSH-major] Adenocarcinoma / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 19916245.001).
  • [ISSN] 1473-5687
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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86. Esni F, Miyamoto Y, Leach SD, Ghosh B: Primary explant cultures of adult and embryonic pancreas. Methods Mol Med; 2005;103:259-71
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  • [Title] Primary explant cultures of adult and embryonic pancreas.
  • The developmental plasticity of adult pancreas is evidenced by the ability to undergo conversion between different epithelial cell types.
  • Specific examples of such conversions include acinar to ductal metaplasia, ductal to islet metaplasia, and generation of ductal structures within islets.
  • Although 90% of human pancreatic cancers are classified as ductal adenocarcinoma, markers of all pancreatic epithelial cell types (acini, ductal, and endocrine) as well as markers of gastric and intestinal lineages can be detected in these tumors.
  • In recent years considerable knowledge has been gained regarding regulation of cellular differentiation and various signaling pathways involved in normal and neoplastic pancreas through studies of pancreatic cancer and immortalized ductal cell lines.
  • Here we have described a detailed method for preparation, maintenance, and manipulation of adult and embryonic mouse pancreas.
  • These methods may be utilized in studies involving normal epithelial differentiation, contributing to improved understanding of pancreatic development and disease.
  • [MeSH-minor] Animals. Cell Culture Techniques / methods. Epithelial Cells / cytology. Immunohistochemistry. Male. Mice. Pancreas / cytology. Pancreas / embryology. Rats

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  • (PMID = 15542912.001).
  • [ISSN] 1543-1894
  • [Journal-full-title] Methods in molecular medicine
  • [ISO-abbreviation] Methods Mol. Med.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK56211-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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87. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

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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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88. Weichert W, Schmidt M, Jacob J, Gekeler V, Langrehr J, Neuhaus P, Bahra M, Denkert C, Dietel M, Kristiansen G: Overexpression of Polo-like kinase 1 is a common and early event in pancreatic cancer. Pancreatology; 2005;5(2-3):259-65
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  • [Title] Overexpression of Polo-like kinase 1 is a common and early event in pancreatic cancer.
  • Therefore, PLK1 has been proposed as a new target for antineoplastic treatment strategies.
  • METHODS: We conducted an immunohistochemical expression study for PLK1 on 86 cases of pancreatic adenocarcinoma as well as on 5 cases of chronic pancreatitis.
  • RESULTS: PLK1 was found overexpressed in pancreatic neoplasia as early as in pancreatic intraepithelial neoplasia III lesions, whereas benign acinar pancreatic parenchyma and ductal epithelia showed only focal PLK1 positivity.
  • Invasive pancreatic adenocarcinomas were PLK1 positive in 47.7% of cases.
  • CONCLUSIONS: The fact that half of the invasive pancreatic carcinomas strongly overexpressed PLK1 indicates that inhibition of this mitotic key regulator might represent a rewarding approach in the treatment of early and late pancreatic carcinoma.
  • [MeSH-major] Carcinoma in Situ / metabolism. Cell Cycle Proteins / metabolism. Pancreatic Neoplasms / metabolism. Protein Kinases / metabolism. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / mortality. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Humans. Immunohistochemistry. Middle Aged. Prognosis. Protein-Serine-Threonine Kinases. Survival Analysis

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  • (PMID = 15855824.001).
  • [ISSN] 1424-3903
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Proto-Oncogene Proteins; EC 2.7.- / Protein Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / polo-like kinase 1
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89. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • OBJECTIVE: Our goal was to evaluate a large population-based cohort of patients with ACC and compare their demographic factors and outcomes to those of patients with pancreatic adenocarcinoma (PA).
  • The mean age at the time of diagnosis was significantly lower for ACC than PA (56 years vs 70 years, P < .001).
  • Multivariate Cox proportional hazards regression model results suggested patients with ACC were less likely to die (hazard ratio = 0.241; 95% confidence interval, 0.22-0.27) than patients with PA after controlling for gender, race, stage, SEER region of diagnosis, and surgical resection status.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology

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