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1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • [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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2. Svrcek M, Lesurtel M, Lewin M, Afchain P, Fabre M, Scoazec JY, Parc R, Fléjou JF: [Acinar cell carcinoma of the pancreas with predominant intraductal growth: report of a case]. Gastroenterol Clin Biol; 2007 May;31(5):543-6
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  • [Title] [Acinar cell carcinoma of the pancreas with predominant intraductal growth: report of a case].
  • [Transliterated title] Carcinome à cellules acineuses du pancréas, de développement essentiellement intracanalaire: à propos d'un cas.
  • Acinar cell carcinoma (ACC) of the pancreas accounts for approximately 1% of all exocrine pancreatic tumours.
  • Abdominal computed tomography showed a hypodense, well-demarcated, heterogeneous lesion, in the head of the pancreas, measuring 4.2 cm in diameter.
  • There was a marked dilatation of the main pancreatic duct upstream, with tumour spreading within this duct.
  • The diagnosis of ACC was made on the fine needle aspiration cytology performed during endoscopic ultrasound examination.
  • On the pancreaticoduodenectomy specimen, the dilated main pancreatic duct (2.5 cm in diameter) was filled by an exophytic tumour.
  • Histological examination showed an ACC, with predominant intraductal growth (main and accessory pancreatic ducts), with pancreatic parenchymal and duodenal invasion.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Ducts / pathology. Pancreatic Neoplasms / diagnosis

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  • (PMID = 17541347.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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3. Zhang Q, Li J, Deavers M, Abbruzzese JL, Ho L: The subcellular localization of syntaxin 17 varies among different cell types and is altered in some malignant cells. J Histochem Cytochem; 2005 Nov;53(11):1371-82
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  • [Title] The subcellular localization of syntaxin 17 varies among different cell types and is altered in some malignant cells.
  • We recently independently identified STX17 as a novel Ras-interacting protein, but immunohistochemical studies suggested that STX17 is localized to the nucleus in normal pancreatic ductal epithelial, acinar, and islet cells in contrast to previous reports of cytoplasmic localization, albeit in other cell types.
  • Therefore, we have conducted a more thorough survey of various human and mouse tissues to better establish the expression pattern of STX17 in different tissues and cell types.
  • Although RT-PCR experiments demonstrate ubiquitous expression of STX17, closer examination by immunohistochemistry reveal that STX17 expression is limited to certain cell types.
  • Furthermore, in contrast to the cytoplasmic localization previously reported in a limited number of cell types, we find that in many other cell types, syntaxin 17 can be found in the nucleus.
  • Finally, we demonstrate that in human hepatocellular carcinoma cell lines, STX17 localization is altered relative to normal hepatocytes, although the localization of STX17 differs even between these established human cancer cell lines and fresh human hepatocellular carcinoma cells, emphasizing the caution that must be exercised in drawing conclusions from data gathered in cell lines.
  • The sequence divergence of STX17, the unexpected nuclear localization of STX17 in many cell types, and the altered localization of STX17 in malignant cells argue for a novel function of syntaxin 17 distinct from its hypothesized role in mediating membrane fusion events.
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Liver Neoplasms / metabolism. Pancreatic Neoplasms / metabolism. Qa-SNARE Proteins / metabolism
  • [MeSH-minor] Alternative Splicing. Animals. Cell Fractionation. Cell Line. Cell Line, Tumor. Cell Nucleus / metabolism. Cytoplasm / metabolism. Hepatocytes / metabolism. Hepatocytes / ultrastructure. Humans. Immunohistochemistry. Mice. Organ Specificity. Pancreas / cytology. Pancreas / metabolism. Pancreas / ultrastructure. Protein Isoforms / genetics. Protein Isoforms / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Steroids / metabolism

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  • (PMID = 15956034.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA71555; United States / NCI NIH HHS / CA / P30 CA16672
  • [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 / Protein Isoforms; 0 / Qa-SNARE Proteins; 0 / Steroids
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4. Hervieu V, Lombard-Bohas C, Dumortier J, Boillot O, Scoazec JY: Primary acinar cell carcinoma of the liver. Virchows Arch; 2008 Mar;452(3):337-41
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  • [Title] Primary acinar cell carcinoma of the liver.
  • We report a case of acinar cell carcinoma primary to the liver.
  • In well-differentiated areas, tumor cells formed acinar structures, had a pyramidal shape and a highly eosinophilic, granular cytoplasm, PAS diastase resistant.
  • The final diagnosis, based on histological, immunohistochemical, and ultrastructural arguments, was extra-pancreatic acinar cell carcinoma, primary to the liver.
  • This unusual lesion is likely to be the result of an abnormal differentiation pathway involving a transformed multipotential progenitor cell.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Liver / pathology. Liver Neoplasms / pathology

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  • (PMID = 18193278.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / alpha 1-Antitrypsin; 0 / alpha-Fetoproteins
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5. Kobayashi S, Asakura T, Ohike N, Enomoto T, Sakurai J, Koizumi S, Watanabe T, Nakano H, Otsubo T: Mixed acinar-endocrine carcinoma of the pancreas with intraductal growth into the main pancreatic duct: Report of a case. Surg Today; 2010 Apr;40(4):380-4
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  • [Title] Mixed acinar-endocrine carcinoma of the pancreas with intraductal growth into the main pancreatic duct: Report of a case.
  • The patient was a 75-year-old asymptomatic man, in whom a tumor mass in the pancreatic tail had been found 6 months earlier.
  • Endoscopic retrograde cholangiopancreatography showed a filling defect in the main pancreatic duct.
  • The tumor consisted of a lobular invasive growth component and a component with intraductal growth into the main pancreatic duct, and histologically the tumor cells had solid acinar to partially trabecular/tubular patterns.
  • Trypsin (an acinic cell marker) expression was widely observed, followed by the expression of chromogranin A (an endocrine cell marker) in about 30% of the tumor cells.
  • The tumor was diagnosed as mixed acinar-endocrine carcinoma according to the WHO classification.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Endocrine Gland Neoplasms / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 20339996.001).
  • [ISSN] 1436-2813
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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6. Rodriguez S, Faigel D: Absence of a dilated duct predicts benign disease in suspected pancreas cancer: a simple clinical rule. Dig Dis Sci; 2010 Apr;55(4):1161-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Absence of a dilated duct predicts benign disease in suspected pancreas cancer: a simple clinical rule.
  • BACKGROUND: Pancreatic cancer can be difficult to diagnose.
  • METHODS: Patients presenting for endoscopic ultrasound (EUS) evaluation for suspected pancreatic mass were prospectively enrolled.
  • The characteristics of patients with cancer were compared to the characteristics of patients without cancer using Chi-square testing and t-tests.
  • Thirty-three patients had cancer and 40 had benign disease.
  • On multivariate analysis, only vascular or organ invasion and dilation of the pancreatic duct (PD) were significantly associated with cancer.
  • PD dilation was examined as a stand-alone feature.
  • CONCLUSIONS: The most significant negative predictive endosonographic finding in patients with suspected pancreatic cancer is a non-dilated PD.
  • If a patient with suspected pancreatic cancer does not have a dilated PD and the FNA is negative for malignancy, the likelihood of cancer is low.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnostic imaging. Carcinoma, Pancreatic Ductal / diagnostic imaging. Endosonography. Pancreatic Ducts / diagnostic imaging. Pancreatic Neoplasms / diagnostic imaging
  • [MeSH-minor] Aged. Biopsy, Fine-Needle. Diagnosis, Differential. Dilatation, Pathologic / diagnostic imaging. Dilatation, Pathologic / pathology. Female. Humans. Male. Middle Aged. Multivariate Analysis. Neoplasm Invasiveness. Pancreas / diagnostic imaging. Pancreas / pathology. Pancreatic Diseases / diagnostic imaging. Pancreatic Diseases / pathology. Predictive Value of Tests. Prospective Studies

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  • (PMID = 19590960.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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7. 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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8. Stelow EB, Bardales RH, Shami VM, Woon C, Presley A, Mallery S, Lai R, Stanley MW: Cytology of pancreatic acinar cell carcinoma. Diagn Cytopathol; 2006 May;34(5):367-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytology of pancreatic acinar cell carcinoma.
  • Acinar cell carcinoma (ACC) of the pancreas is extremely uncommon and its cytologic features have rarely been described.
  • We describe the cytologic features of cases we have seen, review the literature regarding its cytologic features and discuss the pitfalls that may be encountered and the use of immunohistochemistry for its diagnosis.
  • We searched our databases for all cases of histologically confirmed pancreatic ACC which had undergone prior fine needle aspiration (FNA) of the primary pancreatic lesion.
  • Four cases of pancreatic ACC were found that had undergone FNA prior to histologic confirmation of the diagnoses.
  • All masses were in the head of the pancreas, 2 had apparent peri-pancreatic adenopathy and 1 had an apparent liver metastasis.
  • Original cytologic diagnoses included "acinar cell carcinoma," "pancreatic endocrine tumor," "favor neuroendocrine tumor, low-grade" and "non-diagnostic specimen."
  • The cytologic features included small to moderate-sized loose groups with numerous single cells, prominent acinar formation, little anisonucleosis and prominent nucleoli.
  • The cytologic features showed significant overlap with those of pancreatic endocrine tumors.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Biopsy, Fine-Needle. Female. Humans. Keratins / analysis. Liver Neoplasms / chemistry. Liver Neoplasms / secondary. Lymph Nodes / pathology. Male. Middle Aged. Pancreas / chemistry. Pancreas / pathology

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  • (PMID = 16604543.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 68238-35-7 / Keratins
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9. 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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10. 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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11. Borowicz J, Morrison M, Hogan D, Miller R: Subcutaneous fat necrosis/panniculitis and polyarthritis associated with acinar cell carcinoma of the pancreas: a rare presentation of pancreatitis, panniculitis and polyarthritis syndrome. J Drugs Dermatol; 2010 Sep;9(9):1145-50
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  • [Title] Subcutaneous fat necrosis/panniculitis and polyarthritis associated with acinar cell carcinoma of the pancreas: a rare presentation of pancreatitis, panniculitis and polyarthritis syndrome.
  • He was under the care of hospice for end-stage acinar cell carcinoma of the pancreas.
  • An incisional biopsy revealed lobular inflammation of subcutaneous fat, focal fat necrosis with saponification/ghost cells and scattered foreign-body type giant cells consistent with pancreatic fat necrosis/pancreatic panniculitis.
  • This is hypothesized to be initiated by autodigestion of subcutaneous fat secondary to systemic spillage of excess digestive pancreatic enzymes.
  • This report, along with the patient's clinical findings, was consistent with PPP syndrome: pancreatic disease, polyarthritis and panniculitis.
  • Although the pancreatic disease of PPP syndrome usually includes pancreatitis, this case represents a report of polyarthritis and panniculitis occurring in the presence of pancreatic carcinoma.
  • [MeSH-major] Arthritis / pathology. Carcinoma, Acinar Cell / complications. Pancreatic Neoplasms / complications. Pancreatitis / complications. Panniculitis / pathology. Skin / pathology. Subcutaneous Fat / pathology


12. Roy S, Dhingra KK, Gupta P, Khurana N, Gupta B, Meher R: Acinic cell carcinoma with extensive neuroendocrine differentiation: a diagnostic challenge. Head Neck Pathol; 2009 Jun;3(2):163-8
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  • [Title] Acinic cell carcinoma with extensive neuroendocrine differentiation: a diagnostic challenge.
  • Primary salivary gland carcinoma with neuroendocrine differentiation is of rare occurrence, especially so in the parotid gland.
  • Amongst the various reported primary tumors with neuroendocrine differentiation, acinic cell carcinoma (ACC) one such tumor.
  • Contrast Enhanced Computed Tomography (CECT) suggested diagnosis of Pleomorphic Adenoma.
  • Initial histopathological examination of the tumor was suggestive of neuroendocrine carcinoma.
  • Immunoexpression of S-100, Neuron specific Enolase (NSE), Chromogranin A and Synaptophysin confirmed the diagnosis.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Parotid Neoplasms / pathology
  • [MeSH-minor] Adenolymphoma / pathology. Biopsy, Fine-Needle. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Middle Aged

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  • [ISO-abbreviation] Head Neck Pathol
  • [Language] eng
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  • [Publication-country] United States
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13. 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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14. Yamaue H: [Clinical characteristics of invasive ductal carcinomas of the pancreas according to the histological differentiation]. Nihon Rinsho; 2006 Jan;64 Suppl 1:48-51
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  • [Title] [Clinical characteristics of invasive ductal carcinomas of the pancreas according to the histological differentiation].
  • [MeSH-major] Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Carcinoma / epidemiology. Carcinoma / pathology. Carcinoma, Acinar Cell / epidemiology. Carcinoma, Acinar Cell / pathology. Humans. Neoplasm Invasiveness / pathology. Prognosis. Survival Rate. Time Factors

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  • (PMID = 16457220.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 14
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15. 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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16. Murtaugh LC, Leach SD: A case of mistaken identity? Nonductal origins of pancreatic "ductal" cancers. Cancer Cell; 2007 Mar;11(3):211-3
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  • [Title] A case of mistaken identity? Nonductal origins of pancreatic "ductal" cancers.
  • In this issue of Cancer Cell, Guerra and colleagues provide important new insights regarding the ability of specific pancreatic cell types to generate invasive pancreatic cancer.
  • First, they demonstrate that classical pancreatic "ductal" neoplasia can be induced by activation of oncogenic Kras in nonductal exocrine cells.
  • Second, they show that, while Kras activation in immature acinar and centroacinar cells is readily able to induce ductal neoplasia, Kras-mediated tumorigenesis in mature exocrine pancreas requires the induction of chronic epithelial injury.
  • The results shed new light on the "cell of origin" of pancreatic ductal cancer and demonstrate that chronic pancreatitis provides a permissive environment for Kras-induced pancreatic neoplasia.
  • [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. Humans. Mice. Mutation. Neoplasm Invasiveness

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  • [CommentOn] Cancer Cell. 2007 Mar;11(3):291-302 [17349585.001]
  • (PMID = 17349578.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK56211; United States / NIDDK NIH HHS / DK / DK61215
  • [Publication-type] Comment; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 888Y08971B / Ceruletide
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17. Du YC, Klimstra DS, Varmus H: Activation of PyMT in beta cells induces irreversible hyperplasia, but oncogene-dependent acinar cell carcinomas when activated in pancreatic progenitors. PLoS One; 2009 Sep 07;4(9):e6932
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  • [Title] Activation of PyMT in beta cells induces irreversible hyperplasia, but oncogene-dependent acinar cell carcinomas when activated in pancreatic progenitors.
  • It is unclear whether the cellular origin of various forms of pancreatic cancer involves transformation or transdifferentiation of different target cells or whether tumors arise from common precursors, with tumor types determined by the specific genetic alterations.
  • Previous studies suggested that pancreatic ductal carcinomas might be induced by polyoma middle T antigen (PyMT) expressed in non-ductal cells.
  • Induction of PyMT in beta cells causes beta-cell hyperplastic lesions that do not progress to malignant neoplasms.
  • When PyMT is de-induced, beta cell proliferation and growth cease; however, regression does not occur, suggesting that continued production of PyMT is not required to maintain the viable expanded beta cell population.
  • In contrast, induction of PyMT in early pancreatic progenitor cells under the control of Pdx1 produces acinar cell carcinomas and beta-cell hyperplasia.
  • The survival of acinar tumor cells is dependent on continued expression of PyMT.
  • Our findings indicate that PyMT can induce exocrine tumors from pancreatic progenitor cells, but cells in the beta cell lineage are not transdifferentiated toward exocrine cell types by PyMT; instead, they undergo oncogene-dependent hyperplastic growth, but do not require PyMT for survival.

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  • (PMID = 19812721.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA105492; United States / NCI NIH HHS / CA / P30 CA08748; United States / NCI NIH HHS / CA / P01 CA94060; United States / NCI NIH HHS / CA / P30 CA008748; United States / NCI NIH HHS / CA / P30-CA 08748; United States / NCI NIH HHS / CA / P01 CA094060; United States / NCI NIH HHS / CA / R24 CA83084; United States / NCI NIH HHS / CA / 5U01CA105492; United States / NCI NIH HHS / CA / R24 CA083084
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; EC 1.13.12.- / Luciferases; F8VB5M810T / Tetracycline
  • [Other-IDs] NLM/ PMC2758666
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18. 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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  • [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.
  • [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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19. 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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20. Díaz Sánchez A, Ponferrada Díaz A, Senosiain Labiano M, Huerta Madrigal A: [Upper digestive hemorrhage as the first manifestation of acinar cell carcinoma of the pancreas]. Gastroenterol Hepatol; 2006 Jun-Jul;29(6):380
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  • [Title] [Upper digestive hemorrhage as the first manifestation of acinar cell carcinoma of the pancreas].
  • [Transliterated title] Hemorragia digestiva alta como presentación de un carcinoma acinar pancreático.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Gastrointestinal Hemorrhage / etiology. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Aged. Duodenal Neoplasms / diagnosis. Female. Humans. Neoplasm Invasiveness

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  • (PMID = 16790192.001).
  • [ISSN] 0210-5705
  • [Journal-full-title] Gastroenterología y hepatología
  • [ISO-abbreviation] Gastroenterol Hepatol
  • [Language] spa
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Spain
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21. 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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22. Gerloff A, Singer MV, Feick P: Beer and its non-alcoholic compounds: role in pancreatic exocrine secretion, alcoholic pancreatitis and pancreatic carcinoma. Int J Environ Res Public Health; 2010 03;7(3):1093-104
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  • [Title] Beer and its non-alcoholic compounds: role in pancreatic exocrine secretion, alcoholic pancreatitis and pancreatic carcinoma.
  • In this article we provide an overview of the newest data concerning the effect of non-alcoholic constituents of alcoholic beverages, especially of beer, on pancreatic secretion, and their possible role in alcoholic pancreatitis and pancreatic carcinoma.
  • The data indicate that non-alcoholic constituents of beer stimulate pancreatic enzyme secretion in humans and rats, at least in part, by direct action on pancreatic acinar cells.
  • Some non-alcoholic compounds of beer, such as quercetin, resveratrol, ellagic acid or catechins, have been shown to be protective against experimentally induced pancreatitis by inhibiting pancreatic secretion, stellate cell activation or by reducing oxidative stress.
  • Their relevance in beer-induced functional alterations of pancreatic cells leading to pancreatitis and pancreatic cancer in humans needs to be further evaluated.
  • [MeSH-major] Beer. Catechin / pharmacology. Ellagic Acid / pharmacology. Pancreas / secretion. Pancreatic Neoplasms / physiopathology. Pancreatitis, Alcoholic / physiopathology. Quercetin / pharmacology. Stilbenes / pharmacology

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  • (PMID = 20617020.001).
  • [ISSN] 1660-4601
  • [Journal-full-title] International journal of environmental research and public health
  • [ISO-abbreviation] Int J Environ Res Public Health
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Stilbenes; 19YRN3ZS9P / Ellagic Acid; 8R1V1STN48 / Catechin; 9IKM0I5T1E / Quercetin; Q369O8926L / resveratrol
  • [Other-IDs] NLM/ PMC2872306
  • [Keywords] NOTNLM ; beer (major topic) / non-alcoholic constituents (major topic) / pancreatic carcinoma (major topic) / pancreatitis (major topic)
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23. Reske SN: [PET and PET-CT of malignant tumors of the exocrine pancreas]. Radiologe; 2009 Feb;49(2):131-6
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  • [Title] [PET and PET-CT of malignant tumors of the exocrine pancreas].
  • [Transliterated title] PET und PET-CT maligner Tumoren des exokrinen Pankreas.
  • Adenocarcinomas of the pancreas represent the majority (>95%) of all malignant pancreatic tumors.
  • They are formed from malignant degeneration of the exocrine part of the pancreas.
  • Cystic acinar tumors are much rarer and originate from secretion-producing parenchymal cells of the pancreas.
  • Endocrine tumors of the pancreas will not be dealt with in this context.
  • [MeSH-major] Adenocarcinoma / diagnostic imaging. Carcinoma, Acinar Cell / diagnostic imaging. Carcinoma, Pancreatic Ductal / diagnostic imaging. Image Processing, Computer-Assisted. Pancreatic Neoplasms / diagnostic imaging. Positron-Emission Tomography. Tomography, X-Ray Computed
  • [MeSH-minor] Diagnosis, Differential. Disease Progression. Fluorodeoxyglucose F18. Humans. Lymphatic Metastasis / diagnostic imaging. Lymphatic Metastasis / pathology. Neoplasm Recurrence, Local / diagnostic imaging. Neoplasm Staging. Pancreas / diagnostic imaging. Pancreas / pathology. Sensitivity and Specificity

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  • (PMID = 19219476.001).
  • [ISSN] 1432-2102
  • [Journal-full-title] Der Radiologe
  • [ISO-abbreviation] Radiologe
  • [Language] ger
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
  • [Number-of-references] 43
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24. Machado MC, Machado MA, Perini MV, Herman P, Jukemura J, Leite KR, Bacchella T: Acinar cell carcinoma of the pancreas: is the absence of neuroendocrine component related to a more malignant behavior? Hepatogastroenterology; 2008 Mar-Apr;55(82-83):708-10
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  • [Title] Acinar cell carcinoma of the pancreas: is the absence of neuroendocrine component related to a more malignant behavior?
  • BACKGROUND/AIMS: Acinar cell carcinomas are uncommon malignant tumors of the pancreas, accounting for 1-2% of all the cases of exocrine pancreatic tumor.
  • Some authors have estimated acinar cell tumors to be as aggressive as ductal adenocarcinoma of the pancreas whereas other series showed acinar cell tumors to have a favorable clinical outcome.
  • METHODOLOGY: With the aim to evaluate the possible relationship between the presence of neuroendocrine differentiation and behavior of these tumors, the authors reviewed all patients presenting acinar cell carcinoma of the pancreas in the last 5 years with emphasis in the immunohistochemical evaluation.
  • This data suggests that this tumor is less aggressive than ductal adenocarcinoma and even with nodal involvement, long-term survival after complete resection can be achieved.
  • Due to the rarity of this pancreatic tumor, this relationship remains to be confirmed with a multicentric study including a larger number of patients.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18613439.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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25. Minakawa K, Oka K, Nihei T, Sando N, Oikawa H, Toda J, Hosokawa Y, Matsumoto T, Yanagisawa A: Pancreatic endocrine tumor with partial acinar cell differentiation. APMIS; 2006 Oct;114(10):720-5
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  • [Title] Pancreatic endocrine tumor with partial acinar cell differentiation.
  • We examined a 70-year-old woman in whom a pancreatic endocrine tumor with partial acinar cell differentiation had been diagnosed.
  • The tumor was located in the pancreatic tail and measured 12.5 x 9.5 x 8 cm.
  • The cells had proliferated in islet-like solid medullary, trabecular, acinar, and papillary patterns.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Islet Cell / diagnosis. Neoplasms, Multiple Primary / diagnosis. Pancreas / pathology. Pancreatic Neoplasms / diagnosis

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  • (PMID = 17004975.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Synaptophysin; 0 / alpha 1-Antitrypsin
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26. 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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27. Stanger BZ, Stiles B, Lauwers GY, Bardeesy N, Mendoza M, Wang Y, Greenwood A, Cheng KH, McLaughlin M, Brown D, Depinho RA, Wu H, Melton DA, Dor Y: Pten constrains centroacinar cell expansion and malignant transformation in the pancreas. Cancer Cell; 2005 Sep;8(3):185-95
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  • [Title] Pten constrains centroacinar cell expansion and malignant transformation in the pancreas.
  • To determine the role of the phosphatidylinositol 3-kinase (PI3-K) pathway in pancreas development, we generated a pancreas-specific knockout of Pten, a negative regulator of PI3-K signaling.
  • Knockout mice display progressive replacement of the acinar pancreas with highly proliferative ductal structures that contain abundant mucins and express Pdx1 and Hes1, two markers of pancreatic progenitor cells.
  • We provide evidence that ductal metaplasia results from the expansion of centroacinar cells rather than transdifferentiation of acinar cells.
  • These results indicate that Pten actively maintains the balance between different cell types in the adult pancreas and that misregulation of the PI3-K pathway in centroacinar cells may contribute to the initiation of pancreatic carcinoma in vivo.
  • [MeSH-major] Pancreatic Neoplasms / pathology. Protein Tyrosine Phosphatases / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Animals. Cell Differentiation. Cell Transformation, Neoplastic. Metaplasia / pathology. Mice. PTEN Phosphohydrolase. Pancreas / pathology. Pancreas / physiopathology. Pancreas / ultrastructure

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  • (PMID = 16169464.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK064136
  • [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
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
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28. Salla C, Chatzipantelis P, Konstantinou P, Karoumpalis I, Pantazopoulou A, Dappola V: Endoscopic ultrasound-guided fine-needle aspiration cytology diagnosis of solid pseudopapillary tumor of the pancreas: a case report and literature review. World J Gastroenterol; 2007 Oct 14;13(38):5158-63
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  • [Title] Endoscopic ultrasound-guided fine-needle aspiration cytology diagnosis of solid pseudopapillary tumor of the pancreas: a case report and literature review.
  • We describe the clinical, imaging and cytopathological features of solid pseudopapillary tumor of the pancreas (SPTP) diagnosed by endoscopic ultrasound-guided (EUS-guided) fine-needle aspiration (FNA).
  • Computed tomography (CT) analysis revealed a mass of the pancreatic tail with solid and cystic consistency.
  • EUS confirmed the mass, both in body and tail of the pancreas, with distinct borders, which caused dilation of the peripheral part of the pancreatic duct (major diameter 3.7 mm).
  • Biopsy confirmed the above cytologic diagnosis.
  • EUS-guided FNA diagnosis of SPTP is accurate.
  • EUS findings, cytomorphologic features and immunostains of cell block help distinguish SPTP from pancreatic endocrine tumors, acinar cell carcinoma and papillary mucinous carcinoma.
  • [MeSH-major] Carcinoma, Papillary / diagnosis. Carcinoma, Papillary / pathology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma, Mucinous / diagnosis. Adenocarcinoma, Mucinous / pathology. Adolescent. Biopsy, Fine-Needle / methods. Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / pathology. Diagnosis, Differential. Endosonography / methods. Female. Humans. Pancreas / pathology. Pancreas / ultrasonography

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  • (PMID = 17876886.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] China
  • [Number-of-references] 59
  • [Other-IDs] NLM/ PMC4434650
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29. 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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30. Karafin MS, Cummings CT, Fu B, Iacobuzio-Donahue CA: The developmental transcription factor Gata4 is overexpressed in pancreatic ductal adenocarcinoma. Int J Clin Exp Pathol; 2009 Aug 30;3(1):47-55
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  • [Title] The developmental transcription factor Gata4 is overexpressed in pancreatic ductal adenocarcinoma.
  • GATA4 is a transcription factor that plays a role in regulating the normal development of many mesoderm and endoderm derived tissues, including the pancreas.
  • By contrast, GATA4 mRNA expression is upregulated in pancreatic cancer cell lines and tissues.
  • To further clarify the relationship of GATA4 to pancreatic cancer, we immunolabeled 90 samples of pancreatic ductal adenocarcinoma using a GATA4 specific monoclonal antibody.
  • Both the intensity and percent of labeling was recorded for each carcinoma and correlated to the clinic opathologic features available for each patient.
  • Samples of normal adult (n=26) and fetal pancreatic tissue (n=8) were also immunolabeled for comparison to expression patterns in pancreatic carcinoma tissues.
  • Immunolabeling for GATA4 indicated robust nuclear expression in developing acini in fetal pancreatic tissues, consistent with the role of GATA4 in embryologic development, and in mature pancreatic acinar epithelium.
  • Immunolabeling for GATA4 was also noted within normal duct epithelial cells, although it was always lesser in intensity than for acinar cell nuclei in the same section.
  • Positive GATA4 immunolabeling was seen in 61/90 (68%) infiltrating pancreatic cancers of which 27/90 (30%) showed strong positive labeling.
  • These findings support previous studies implicating GATA4 in pancreatic cancer and offer new avenues for investigation into this aggressive tumor type.

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  • (PMID = 19918328.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA106610; United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / CA106610; United States / NCI NIH HHS / CA / CA62924
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GATA4 Transcription Factor; 0 / GATA4 protein, human; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2776266
  • [Keywords] NOTNLM ; Pancreatic cancer / development / embryology / transcription factor
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31. Ambrosini-Spaltro A, Potì O, De Palma M, Filotico M: Pancreatic-type acinar cell carcinoma of the stomach beneath a focus of pancreatic metaplasia of the gastric mucosa. Hum Pathol; 2009 May;40(5):746-9
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  • [Title] Pancreatic-type acinar cell carcinoma of the stomach beneath a focus of pancreatic metaplasia of the gastric mucosa.
  • Acinar cell carcinoma is an uncommon type of carcinoma of the pancreas that can exceptionally arise in ectopic pancreatic tissue.
  • Herein, we report a case of a 52-year-old man with pancreatic-type acinar cell carcinoma of the stomach and concomitant pancreatic metaplasia of the adjacent nonneoplastic gastric mucosa.
  • There was neither clinical nor radiographic evidence of a tumor in the pancreas itself.
  • The neoplastic cells and those of the adjacent metaplastic mucosa were both strongly immunoreactive for alpha-1-antitrypsin, consistent with pancreatic acinar cell differentiation.
  • Ectopic pancreatic-type acinar cell carcinoma is an extremely rare condition, having been previously reported only in 5 occasions, none of them in association with pancreatic acinar cell metaplasia of the gastric mucosa.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Gastric Mucosa / pathology. Pancreas / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Cell Differentiation. Humans. Male. Metaplasia / pathology. Middle Aged. alpha 1-Antitrypsin / biosynthesis


32. Kawakami H, Kuwatani M, Hirano S, Kondo S, Nakanishi Y, Itoh T, Asaka M: Pancreatic endocrine tumors with intraductal growth into the main pancreatic duct and tumor thrombus within the portal vein: a case report and review of the literature. Intern Med; 2007;46(6):273-7
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  • [Title] Pancreatic endocrine tumors with intraductal growth into the main pancreatic duct and tumor thrombus within the portal vein: a case report and review of the literature.
  • Pancreatic endocrine tumors are rare tumors classified into "functioning" and "nonfunctioning" tumors.
  • Various imaging studies demonstrated a mass in the head of the pancreas with intraductal growth into the main pancreatic duct and an intraportal mass.
  • Histopathological examination revealed that it was nonfunctioning endocrine carcinoma of the pancreas.
  • This is the first reported case of a pancreatic endocrine tumor with intraductal growth into the main pancreatic duct and tumor thrombus within the portal vein.
  • [MeSH-major] Pancreatic Neoplasms / complications. Pancreatic Neoplasms / diagnosis. Portal Vein. Venous Thrombosis / etiology
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / blood. Carcinoma, Acinar Cell / diagnosis. Carcinoma, Pancreatic Ductal / diagnosis. Diagnosis, Differential. Endosonography. Fatal Outcome. Female. Humans. Male. Middle Aged. Pancreaticoduodenectomy

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  • (PMID = 17379993.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 15
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33. Zhu L, Shi G, Schmidt CM, Hruban RH, Konieczny SF: Acinar cells contribute to the molecular heterogeneity of pancreatic intraepithelial neoplasia. Am J Pathol; 2007 Jul;171(1):263-73
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  • [Title] Acinar cells contribute to the molecular heterogeneity of pancreatic intraepithelial neoplasia.
  • A number of studies have shown that pancreatic ductal adenocarcinoma develops through precursor lesions termed pancreatic intraepithelial neoplasia (PanIN).
  • PanINs are thought to initiate in the small ducts of the pancreas through activating mutations in the KRAS proto-oncogene.
  • What remains unanswered is the identification of the individual cell type(s) that contributes to pancreatic ductal adenocarcinoma formation.
  • To follow the cellular and molecular changes that occur in acinar and duct cell properties on Kras(G12D) expression, we took advantage of LSL-Kras(G12D/+)/p48(Cre/+) mice, which faithfully mimic the human disease.
  • In young animals (4 weeks), the predominant cellular alteration in the exocrine pancreas was acinar metaplasia in which individual acini consisted of acinar cells and duct-like cells.
  • Metaplastic acinar structures were highly proliferative, expressed Notch target genes, and exhibited mosaic expression patterns for epidermal growth factor receptor, ErbB2, and pErk.
  • This expression pattern paralleled the expression pattern detected in mouse PanINs, suggesting that mouse PanINs and acinar-ductal metaplasia follow similar molecular pathways.
  • Indeed, immunofluorescence studies confirmed the presence of acinar cells within mPanIN lesions, raising the possibility that Kras(G12D)-induced mPanINs develop from acinar cells that undergo acinar-ductal metaplasia.
  • Identification of an acinar contribution to PanIN formation offers new directions for successful targeted therapeutic approaches to combat this disease.

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  • (PMID = 17591971.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA062924; United States / NIDDK NIH HHS / DK / DK55489; United States / NCI NIH HHS / CA / P50 CA62924; United States / NIDDK NIH HHS / DK / R01 DK055489; United States / NCI NIH HHS / CA / R01 CA124586
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Erbb2ip protein, mouse; 0 / Interferon-Stimulated Gene Factor 3, gamma Subunit; 0 / Isgf3g protein, mouse; 0 / Receptors, Notch
  • [Other-IDs] NLM/ PMC1941579
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34. 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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35. 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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36. 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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37. 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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38. Ban D, Shimada K, Sekine S, Sakamoto Y, Kosuge T, Kanai Y, Hiraoka N: Pancreatic ducts as an important route of tumor extension for acinar cell carcinoma of the pancreas. Am J Surg Pathol; 2010 Jul;34(7):1025-36
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  • [Title] Pancreatic ducts as an important route of tumor extension for acinar cell carcinoma of the pancreas.
  • Acinar cell carcinoma (ACC) of the pancreas is very rare, which usually grows expansively.
  • Recently, a variant of ACC with predominant growth in the pancreatic ducts has been proposed, and is speculated to have potentially less aggressive behavior.
  • The aim of this study was to investigate how the pancreatic duct system is related to the growth and extension of ACC.
  • We reviewed the detailed gross and histologic features of 13 cases of ACC, of which 7 (54%) showed intraductal polypoid growth (IPG) of the tumor in the large pancreatic ducts with a mean IPG length of 24.8 mm.
  • Tumors with IPG were found to spread characteristically along the pancreatic ducts as extending polypoid projections, filling the ducts and destroying the duct walls, although tumors did not tend to extend beyond the pancreatic parenchyma.
  • Comparison of the clinicopathologic characteristics showed that ACC with IPG had less infiltrative features including lymphatic, venous, and neural invasion, formation of tumor thrombus in the portal vein, nodal metastasis, and invasion beyond the pancreas to the surrounding organs; death in only 1 case (14%) of ACC with IPG was the result of ACC itself.
  • Intraductal dissemination of ACC in pancreatic ducts was proven in 1 case of ACC with IPG.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 20534994.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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39. 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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40. 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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41. Lakhani A, Maas L: Necrotizing panniculitis: a skin condition associated with acinar cell carcinoma of the pancreas. South Med J; 2008 May;101(5):554-5
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  • [Title] Necrotizing panniculitis: a skin condition associated with acinar cell carcinoma of the pancreas.
  • Pancreatic panniculitis (PP) is a rare cutaneous eruption that is associated with severe pancreatic disease.
  • Thorough investigation revealed stage IV acinar cell carcinoma of the pancreas.
  • Panniculitis should be kept in mind in the differential diagnosis of inflamed appearing nodules and pustules with an erythematous base, particularly when they are progressive and unrelenting.
  • [MeSH-major] Carcinoma, Acinar Cell / complications. Pancreatic Neoplasms / complications. Panniculitis / etiology
  • [MeSH-minor] Amylases / blood. Cellulitis / diagnosis. Diagnosis, Differential. Exanthema / etiology. Humans. Lipase / blood. Male. Middle Aged. Necrosis

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  • (PMID = 18414166.001).
  • [ISSN] 1541-8243
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.1.1.3 / Lipase; EC 3.2.1.- / Amylases
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42. Chung WJ, Byun JH, Lee SS, Lee MG: Imaging findings in a case of mixed acinar-endocrine carcinoma of the pancreas. Korean J Radiol; 2010 May-Jun;11(3):378-81
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  • [Title] Imaging findings in a case of mixed acinar-endocrine carcinoma of the pancreas.
  • Mixed acinar-endocrine carcinoma (MAEC) of the pancreas is extremely uncommon.
  • We report here a rare case of MAEC of the pancreas presenting as watery diarrhea.
  • This is the first report in the English-language literature that describes the imaging findings of MAEC of the pancreas, including computed tomography (CT), magnetic resonance (MR) imaging, and MR cholangiopancreatography features.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / radiography. Endocrine Gland Neoplasms / pathology. Endocrine Gland Neoplasms / radiography. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / radiography
  • [MeSH-minor] Cholangiopancreatography, Magnetic Resonance / methods. Diagnosis, Differential. Diarrhea. Female. Humans. Magnetic Resonance Imaging / methods. Middle Aged. Pancreas / pathology. Pancreas / radiography. Pancreas / surgery. Pancreatectomy. Splenectomy. Tomography, X-Ray Computed / methods

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  • (PMID = 20461195.001).
  • [ISSN] 2005-8330
  • [Journal-full-title] Korean journal of radiology
  • [ISO-abbreviation] Korean J Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2864868
  • [Keywords] NOTNLM ; Endocrine / Exocrine / Mixed acinar-endocrine carcinoma / Pancreas
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43. 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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44. 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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45. Rouleau C, Serre I, Roger P, Guibal MP, Galifer RB, Bonardet A, Baldet P: Acinar cell carcinoma of the pancreas in a young patient with cells immunoreactive for somatostatin. Histopathology; 2006 Feb;48(3):307-9
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  • [Title] Acinar cell carcinoma of the pancreas in a young patient with cells immunoreactive for somatostatin.
  • [MeSH-major] Carcinoma, Acinar Cell / chemistry. Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / chemistry. Pancreatic Neoplasms / pathology. Somatostatin / analysis

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  • (PMID = 16430479.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranins; 0 / Mucin-1; 0 / alpha-Fetoproteins; 51110-01-1 / Somatostatin; 68238-35-7 / Keratins; EC 3.2.1.- / Amylases; EC 3.4.21.4 / Trypsin
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46. Bockman DE: Transition to pancreatic cancer in response to carcinogen. Langenbecks Arch Surg; 2008 Jul;393(4):557-60
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  • [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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47. Jiang X, Gillen S, Esposito I, Giese NA, Michalski CW, Friess H, Kleeff J: Reduced expression of the membrane skeleton protein beta1-spectrin (SPTBN1) is associated with worsened prognosis in pancreatic cancer. Histol Histopathol; 2010 12;25(12):1497-506
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  • [Title] Reduced expression of the membrane skeleton protein beta1-spectrin (SPTBN1) is associated with worsened prognosis in pancreatic cancer.
  • Spectrins are members of the superfamily of F-actin cross linking proteins that are important as scaffolding proteins for protein sorting, cell adhesion, and migration.
  • The aim of the present study was to analyze the expression and localization of beta1-spectrin (SPTBN1) in pancreatic tissues. mRNA levels of SPTBN1 in cultured pancreatic cancer cell lines, as well as in normal pancreatic tissues (n=18), chronic pancreatitis (n=48) and pancreatic cancer tissues (n=66) were analyzed by real time quantitative RT-PCR.
  • Localization of SPTBN1 in pancreatic tissues was determined by immunohistochemistry.
  • SPTBN1 staining was assessed semi-quantitatively in 55 cancer tissues and survival analysis was carried out using the Kaplan-Meier method.
  • Median SPTBN1 mRNA levels were 6.0-fold higher in pancreatic cancer tissues compared to the normal pancreas (p<0.0001) and 2.2-fold higher compared to chronic pancreatitis tissues (p=0.0002).
  • In the normal pancreas, SPTBN1 was present in the cytoplasm of normal ductal cells and occasionally in pancreatic acinar and centroacinar cells.
  • In pancreatic cancer tissues, SPTBN1 was present in the cytoplasm of pancreatic cancer cells.
  • In conclusion, reduced SPTBN1 expression correlated with shorter survival of pancreatic cancer patients, suggesting a tumor suppressor function of this gene, as has already been shown for other malignancies of the gastrointestinal tract.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Pancreatic Neoplasms / metabolism. Spectrin / biosynthesis

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  • (PMID = 20886430.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / SPTBN1 protein, human; 12634-43-4 / Spectrin
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48. National Toxicology Program: Toxicology and carcinogenesis studies of 2,3',4,4',5-pentachlorobiphenyl (PCB 118) (CAS No. 31508-00-6) in female harlan Sprague-Dawley rats (gavage studies). Natl Toxicol Program Tech Rep Ser; 2010 Nov;(559):1-174
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  • Since human exposure to DLCs always occurs as a complex mixture, the toxic equivalency factor (TEF) methodology has been developed as a mathematical tool to assess the health risk posed by complex mixtures of these compounds.
  • The toxic equivalency of DLCs was nominated for evaluation because of the widespread human exposure to DLCs and the lack of data on the adequacy of the TEF methodology for predicting relative potency for cancer risk.
  • There were increases in hepatic cell proliferation in the 4,600 g/kg group at 14, 31, and 53 weeks.
  • At 2 years, a significant dose-related increase in hepatic toxicity was observed and was characterized by increased incidences of numerous lesions including hepatocyte hypertrophy, inflammation, oval cell hyperplasia, pigmentation, multinucleated hepatocyte, eosinophilic and mixed cell foci, diffuse fatty change, toxic hepatopathy, nodular hyperplasia, necrosis, bile duct hyperplasia and cyst, and cholangiofibrosis.
  • The incidence of carcinoma of the uterus in the 4,600 g/kg stop-exposure group was significantly greater than those in the vehicle control and 4,600 g/kg core study groups at 2 years.
  • A marginal increase in squamous cell carcinoma occurred in the 220 g/kg group.
  • At 2 years, there were marginally increased incidences of exocrine pancreatic adenoma or carcinoma in the 460, 1,000, and 4,600 g/kg core study groups.
  • Numerous nonneoplastic effects were seen in other organs including: adrenal cortical atrophy and cytoplasmic vacuolization, pancreatic acinar cell cytoplasmic vacuolization and arterial chronic active inflammation, follicular cell hypertrophy of the thyroid gland, inflammation and respiratory epithelial hyperplasia of the nose, and kidney pigmentation.
  • Occurrences of carcinoma in the uterus were considered to be related to the administration of PCB 118.
  • Occurrences of squamous cell carcinoma of the uterus and acinar neoplasms of the pancreas may have been related to administration of PCB 118.
  • Administration of PCB 118 caused increased incidences of nonneoplastic lesions in the liver, lung, adrenal cortex, pancreas, thyroid gland, nose, and kidney.

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  • (PMID = 21383778.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 31508-00-6 / 2,3',4,4',5-pentachlorobiphenyl; DFC2HB4I0K / Polychlorinated Biphenyls; DO80M48B6O / Tetrachlorodibenzodioxin
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49. 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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50. Colby JK, Klein RD, McArthur MJ, Conti CJ, Kiguchi K, Kawamoto T, Riggs PK, Pavone AI, Sawicki J, Fischer SM: Progressive metaplastic and dysplastic changes in mouse pancreas induced by cyclooxygenase-2 overexpression. Neoplasia; 2008 Aug;10(8):782-96
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  • [Title] Progressive metaplastic and dysplastic changes in mouse pancreas induced by cyclooxygenase-2 overexpression.
  • We generated transgenic mice (BK5.COX-2) in which elevation of COX-2 and its effectors trigger a metaplasia-dysplasia sequence in exocrine pancreas.
  • Histologic evaluation revealed a chronic pancreatitis-like state characterized by acinar-to-ductal metaplasia and a well-vascularized fibroinflammatory stroma that develops by 3 months.
  • By 6 to 8 months, strongly dysplastic features suggestive of pancreatic ductal adenocarcinoma emerge in the metaplastic ducts.
  • Increased proliferation, cellular atypia, and loss of normal cell/tissue organization are typical features in transgenic pancreata.
  • Alterations in biomarkers associated with human inflammatory and neoplastic pancreatic disease were detected using immunohistochemistry.
  • The abnormal pancreatic phenotype can be completely prevented by maintaining mice on a diet containing celecoxib, a well-characterized COX-2 inhibitor.
  • However, cell lines derived from spontaneous lesions are aggressively tumorigenic when injected into syngeneic or nude mice.

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  • (PMID = 18670639.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA122815; United States / NCI NIH HHS / CA / R25 CA057730; United States / NIEHS NIH HHS / ES / T32 ES07247; United States / NCI NIH HHS / CA / R21 CA122815; United States / NIEHS NIH HHS / ES / P30 ES007784; United States / NIEHS NIH HHS / ES / ES07784; United States / NIEHS NIH HHS / ES / T32 ES007247; United States / NCI NIH HHS / CA / R25CA57730; United States / NCI NIH HHS / CA / CA105345; United States / NCI NIH HHS / CA / U01 CA105345
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Pyrazoles; 0 / Sulfonamides; 63231-63-0 / RNA; EC 1.14.99.1 / Cyclooxygenase 2; JCX84Q7J1L / Celecoxib; K7Q1JQR04M / Dinoprostone
  • [Other-IDs] NLM/ PMC2481568
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51. Mizgireuv IV, Revskoy SY: Transplantable tumor lines generated in clonal zebrafish. Cancer Res; 2006 Mar 15;66(6):3120-5
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  • Transplantable zebrafish tumors are a novel and very promising model in cancer research.
  • The histologic analysis of these tumors revealed different types of hepatocellular carcinomas, hepatoblastomas, hepatoma, cholangiocarcinoma, and pancreatic carcinoma.
  • Four spontaneous acinar cell carcinomas of pancreas were also found in 10- to 18-month-old CB1 fish.
  • Small pieces of tissue or cell suspensions of either DEN-induced or spontaneous tumors were serially transplanted into the peritoneal cavity of syngeneic fish at different stages of development from 5-day-old larvae to adult fish.
  • [MeSH-minor] Animals. Cell Line, Tumor. Diethylnitrosamine. Diploidy. Disease Models, Animal. Homozygote. Humans. Male. Neoplasm Transplantation

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  • (PMID = 16540662.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 3IQ78TTX1A / Diethylnitrosamine
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52. Klipin M, Sparaco A, Omoshoro-Jones J, Smith MD: Acinar cell carcinoma--a rare tumour of the pancreas. S Afr J Surg; 2008 Aug;46(3):88
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  • [Title] Acinar cell carcinoma--a rare tumour of the pancreas.
  • [MeSH-major] Carcinoma, Acinar Cell / therapy. Pancreatic Neoplasms / therapy

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  • (PMID = 18807305.001).
  • [ISSN] 0038-2361
  • [Journal-full-title] South African journal of surgery. Suid-Afrikaanse tydskrif vir chirurgie
  • [ISO-abbreviation] S Afr J Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] South Africa
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
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53. Chetty R, El-Shinnawy I: Intraductal pancreatic neuroendocrine tumor. Endocr Pathol; 2009;20(4):262-6
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  • [Title] Intraductal pancreatic neuroendocrine tumor.
  • Intraductal lesions of the pancreas are usually due to intraductal papillary mucinous neoplasms and the less common intraductal tubular adenoma.
  • Cases of acinar cell carcinoma within intraductal location have also been encountered recently.
  • Pancreatic neuroendocrine tumors are rarely encountered within the main pancreatic duct.
  • A 74-year-old male presented with non-specific abdominal symptoms and was found to have an obstructive lesion in the main pancreatic duct with associated chronic pancreatitis.
  • A distal pancreatectomy was performed which revealed a solid and cystic tumor measuring 6 x 3 x 2 cm situated wholly within the main pancreatic duct.
  • Microscopic evaluation of the mass showed it to be a well-differentiated pancreatic neuroendocrine tumor with entrapped, non-malignant tubules.
  • Intraductal pancreatic neuroendocrine tumors may occur in two settings.
  • Firstly, and more commonly, there is a parenchymal-based tumor that then encroaches on and pushes into the main pancreatic duct.
  • The less common scenario is of a primary intraductal location without a pancreatic parenchymal lesion.
  • While an intraductal location of a pancreatic neuroendocrine tumor is rare, it should be borne in mind when confronted by an intraductal lesion in the pancreas.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / diagnosis. Neuroendocrine Tumors / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 19763904.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromogranins; 0 / Synaptophysin
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54. Awadallah NS, Shroyer KR, Langer DA, Torkko KC, Chen YK, Bentz JS, Papkoff J, Liu W, Nash SR, Shah RJ: Detection of B7-H4 and p53 in pancreatic cancer: potential role as a cytological diagnostic adjunct. Pancreas; 2008 Mar;36(2):200-6
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  • [Title] Detection of B7-H4 and p53 in pancreatic cancer: potential role as a cytological diagnostic adjunct.
  • OBJECTIVES: This study compared p53 expression with B7-H4, a novel cancer biomarker, in pancreatic ductal adenocarcinoma (PDA) resection specimens and in a pilot series of endoscopic ultrasound-guided fine-needle aspirations (EUS-FNAs).
  • Some benign tissue components (intercalated cells/ducts, main pancreatic ducts, and acinar cells) were also positive for B7-H4 and/or p53.
  • Overall expression of B7-H4 in benign tissues, however, was relatively low compared with that seen in most carcinoma cases.
  • [MeSH-major] Antigens, CD80 / analysis. Biomarkers, Tumor / analysis. Carcinoma, Pancreatic Ductal / chemistry. Pancreatic Neoplasms / chemistry. Tumor Suppressor Protein p53 / analysis
  • [MeSH-minor] Adult. Aged. Biopsy, Fine-Needle / methods. Endosonography. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Staging. Pancreas / chemistry. Pilot Projects. Predictive Value of Tests. Reproducibility of Results. Tissue Fixation. V-Set Domain-Containing T-Cell Activation Inhibitor 1

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  • (PMID = 18376314.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Biomarkers, Tumor; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / V-Set Domain-Containing T-Cell Activation Inhibitor 1; 0 / VTCN1 protein, human
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55. Stelow EB, Shaco-Levy R, Bao F, Garcia J, Klimstra DS: Pancreatic acinar cell carcinomas with prominent ductal differentiation: Mixed acinar ductal carcinoma and mixed acinar endocrine ductal carcinoma. Am J Surg Pathol; 2010 Apr;34(4):510-8
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  • [Title] Pancreatic acinar cell carcinomas with prominent ductal differentiation: Mixed acinar ductal carcinoma and mixed acinar endocrine ductal carcinoma.
  • BACKGROUND: Pancreatic acinar cell carcinomas (ACCs) are clinically and pathologically distinct from pancreatic ductal adenocarcinomas (PDAs).
  • DESIGN: Cases of pancreatic ACCs with significant ductal differentiation were identified in the surgical pathology databases of 2 academic centers.
  • Ten were located in the head of the pancreas.
  • All cases showed significant evidence of both acinar and ductal differentiation, estimated to be at least 25% of the neoplastic cells, and 3 cases in addition had endocrine differentiation in more than 25% of cells.
  • Five cases were predominately acinar with intracellular and sometimes extracellular mucin ("mucinous acinar cell carcinoma" pattern).
  • Six cases seemed more mixed with areas recapitulating typical PDAs whereas the other portions of the tumors seemed akin to typical acinar cell carcinomas ("combined acinar and ductal" pattern).
  • CONCLUSION: Despite the early embryologic divergence of acinar and ductal cell lineages, rare pancreatic tumors have both acinar and ductal differentiation, usually predominantly the former.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Carcinoma, Islet Cell / pathology. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Combined Modality Therapy. DNA Mutational Analysis. DNA, Neoplasm / analysis. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Mucins / metabolism. Mutation. Neoplasms, Multiple Primary. New York / epidemiology. Pancreatectomy. Proto-Oncogene Proteins / genetics. Survival Rate. Virginia / epidemiology. ras Proteins / genetics

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  • (PMID = 20182344.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / KRAS protein, human; 0 / Mucins; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
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56. National Toxicology Program: NTP technical report on the toxicology and carcinogenesis studies of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (CAS No. 1746-01-6) in female Harlan Sprague-Dawley rats (Gavage Studies). Natl Toxicol Program Tech Rep Ser; 2006 Apr;(521):4-232
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  • Since human exposure to DLCs always involves a complex mixture, the toxic equivalency factor (TEF) methodology has been developed as a mathematical tool to assess the health risk posed by complex mixtures of these compounds.
  • The toxic equivalency of DLCs was nominated for evaluation because of the widespread human exposure to DLCs and the lack of data on the adequacy of the TEF methodology for predicting relative potency for cancer risk.
  • TCDD (dioxin) was selected for study by the National Toxicology Program as a part of the dioxin TEF evaluation to assess the cancer risk posed by complex mixtures of polychlorinated dibenzodioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and PCBs.
  • HEPATIC CELL PROLIFERATION DATA: To evaluate hepatocyte replication, analysis of labeling of replicating hepatocytes with 5-bromo-2'-deoxyuridine was conducted at the 14-, 31-, and 53-week interim evaluations.
  • At 2 years, there was a significant increase in toxic hepatopathy characterized by increased incidences of numerous nonneoplastic liver lesions including hepatocyte hypertrophy, multinucleated hepatocytes, altered hepatocellular foci, inflammation, pigmentation, diffuse fatty change, necrosis, portal fibrosis, oval cell hyperplasia, bile duct hyperplasia, bile duct cysts, cholangiofibrosis, and nodular hyperplasia At 2 years, the incidence of hepatocellular adenoma was significantly increased in the 100 ng/kg core study group.
  • The incidence of gingival squamous cell carcinoma of the oral mucosa was significantly increased in the 100 ng/kg core study group at 2 years and was accompanied by an increased incidence of gingival squamous hyperplasia.
  • At 2 years, the incidence of squamous cell carcinoma of the uterus in the 46 ng/kg group was significantly increased, and there were two squamous cell carcinomas in the 100 ng/kg stop-exposure group.
  • At 2 years, one acinar adenoma and two acinar cell carcinomas of the pancreas were seen in the 100 ng/kg core study group; one acinar carcinoma was seen in the 100 ng/kg stop-exposure group.
  • The incidences of acinar cell adenoma or carcinoma (combined) exceeded the historical vehicle control range.
  • Nonneoplastic effects in the lung included acinar cytoplasmic vacuolization, chronic active inflammation, acinar atrophy, and arterial chronic active inflammation. (ABSTRACT TRUNCATED)

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  • (PMID = 16835633.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; DO80M48B6O / Tetrachlorodibenzodioxin
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57. Kuo FY, Swanson PE, Yeh MM: Pancreatic acinar tissue in liver explants: a morphologic and immunohistochemical study. Am J Surg Pathol; 2009 Jan;33(1):66-71
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  • [Title] Pancreatic acinar tissue in liver explants: a morphologic and immunohistochemical study.
  • BACKGROUND: Pancreatic acini-like tissue is occasionally seen in the liver.
  • To gain further insight into this issue, we performed a pathologic and immunohistochemical study in liver explants to identify pancreatic acinar tissue.
  • Formalin-fixed, paraffin-embedded tissues were stained with hematoxylin-eosin, and immunohistochemical analyses using antibodies against CK7, CK8, and CK19 (biliary type cytokeratins), CD56 (positive in reactive bile ductules), chromogranin A (positive in reactive bile ductules and human oval-like/hepatic progenitor cells), pancreatic amylase, and PDX-1 were performed.
  • The immunohistochemical comparison group consisted of 3 gastric biopsies diagnosed as autoimmune gastritis with pancreatic metaplasia and 3 normal pancreatic tissues from pancreatectomy specimens.
  • RESULTS: Sixteen (4.2%) of 382 liver explants contained pancreatic acini-like tissue.
  • Fifteen of these were cirrhotic livers due to cryptogenic cirrhosis (n=1), primary biliary cirrhosis (n=3), primary sclerosing cholangitis (n=1), chronic hepatitis C-related cirrhosis (n=5), and cirrhosis with hepatitis C and hepatocellular carcinoma (n=5).
  • The pancreatic acini-like tissue appeared as small clusters of compactly packed cells that either blended imperceptibly with or were in close proximity to adjacent bile ducts or ductules.
  • The pancreatic acinar tissue was diffusely reactive for amylase, was occasionally positive for keratin 8 and chromogranin A, and was negative for CD56, keratin 7, and keratin 19.
  • CONCLUSIONS: Our results collectively indicate that pancreatic acini-like tissue in liver represent aggregates of pancreatic acinar cells admixed with small intra-acinar terminal ductules.
  • Given the close spatial relationship with reactive bile ductules and the apparent transition in immunophenotype from bile ductules to pancreatic acinar tissue, the latter is likely of metaplastic origin derived from a hepatic progenitor lineage.
  • [MeSH-major] Cell Transdifferentiation / physiology. Choristoma / etiology. Choristoma / pathology. Liver Diseases / pathology. Pancreas

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  • (PMID = 18987542.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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58. 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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59. Saif MW: Pancreatoblastoma. JOP; 2007;8(1):55-63
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  • Pancreatoblastoma (PB), or infantile pancreatic carcinoma, is an extremely rare pancreatic tumor in childhood, comprising 0.5% of pancreatic non-endocrine tumors.
  • Mechanical obstruction of the upper duodenum and gastric outlet by tumor in the head of the pancreas may be associated with vomiting, jaundice and gastrointestinal bleeding.
  • Histologically, PB is characterized with distinct acinar and squamoid cell differentiation.
  • The majority of these tumors arise in the head of the pancreas.
  • Ultrasound and CT scan may be useful but preoperative diagnosis is often quite difficult.
  • On the whole, PB is regarded to be a curable tumor; hence the clinical diagnosis should be made early.
  • Awareness of this rare tumor of pancreas is essential for early detection and proper management.
  • The author review the clinical presentation, etiology, diagnosis, treatment and prognosis of PB in this presentation.
  • [MeSH-major] Carcinoma / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Infant. Male. Middle Aged. Pancreas / pathology

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  • (PMID = 17228135.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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60. 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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61. Esposito I, Seiler C, Bergmann F, Kleeff J, Friess H, Schirmacher P: Hypothetical progression model of pancreatic cancer with origin in the centroacinar-acinar compartment. Pancreas; 2007 Oct;35(3):212-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypothetical progression model of pancreatic cancer with origin in the centroacinar-acinar compartment.
  • OBJECTIVES: Based mainly on animal models, 2 lesions have been suggested as possible precursors of pancreatic ductal adenocarcinoma (PDAC): pancreatic intraepithelial neoplasia (PanIN) and tubular complexes (TCs).
  • 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


62. Lin YC, Lee PH, Yao YT, Hsiao JK, Sheu JC, Chen CH: Alpha-fetoprotein-producing pancreatic acinar cell carcinoma. J Formos Med Assoc; 2007 Aug;106(8):669-72
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  • [Title] Alpha-fetoprotein-producing pancreatic acinar cell carcinoma.
  • A pancreatic tail tumor, instead of liver tumor, was detected.
  • He underwent elective distal pancreatectomy and splenectomy and the pathology turned out to be acinar cell carcinoma of the pancreas.
  • No cancer recurrence was noted after 3 years of follow-up.
  • Alpha-fetoprotein is commonly used as a tumor marker to screen for hepatocellular carcinoma in high-risk patients.
  • However, elevated alpha-fetoprotein could occur in a much rarer disease, acinar cell carcinoma of the pancreas.

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  • (PMID = 17711801.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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63. Frankel WL: Update on pancreatic endocrine tumors. Arch Pathol Lab Med; 2006 Jul;130(7):963-6
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  • [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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64. 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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  • [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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  • [Cites] Cancer. 1987 Feb 15;59(4):739-47 [3542187.001]
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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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65. Sipos B, Klöppel G: [Acinar cell carcinomas and pancreatoblastomas: related but not the same]. Pathologe; 2005 Feb;26(1):37-40
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  • [Title] [Acinar cell carcinomas and pancreatoblastomas: related but not the same].
  • Acinar cell carcinomas and pancreatoblastomas are malignant tumors of the pancreas, showing predominantly acinar differentiation characterized by the immunohistochemical expression of pancreatic enzymes.
  • Histologically, they usually display acinar and/or solid patterns, but may occasionally also exhibit cystic structures.
  • Acinar cell carcinomas predominantly occur in adults, pancreatoblastomas in children.
  • Pancreatoblastomas, in contrast to acinar cell carcinomas, are potentially curable.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Cell Differentiation. Diagnosis, Differential. Female. Humans. Male. Prognosis. Sex Characteristics

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  • (PMID = 15614488.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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66. Ballas KD, Rafailidis SF, Demertzidis C, Alatsakis MB, Pantzaki A, Sakadamis AK: Mixed exocrine-endocrine tumor of the pancreas. JOP; 2005 Sep;6(5):449-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mixed exocrine-endocrine tumor of the pancreas.
  • CONTEXT: Neoplasms of the pancreas usually show ductal, acinar or endocrine differentiation.
  • CASE REPORT: A 65-year-old woman was referred to our department with a diagnosis of carcinoma of the tail of the pancreas.
  • Upper gastrointestinal endoscopy revealed gastric fundus varices and CT scan demonstrated an inhomogeneous tumor located in the tail of the pancreas infiltrating the spleen and the splenic vein.
  • [MeSH-major] Carcinoma, Islet Cell / pathology. Carcinoma, Pancreatic Ductal / pathology. Mixed Tumor, Malignant / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 16186667.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Chromogranins; 0 / Gastrins; 51110-01-1 / Somatostatin; 9007-92-5 / Glucagon; EC 4.2.1.11 / Phosphopyruvate Hydratase
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67. Shah S, Mortele KJ: Uncommon solid pancreatic neoplasms: ultrasound, computed tomography, and magnetic resonance imaging features. Semin Ultrasound CT MR; 2007 Oct;28(5):357-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Uncommon solid pancreatic neoplasms: ultrasound, computed tomography, and magnetic resonance imaging features.
  • This article reviews the ultrasound, computed tomography, and magnetic resonance imaging features of rare solid tumors of the pancreas with attention to distinctive imaging appearances, which can help radiologists to discriminate between the different entities.
  • Various uncommon solid pancreatic neoplasms, including exocrine and endocrine epithelial tumors, mesenchymal tumors, and metastases, are reviewed, with emphasis on key differential points, including morphologic features and patterns of contrast enhancement.
  • [MeSH-major] Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / pathology. Carcinoma, Giant Cell / diagnosis. Carcinoma, Giant Cell / pathology. Contrast Media. Diagnosis, Differential. Endocrine Gland Neoplasms / diagnosis. Endocrine Gland Neoplasms / pathology. Humans. Lymphoma / diagnosis. Lymphoma / pathology. Magnetic Resonance Imaging. Neoplasm Metastasis. Neoplasm Staging. Neoplasms, Complex and Mixed / diagnosis. Neoplasms, Complex and Mixed / pathology. Tomography, X-Ray Computed

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  • (PMID = 17970552.001).
  • [ISSN] 0887-2171
  • [Journal-full-title] Seminars in ultrasound, CT, and MR
  • [ISO-abbreviation] Semin. Ultrasound CT MR
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
  • [Number-of-references] 41
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68. Mataki Y, Shinchi H, Kurahara H, Maemura K, Minami K, Setoyama T, Ueno S, Sakoda M, Yamamoto T, Takao S, Natsugoe S: [A case of acinar cell carcinoma diagnosed by endoscopic ultrasound-guided fine-needle aspiration prior to surgical treatment]. Nihon Shokakibyo Gakkai Zasshi; 2010 Aug;107(8):1328-34
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  • [Title] [A case of acinar cell carcinoma diagnosed by endoscopic ultrasound-guided fine-needle aspiration prior to surgical treatment].
  • She was given a diagnosis of acute pancreatitis and treated with intravenous infusion.
  • After recovering, abdominal enhanced-CT showed a low density area in the head of the pancreas, measuring 2 cm in maximum dimension.
  • Endoscopic ultrasound guided fine-needle aspiration (EUS-FNA) revealed acinar cell carcinoma (ACC).
  • The definitive diagnosis, based on the histopathological examinations including immunohistochemical staining, was ACC.
  • ACC of the pancreas is extremely rare, occurring in approximately 1% of all cases of pancreatic neoplasm.
  • [MeSH-major] Biopsy, Fine-Needle / methods. Carcinoma, Acinar Cell / pathology. Endosonography. Pancreatic Neoplasms / pathology

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  • (PMID = 20693758.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 26
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69. Scoazec JY: [Case 8: Liver metastasis of pancreatic acinar cell carcinoma]. Ann Pathol; 2007 Apr;27(2):120-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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70. 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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71. Martin SK, Agarwal G, Lynch GR: Subcutaneous fat necrosis as the presenting feature of a pancreatic carcinoma: the challenge of differentiating endocrine and acinar pancreatic neoplasms. Pancreas; 2009 Mar;38(2):219-22
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  • [Title] Subcutaneous fat necrosis as the presenting feature of a pancreatic carcinoma: the challenge of differentiating endocrine and acinar pancreatic neoplasms.
  • The association between pancreatic panniculitis and pancreatic disease is well described, but differentiation among the neoplastic causes of the syndrome remains difficult due to substantial overlap in histological and immunohistochemical features.
  • We report a case of subcutaneous fat necrosis as the presenting feature in a 61-year-old man with metastatic carcinoma of pancreatic origin.
  • Previous pathological evaluation of the patient's liver biopsy led to an initial diagnosis of adenocarcinoma of unknown primary site.
  • One month later, the patient presented with pancreatic panniculitis, prompting further investigation.
  • Immunohistochemistry was consistent with neuroendocrine differentiation, but the patient rapidly decompensated and died before the evaluation was complete, leaving the definitive diagnosis in question.
  • In our review of the published reports of tumor types associated with pancreatic panniculitis, we found that immunohistochemical staining and electron microscopy can and should be used in conjunction with clinical correlation to accurately differentiate neuroendocrine tumors from carcinomas with acinar cell features.
  • Accurate diagnosis of these tumors is necessary to determine prognosis and define appropriate therapy.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Fat Necrosis / pathology. Neuroendocrine Tumors / pathology. Pancreatic Neoplasms / pathology. Panniculitis / pathology. Skin / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry. Male. Middle Aged

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  • (PMID = 19238022.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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72. 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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  • [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


73. Kusafuka K, Bando E, Muramatsu K, Ito H, Tanizawa Y, Kawamura T, Mochizuki T, Terashima M, Nakajima T: Pancreatic-type mixed acinar-endocrine carcinoma with alpha-fetoprotein production arising from the stomach: a report of an extremely rare case. Med Mol Morphol; 2009 Sep;42(3):167-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic-type mixed acinar-endocrine carcinoma with alpha-fetoprotein production arising from the stomach: a report of an extremely rare case.
  • An extremely rare case of mixed acinar-endocrine carcinoma (MAEC) arising from the stomach in a 56-year-old Japanese woman is herein presented.
  • Histologically, the intragastric tumor consisted of large or small solid nests with acinar appearance.
  • The cancer cells had an ovoid nuclei and polygonal cytoplasm, which was frequently amphophilic.
  • Immunohistochemical examination showed that the cancer cells were positive for chromogranin-A, synaptophysin, alpha-amylase, lipase, and alpha-fetoprotein (AFP) but were negative for CD56, insulin, and other hormones.
  • Ultrastructurally, the cancer cells contained 500-nm electron-lucent zymogen granules and 230-nm electron-dense neuroendocrine granules.
  • Although no ectopic pancreas was found in the stomach, this tumor may originate from ectopic pancreas.
  • [MeSH-major] Carcinoma, Acinar Cell. Endocrine Gland Neoplasms. Stomach Neoplasms. alpha-Fetoproteins / metabolism
  • [MeSH-minor] Female. Humans. Middle Aged. Pancreatic Neoplasms / pathology

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  • [CommentIn] Med Mol Morphol. 2010 Mar;43(1):65 [20340009.001]
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  • (PMID = 19784744.001).
  • [ISSN] 1860-1499
  • [Journal-full-title] Medical molecular morphology
  • [ISO-abbreviation] Med Mol Morphol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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74. 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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75. 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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76. 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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77. Tapia B, Ahrens W, Kenney B, Touloukian R, Reyes-Múgica M: Acinar cell carcinoma versus solid pseudopapillary tumor of the pancreas in children: a comparison of two rare and overlapping entities with review of the literature. Pediatr Dev Pathol; 2008 Sep-Oct;11(5):384-90
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  • [Title] Acinar cell carcinoma versus solid pseudopapillary tumor of the pancreas in children: a comparison of two rare and overlapping entities with review of the literature.
  • Primary epithelial tumors of the pancreas are extremely uncommon in children, and among these, acinar cell carcinoma (ACC) is the most rare.
  • The histologic diagnosis of ACC was supported by both immunohistochemistry and electron microscopy.
  • Despite its rarity, ACC should be kept in the differential diagnosis of pediatric pancreatic exocrine tumors.
  • We also provide a comparison with an example of solid pseudopapillary tumor, another relatively infrequent epithelial tumor of the pancreas in the young.
  • We review the relevant literature addressing the clinical and pathologic features of ACC and its distinction from other pancreatic neoplasms.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / pathology. Pancreatic Cyst / pathology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Child. Diagnosis, Differential. Humans. Immunohistochemistry. Male. Pancreatectomy. Treatment Outcome. alpha 1-Antitrypsin / metabolism

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  • (PMID = 19006424.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / SERPINA1 protein, human; 0 / alpha 1-Antitrypsin
  • [Number-of-references] 37
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78. Sabbagh C, Fuks D, Chatelain D, Flamant M, Delcenserie R, Yzet T, Regimbeau JM: [Acinar cell carcinoma of the pancreas: a rare tumor with particular clinical and paraclinical presentation]. Rev Med Interne; 2008 Dec;29(12):1046-9
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  • [Title] [Acinar cell carcinoma of the pancreas: a rare tumor with particular clinical and paraclinical presentation].
  • [Transliterated title] Carcinome à cellules acineuses du pancréas : une tumeur rare avec des caractéristiques cliniques et paracliniques particulières.
  • Acinar cell carcinoma of the pancreas is a rare tumour with specific clinical and paraclinical presentation.

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  • (PMID = 18433943.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin
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79. Sanchez D, Mueller CM, Zenilman ME: Pancreatic regenerating gene I and acinar cell differentiation: influence on cellular lineage. Pancreas; 2009 Jul;38(5):572-7
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  • [Title] Pancreatic regenerating gene I and acinar cell differentiation: influence on cellular lineage.
  • OBJECTIVES: Pancreatic regenerating gene I (reg I) has been implicated in cellular differentiation.
  • Acinar cells can transdifferentiate into other pancreatic-derived cells, and we postulated that changes in intracellular levels of reg I would affect the state of differentiation.
  • Specifically, amylase mRNA and protein levels increased in SS cells, whereas AS cells showed increased pancreatic and duodenal homeobox 1 (Pdx1) and insulin mRNAs and cytokeratin protein.
  • CONCLUSIONS: These data demonstrate that in acinar cells, reg I overexpression is linked to acinar cell differentiation, whereas inhibition of reg I leads to beta cell and possibly ductal phenotype.
  • Reg I expression in acinar cells is important in maintaining pancreatic cell lineage, and when decreased, cells can dedifferentiate and move toward becoming other pancreatic cells.

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  • (PMID = 19557902.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK054511; United States / NIDDK NIH HHS / DK / DK054511-03; United States / NIDDK NIH HHS / DK / R01 DK054511-04; United States / NIDDK NIH HHS / DK / DK054511-04; United States / NIDDK NIH HHS / DK / R01 DK054511-03; United States / NIDDK NIH HHS / DK / Z01 DK054511
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Homeodomain Proteins; 0 / Insulin; 0 / Lithostathine; 0 / RNA, Messenger; 0 / Reg1 protein, rat; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein; EC 3.2.1.- / Amylases
  • [Other-IDs] NLM/ NIHMS100566; NLM/ PMC2702698
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80. 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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81. 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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82. Valentich MA, Eynard AR, Barotto NN, Díaz MP, Bongiovanni GA: Effect of the co-administration of phenobarbital, quercetin and mancozeb on nitrosomethylurea-induced pancreatic tumors in rats. Food Chem Toxicol; 2006 Dec;44(12):2101-5
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  • [Title] Effect of the co-administration of phenobarbital, quercetin and mancozeb on nitrosomethylurea-induced pancreatic tumors in rats.
  • We have previously shown that a single i.p. injection of nitrosomethylurea (NMU) in 3-day-old rats orally treated with the pesticide mancozeb (MZ), the flavonoid quercetin (Q) or in combination (MZ-Q) induces hyperplasia, atypical acinar cell proliferation and carcinoma in situ (CIS) in the pancreas.
  • This work studies the effect of oral administration of phenobarbital (PB) on this model of pancreatic carcinogenesis.
  • Acinar cell hyperplasia was found in all groups of NMU-treated rats.
  • [MeSH-major] Carcinogens / pharmacology. Carcinoma in Situ / chemically induced. Fungicides, Industrial / toxicity. Maneb / toxicity. Pancreatic Neoplasms / chemically induced. Phenobarbital / pharmacology. Quercetin / pharmacology. Zineb / toxicity

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  • Hazardous Substances Data Bank. QUERCETIN .
  • Hazardous Substances Data Bank. Zineb .
  • Hazardous Substances Data Bank. Maneb .
  • Hazardous Substances Data Bank. Phenobarbital .
  • Hazardous Substances Data Bank. N-NITROSO-N-METHYLUREA .
  • Hazardous Substances Data Bank. Mancozeb .
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  • (PMID = 16965848.001).
  • [ISSN] 0278-6915
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Carcinogens; 0 / Fungicides, Industrial; 12427-38-2 / Maneb; 684-93-5 / Methylnitrosourea; 9IKM0I5T1E / Quercetin; R0HY55EB9E / mancozeb; X1FSB1OZPT / Zineb; YQE403BP4D / Phenobarbital
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83. Klimstra DS: Nonductal neoplasms of the pancreas. Mod Pathol; 2007 Feb;20 Suppl 1:S94-112
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  • [Title] Nonductal neoplasms of the pancreas.
  • Although the majority of pancreatic neoplasms are infiltrating ductal adenocarcinomas or other neoplasms with ductal differentiation, neoplasms with acinar, endocrine, mixed, or uncertain differentiation constitute a diverse and distinctive group.
  • The most common and best-characterized nonductal neoplasms are pancreatic endocrine neoplasm, acinar cell carcinoma, pancreatoblastoma, and solid pseudopapillary neoplasm.
  • [MeSH-major] Adenocarcinoma, Papillary / pathology. Adenoma, Islet Cell / pathology. Carcinoma, Acinar Cell / pathology. Carcinoma, Islet Cell / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 17486055.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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84. Hosoda W, Takagi T, Mizuno N, Shimizu Y, Sano T, Yamao K, Yatabe Y: Diagnostic approach to pancreatic tumors with the specimens of endoscopic ultrasound-guided fine needle aspiration. Pathol Int; 2010 May;60(5):358-64
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  • [Title] Diagnostic approach to pancreatic tumors with the specimens of endoscopic ultrasound-guided fine needle aspiration.
  • Endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) has enabled clinicians to histologically diagnose pancreatic tumors.
  • Using immunostaining of CK7, CDX2, neuroendocrine markers and KRAS mutation analysis, we examined 57 FNA cell block sections and 61 surgically-resected specimens (25 invasive ductal carcinomas, 25 endocrine tumors, and 11 acinar cell tumors).
  • In the majority of the matched pairs, the diagnoses between EUS-FNA and surgical specimens were concordant using the following criteria: neuroendocrine markers negative, CK7 positive, and mutated KRAS gene for invasive ductal carcinomas; neuroendocrine markers diffusely positive, CK7 and CDX2 negative, and wild-type KRAS gene for well-differentiated endocrine tumors; and neuroendocrine markers no more than focal positive, CK7 and CDX2 with various staining patterns, and wild-type KRAS gene for acinar cell carcinomas.
  • The usefulness of these markers was confirmed using 13 additional pancreatic tumors, prospectively.
  • Although minimal in selection, these markers are helpful in making diagnosis from EUS-FNA specimens of the major pancreatic tumors.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Islet Cell / diagnosis. Carcinoma, Pancreatic Ductal / diagnosis. Endosonography / methods. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Biopsy, Fine-Needle. DNA Mutational Analysis. DNA, Neoplasm / analysis. Homeodomain Proteins / metabolism. Humans. Keratin-7 / metabolism. Pancreas / metabolism. Pancreas / pathology. Pancreatectomy. Prognosis. Prospective Studies. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. ras Proteins / genetics. ras Proteins / metabolism

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  • (PMID = 20518885.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / DNA, Neoplasm; 0 / Homeodomain Proteins; 0 / KRAS protein, human; 0 / Keratin-7; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
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85. Borka K: [Claudin expression in different pancreatic cancers and its significance in differential diagnostics]. Magy Onkol; 2009 Sep;53(3):273-8
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  • [Title] [Claudin expression in different pancreatic cancers and its significance in differential diagnostics].
  • The aim of our studies was to compare the different CLDN expression patterns in normal pancreas cells, pancreatic endocrine tumors, adenocarcinomas, mucinous cystic tumors and acinar cell carcinomas.
  • ) In addition to the well-known CLDN-1 and -4 expression CLDN-2, -3 and -7 proteins were demonstrated in ductal cells, while CLDN-3 and -7 proteins showed expression in acinar cells.
  • 4.) This is a first review on childhood acinar cell carcinoma causing Cushing syndrome.
  • The adenocarcinomas and cystic mucinous tumors of exocrine origin denoted CLDN-1, -2, -4 and -7 positivity, whereas acinar cell carcinomas expressed only CLDN-1 and -2.
  • Considering the CLDN expression observed in normal pancreas cells, it can be established that CLDN-1, -2 and -4 proteins are definitely markers of ductal differentiation, CLDN-1 protein of acinar and CLDN-3 of endocrine differentiation. 2).
  • The claudin expression pattern of pancreas tumors may be employed in the differential diagnosis of these tumors and may be of help in deciding dignity.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Claudins / metabolism. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Carcinoma, Pancreatic Ductal / diagnosis. Carcinoma, Pancreatic Ductal / metabolism. Claudin-1. Claudin-3. Claudin-4. Cystadenocarcinoma, Mucinous / diagnosis. Cystadenocarcinoma, Mucinous / metabolism. Diagnosis, Differential. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Luminescence. Membrane Proteins / metabolism. Microscopy, Electron. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19793693.001).
  • [ISSN] 0025-0244
  • [Journal-full-title] Magyar onkologia
  • [ISO-abbreviation] Magy Onkol
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CLDN1 protein, human; 0 / CLDN2 protein, human; 0 / CLDN3 protein, human; 0 / CLDN4 protein, human; 0 / CLDN7 protein, human; 0 / Claudin-1; 0 / Claudin-3; 0 / Claudin-4; 0 / Claudins; 0 / Membrane Proteins
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86. Wu X, Tao R, Lei R, Han B, Cheng D, Shen B, Peng C: Distal pancreatectomy combined with celiac axis resection in treatment of carcinoma of the body/tail of the pancreas: a single-center experience. Ann Surg Oncol; 2010 May;17(5):1359-66
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  • [Title] Distal pancreatectomy combined with celiac axis resection in treatment of carcinoma of the body/tail of the pancreas: a single-center experience.
  • The aim of this study was to assess the safety and efficacy of this extended procedure in treatment of advanced carcinoma of the body/tail of the pancreas.
  • METHODS: This was a retrospective analysis of 206 patients with carcinoma of the body/tail of the pancreas from January 2003 through June 2008.
  • Group A had longer mean operative time than group B (323 versus 225 min, P = 0.000); there was no difference in mean estimated blood loss, percentage of pancreatic fistula or median survival time (14 versus 15 months, P = 0.197).
  • CONCLUSIONS: DP combined with CA resection can be safely performed in certain patients with carcinoma of body/tail of the pancreas and significantly improves patient survival and quality of life.
  • [MeSH-major] Celiac Artery / surgery. Pancreatectomy. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adenocarcinoma. Adenocarcinoma, Clear Cell. Adenocarcinoma, Mucinous. Adult. Aged. Carcinoma, Acinar Cell. Female. Humans. Liver Neoplasms / secondary. Liver Neoplasms / surgery. Male. Middle Aged. Neoplasm Invasiveness. Postoperative Complications / diagnosis. Retrospective Studies. Survival Rate. Tomography, X-Ray Computed. Treatment Outcome

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  • [CommentIn] Ann Surg Oncol. 2011 Dec;18 Suppl 3:S244; author reply S245 [20967503.001]
  • (PMID = 20198445.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
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87. 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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88. 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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89. Mathieu A, Clerc P, Portolan G, Bierkamp C, Lulka H, Pradayrol L, Seva C, Fourmy D, Dufresne M: Transgenic expression of CCK2 receptors sensitizes murine pancreatic acinar cells to carcinogen-induced preneoplastic lesions formation. Int J Cancer; 2005 May 20;115(1):46-54
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  • [Title] Transgenic expression of CCK2 receptors sensitizes murine pancreatic acinar cells to carcinogen-induced preneoplastic lesions formation.
  • In humans, initial events of pancreatic carcinogenesis remain unknown, and the question of whether this cancer, which has a ductal phenotype, exclusively arises from duct cells has been raised.
  • Previous studies have demonstrated that transgenic expression of the CCK2 receptor in acinar cells of ElasCCK2 mice plays a role in the development of pancreatic neoplasia.
  • Transition of acinar cells into duct-like cells expressing Pdx1 and gastrin, as well as proliferation of acinar cells, were transiently observed in both transgenic and control mice.
  • Importantly, expression of the CCK2 receptor increased the susceptibility of pancreas to azaserine.
  • Indeed, treated ElasCCK2 mice exhibited larger areas of pancreatic acinar-ductal transition, increased cellular proliferation as well as larger adenomas areas vs. control mice.
  • [MeSH-major] Carcinoma, Acinar Cell / etiology. Carcinoma, Acinar Cell / genetics. Pancreatic Neoplasms / etiology. Pancreatic Neoplasms / genetics. Receptor, Cholecystokinin B / genetics. Receptor, Cholecystokinin B / physiology. Transgenes
  • [MeSH-minor] Adenoma / metabolism. Animals. Antimetabolites, Antineoplastic / pharmacology. Azaserine / chemistry. Azaserine / pharmacology. Bromodeoxyuridine / pharmacology. Carcinogens. Cell Proliferation. Coloring Agents / pharmacology. Homeodomain Proteins / metabolism. Homozygote. Immunohistochemistry. Inflammation. Lymphocytes / metabolism. Mice. Mice, Transgenic. Phenotype. Precancerous Conditions / metabolism. Receptors, G-Protein-Coupled / metabolism. Risk. Time Factors. Trans-Activators / metabolism

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15688412.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Carcinogens; 0 / Coloring Agents; 0 / Homeodomain Proteins; 0 / Receptor, Cholecystokinin B; 0 / Receptors, G-Protein-Coupled; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein; 87299V3Q9W / Azaserine; G34N38R2N1 / Bromodeoxyuridine
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90. National Toxicology Program: Toxicology and carcinogenesis studies of a binary mixture of 3,3',4,4',5-pentachlorobiphenyl (PCB 126) (Cas No. 57465-28-8) and 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153) (CAS No. 35065-27-1) in female Harlan Sprague-Dawley rats (gavage studies). Natl Toxicol Program Tech Rep Ser; 2006 Aug;(530):1-258
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  • Since human exposure to DLCs always occurs as a complex mixture, the toxic equivalency factor (TEF) methodology has been developed as a mathematical tool to assess the health risk posed by complex mixtures of these compounds.
  • The toxic equivalency of DLCs was nominated for evaluation because of the widespread human exposure to DLCs and the lack of data on the adequacy of the TEF methodology for predicting relative potency for cancer risk.
  • Hepatic Cell Proliferation Data: To evaluate hepatocyte replication, analysis of labeling of replicating hepatocytes with 5-bromo-2'-deoxyuridine was conducted at the 14-, 31-, and 53-week interim evaluations.
  • At the end of the 2-year study, there were significantly increased incidences and severities of toxic hepatopathy characterized by hepatocyte hypertrophy, multinucleated hepatocytes, pigmentation, diffuse and focal fatty change, eosinophilic focus, nodular hyperplasia, cholangiofibrosis, oval cell hyperplasia, bile duct cysts, bile duct hyperplasia, necrosis, and portal fibrosis.
  • In addition, two animals in the highest dose group had hepatocellular carcinoma.
  • In addition, single occurrences of squamous cell carcinoma were seen in the top two dose groups.
  • Significantly increased incidences of squamous cell carcinoma (gingival) of the oral mucosa were seen at the end of the 2-year study and were accompanied by increased incidences of gingival squamous hyperplasia.
  • In the pancreas at 53 weeks, the incidence of acinar cytoplasmic vacuolization was significantly increased in the highest dose group.
  • At 2 years, increased incidences of acinar atrophy and acinar cytoplasmic vacuolization were seen in addition to pancreatic acinar neoplasms in dosed groups.
  • In the uterus at 2 years, there was a marginal increase in the incidence of squamous cell carcinoma in Group 5.
  • Numerous nonneoplastic effects were seen in other organs at the interim time points including atrophy of the thymus and follicular cell hypertrophy of the thyroid gland.

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  • (PMID = 17160104.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; DFC2HB4I0K / Polychlorinated Biphenyls; TSH69IA9XF / 3,4,5,3',4'-pentachlorobiphenyl; ZRU0C9E32O / 2,4,5,2',4',5'-hexachlorobiphenyl
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91. Kataoka Y, Nio Y, Yano S, Koike M, Hashimoto K, Itakura M, Itagaki T, Nishi T, Endo S, Higami T: [Pancreatic acinar cell carcinoma successfully treated with combination of oral TS-1 and intra-arterial cisplatin]. Gan To Kagaku Ryoho; 2006 Apr;33(4):525-8
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  • [Title] [Pancreatic acinar cell carcinoma successfully treated with combination of oral TS-1 and intra-arterial cisplatin].
  • Pancreatic acinar cell carcinomas are rare, and little is reported on their chemotherapy.
  • We report a 49-year old male patient with pancreatic acinar cell carcinoma and multiple liver metastases, which responded to oral TS-1 and hepatic arterial infusion of cisplatin.
  • The patient underwent a partial hepatectomy, MCT abrasions and excision of the pancreatic tumor.
  • Postoperative pathological studies revealed metastases of acinar cell carcinoma to the liver and lymph nodes; the primary lesion was undetermined.
  • Abdominal CT one year after surgery revealed a pancreatic body tumor, which was surgically removed.
  • Pathological studies showed primary pancreatic acinar cell carcinoma, while previous metastases remained under control.
  • To summarize, TS-1 and cisplatin can be effective treatments for pancreatic acinar cell carcinomas.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Pancreatic Neoplasms / drug therapy

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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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92. Tsutsumi M: [Differential genetic pathway of duct and acinar carcinomas of the pancreas]. Gan To Kagaku Ryoho; 2005 May;32(5):593-8
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  • [Title] [Differential genetic pathway of duct and acinar carcinomas of the pancreas].
  • Genetic pathways of various types of pancreatic carcinoma are described.
  • There are many differences in the genetic pathway between duct carcinogenesis and acinar carcinogensis.
  • K-ras mutation is a key event in the early stage of pancreatic duct carcinogenesis and various gene alterations accumulate from precancerous ductal lesions until the development of carcinomas.
  • [MeSH-major] Carcinoma, Acinar Cell / genetics. Carcinoma, Pancreatic Ductal / genetics. Genes, ras. Pancreatic Neoplasms / genetics

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  • (PMID = 15918556.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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93. Pan Z, Erkan M, Streit S, Friess H, Kleeff J: Silencing of GRP94 expression promotes apoptosis in pancreatic cancer cells. Int J Oncol; 2009 Oct;35(4):823-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Silencing of GRP94 expression promotes apoptosis in pancreatic cancer cells.
  • As a molecular chaperone, GRP94 is the most abundant glycoprotein in the endoplasmic reticulum, playing an important role in maintaining cellular homeostasis.
  • Here, we investigated the expression and the role of GRP94 in regulating cell growth and apoptosis in pancreatic cancer cells.
  • Immunohistochemistry was performed to localize GRP94 in tissues of the normal pancreas (n=20), chronic pancreatitis (n=20) and pancreatic ductal adenocarcinoma (n=44).
  • Compared to normal pancreatic tissues, median mRNA levels of GRP94 were 1.5- and 3.7-fold (p<0.05) lower in chronic pancreatitis and pancreatic cancer tissues, respectively.
  • GRP94 protein was strongly expressed in normal acinar cells and moderately expressed in normal ductal cells.
  • GRP94 expression was lost in 48% of the cancer cases.
  • Moderate or strong staining in cancer cells was observed in 32 and 20% of pancreatic cancer tissues, respectively.
  • Silencing GRP94 by siRNA increased apoptosis of pancreatic cancer cells in vitro.
  • Down-regulation of GRP94 decreases apoptosis resistance in pancreatic cancer cells.
  • [MeSH-major] Apoptosis. Biomarkers, Tumor / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Membrane Glycoproteins / metabolism. Pancreatic Neoplasms / metabolism. RNA Interference. RNA, Small Interfering / metabolism
  • [MeSH-minor] Cell Line, Tumor. Dactinomycin / pharmacology. Dose-Response Relationship, Drug. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Neoplasm Staging. Nucleic Acid Synthesis Inhibitors / pharmacology. Prognosis. Protein Synthesis Inhibitors / pharmacology. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Transfection

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  • (PMID = 19724918.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Glycoproteins; 0 / Nucleic Acid Synthesis Inhibitors; 0 / Protein Synthesis Inhibitors; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / endoplasmin; 1CC1JFE158 / Dactinomycin
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94. Kimura W: [Pathogenesis of endocrine tumors of the pancreas]. Nihon Geka Gakkai Zasshi; 2008 May;109(3):133-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Pathogenesis of endocrine tumors of the pancreas].
  • Precise pathohistologic and immunohistochemical investigations of the pancreas in elderly autopsy cases revealed that endocrine tumors are found very frequently.
  • Some endocrine tumors of the pancreas may originate from Langerhans islets, although other endocrine tumors may develop from endocrine cells or stem cells with multiple differentiation ability and occur in the duct cells or acinar cells.
  • This possibility may be supported by the evidence that ductular or tubular structures were found in or adjacent to tumors in about 60% of minute tumors and that hormone production was found in both duct cells and acinar cells based on immunohistochemical findings.
  • The occurrence of ductuloinsular tumors, acinar endocrine cell tumors, and duct-acinar-islet cell tumors may also support these observations.
  • Molecular biological investigations will further analyze the pathogenesis of endocrine tumors of the pancreas.
  • There are three possible origins of endocrine tumors of the pancreas: Langerhans islets cells, ductular cells, and acinar cells.
  • [MeSH-major] Neuroendocrine Tumors. Pancreatic Neoplasms
  • [MeSH-minor] Aged. Animals. Carcinoma, Acinar Cell. Carcinoma, Pancreatic Ductal. Female. Humans. Immunohistochemistry. Islets of Langerhans. Male

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  • (PMID = 18536316.001).
  • [ISSN] 0301-4894
  • [Journal-full-title] Nihon Geka Gakkai zasshi
  • [ISO-abbreviation] Nihon Geka Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 35
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95. Kawakami H, Kuwatani M, Onodera M, Hirano S, Kondo S, Nakanishi Y, Itoh T, Asaka M: Primary acinar cell carcinoma of the ampulla of Vater. J Gastroenterol; 2007 Aug;42(8):694-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary acinar cell carcinoma of the ampulla of Vater.
  • Acinar cell carcinoma of the pancreatobiliary system is a relatively rare malignant neoplasm arising usually in the pancreatic parenchyma.
  • The patient underwent a curative surgical operation, and histopathological examination revealed that the tumor was confined to the ampulla of Vater with no continuity to the pancreatic parenchyma.
  • The tumor cells showed acinar or tubular arrangement with eosinophilic to basophilic granular cytoplasm, findings identical to those of acinar cell carcinoma of the pancreas.
  • From these findings, we concluded that the tumor was primary acinar cell carcinoma arising in the ampulla of Vater, probably originating from heterotopic pancreatic tissue.
  • This is the first reported case of primary acinar cell carcinoma in the ampulla of Vater.
  • [MeSH-major] Ampulla of Vater. Carcinoma, Acinar Cell / diagnosis. Common Bile Duct Neoplasms / diagnosis
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Endosonography. Female. Follow-Up Studies. Humans. Middle Aged. Pancreaticoduodenectomy / methods. Tomography, X-Ray Computed

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  • (PMID = 17701134.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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96. Mueller SB, Micke O, Herbst H, Schaefer U, Willich N: Alpha-fetoprotein-positive carcinoma of the pancreas: a case report. Anticancer Res; 2005 May-Jun;25(3A):1671-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alpha-fetoprotein-positive carcinoma of the pancreas: a case report.
  • We report on the case of a 19-year-old male with an alpha-fetoprotein (AFP)-producing acinar cell carcinoma of the pancreas.
  • Originally, AFP was thought to be specific to hepatocellular carcinoma and germ cell tumours.
  • Rare cases of acinar cell carcinomas of the pancreas were found to express AFP.
  • When present, AFP expression is useful for diagnosis and as a marker for monitoring therapeutic response and recurrence of the disease.
  • [MeSH-major] Pancreatic Neoplasms / metabolism. alpha-Fetoproteins / metabolism

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  • (PMID = 16033080.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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97. Nishii T, Amano R, Nakao S, Doi Y, Yamada N, Ohira M, Hirakawa K: [A case of liver metastasis of mixed acinar-endocrine carcinoma treated with various loco-regional cancer therapies]. Gan To Kagaku Ryoho; 2008 Nov;35(12):2126-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of liver metastasis of mixed acinar-endocrine carcinoma treated with various loco-regional cancer therapies].
  • Mixed acinar-endocrine carcinoma of pancreas is a very rare tumor.
  • We report a 60s female patient with pancreatic mixed acinar-endocrine carcinoma and liver metastasis.
  • The patient admitted for further examination of pancreatic head mass.
  • Computed tomography scan of abdomen showed a large tumor in pancreatic head and liver tumor.
  • We conducted a pylorus-preserved pancreatoduodenectomy with resection of the portal vein on the diagnosis of acinar cell carcinoma by fine needle aspiration biopsy.
  • Pathological examination showed a mixed acinar-endocrine carcinoma.
  • Following the operation, the liver metastasis was controlled with various loco-regional cancer therapies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Carcinoma, Acinar Cell / pathology. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / pathology

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  • (PMID = 19106545.001).
  • [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
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98. 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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99. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.