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

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  • (PMID = 17993731.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 28
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2. Peng HQ, Darwin P, Papadimitriou JC, Drachenberg CB: Liver metastases of pancreatic acinar cell carcinoma with marked nuclear atypia and pleomorphism diagnosed by EUS FNA cytology: a case report with emphasis on FNA cytological findings. Cytojournal; 2006;3:29
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  • [Title] Liver metastases of pancreatic acinar cell carcinoma with marked nuclear atypia and pleomorphism diagnosed by EUS FNA cytology: a case report with emphasis on FNA cytological findings.
  • BACKGROUND: Acinar cell carcinoma of the pancreas is a rare neoplasm.
  • Unlike ductal adenocarcinomas, endocrine tumors, and solid pseudopapillary tumors of the pancreas with their characteristic FNA cytological features, acinar cell carcinomas pose a particular diagnostic challenge by sharing many cytomorphologic features with endocrine tumors of the pancreas.
  • Computed tomography revealed a 7.8 x 7.3 cm irregular, partially cystic mass in the body and tail of the pancreas, and two lesions in the liver compatible with metastases.
  • FNA cytology revealed abundant, loosely cohesive clusters of malignant epithelial cells with vaguely acinar and trabecular formations.
  • A pancreatic endocrine tumor was suspected initially, but acinar cell carcinoma of the pancreas was confirmed by immunohistochemistry, cytochemical and ultrastructural studies.
  • CONCLUSION: We describe a case of pancreatic acinar cell carcinoma with unusual cytomorphologic features mimicking an endocrine tumor of pancreas, encountered in endoscopic ultrasound-guided fine needle aspiration of a metastatic liver mass and discuss the diagnostic approach for this unusual pancreatic tumor in fine needle aspiration cytology.

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  • (PMID = 17196112.001).
  • [ISSN] 1742-6413
  • [Journal-full-title] CytoJournal
  • [ISO-abbreviation] Cytojournal
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1779360
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3. 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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4. 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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5. 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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6. Hsu MY, Pan KT, Chu SY, Hung CF, Wu RC, Tseng JH: CT and MRI features of acinar cell carcinoma of the pancreas with pathological correlations. Clin Radiol; 2010 Mar;65(3):223-9
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  • [Title] CT and MRI features of acinar cell carcinoma of the pancreas with pathological correlations.
  • AIM: To document the computed tomography (CT) and magnetic resonance imaging (MRI) features of acinar cell carcinoma of the pancreas and to correlate them with pathological findings to determine the unique imaging manifestations of this rare subtype tumour of the pancreas.
  • MATERIALS AND METHODS: From January 1986 to August 2008, six patients (five men and one woman, mean age 61.3 years) with histologically proven acinar cell carcinoma of the pancreas underwent CT (n=6) and MRI (n=4) examinations.
  • RESULTS: The tumours were distributed in the head (n=4), body (n=1), and tail (n=1) of the pancreas.
  • In both CT and MRI, the tumours enhanced less than the adjacent normal pancreatic parenchyma.
  • CONCLUSION: Acinar cell carcinoma of the pancreas has distinct imaging features, and both CT and MRI are useful and complementary imaging methods.
  • [MeSH-major] Carcinoma, Acinar Cell. Magnetic Resonance Imaging. Pancreatic Neoplasms. Tomography, X-Ray Computed
  • [MeSH-minor] Adult. Aged. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Pancreas, Exocrine. Retrospective Studies. Sex Distribution. alpha-Fetoproteins / metabolism

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  • [Copyright] Copyright (c) 2010 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.
  • (PMID = 20152279.001).
  • [ISSN] 1365-229X
  • [Journal-full-title] Clinical radiology
  • [ISO-abbreviation] Clin Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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7. 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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8. Wisnoski NC, Townsend CM Jr, Nealon WH, Freeman JL, Riall TS: 672 patients with acinar cell carcinoma of the pancreas: a population-based comparison to pancreatic adenocarcinoma. Surgery; 2008 Aug;144(2):141-8
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  • [Title] 672 patients with acinar cell carcinoma of the pancreas: a population-based comparison to pancreatic adenocarcinoma.
  • BACKGROUND: Acinar cell carcinoma (ACC) is a rare cancer of the pancreas accounting for approximately 1% of nonendocrine tumors.
  • OBJECTIVE: Our goal was to evaluate a large population-based cohort of patients with ACC and compare their demographic factors and outcomes to those of patients with pancreatic adenocarcinoma (PA).
  • The mean age at the time of diagnosis was significantly lower for ACC than PA (56 years vs 70 years, P < .001).
  • Multivariate Cox proportional hazards regression model results suggested patients with ACC were less likely to die (hazard ratio = 0.241; 95% confidence interval, 0.22-0.27) than patients with PA after controlling for gender, race, stage, SEER region of diagnosis, and surgical resection status.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18656619.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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9. Seth AK, Argani P, Campbell KA, Cameron JL, Pawlik TM, Schulick RD, Choti MA, Wolfgang CL: Acinar cell carcinoma of the pancreas: an institutional series of resected patients and review of the current literature. J Gastrointest Surg; 2008 Jun;12(6):1061-7
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  • [Title] Acinar cell carcinoma of the pancreas: an institutional series of resected patients and review of the current literature.
  • INTRODUCTION: Acinar cell carcinoma (ACC) is a rare, malignant neoplasm with a generally poor prognosis.
  • MATERIALS AND METHODS: The Johns Hopkins pathology prospective database was reviewed from 1988 to 2006 to identify patients with pancreatic neoplasms possessing features of acinar cell differentiation.
  • Overall median survival and disease-free survival were 33 and 25 months, respectively, as compared to a median survival of 18 months for pancreatic adenocarcinoma.
  • CONCLUSION: Acinar cell carcinomas are rare, aggressive neoplasms that are difficult to diagnose and treat.
  • These lesions have a better prognosis than the more common pancreatic adenocarcinomas.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatectomy / methods. Pancreatic Neoplasms / pathology. Pancreaticoduodenectomy / methods

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  • (PMID = 17957440.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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10. 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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11. Schmidt CM, Matos JM, Bentrem DJ, Talamonti MS, Lillemoe KD, Bilimoria KY: Acinar cell carcinoma of the pancreas in the United States: prognostic factors and comparison to ductal adenocarcinoma. J Gastrointest Surg; 2008 Dec;12(12):2078-86
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  • [Title] Acinar cell carcinoma of the pancreas in the United States: prognostic factors and comparison to ductal adenocarcinoma.
  • INTRODUCTION: Pancreatic acinar cell carcinoma (ACC) is a rare tumor with poorly defined prognosis.
  • OBJECTIVE: Our objective was to compare a large population of patients with ACC to pancreatic ductal cell adenocarcinoma (DCC) in order to determine distinguishing characteristics and to assess survival.
  • METHODS: Patients were identified from the National Cancer Database.
  • Patients with ACC were more likely to be male, white, and have larger tumor size, no nodal involvement, or pancreatic tail tumors.
  • Aggressive surgical resection with negative margins is associated with long-term survival in these more favorable pancreatic cancers.
  • [MeSH-major] Carcinoma, Acinar Cell / epidemiology. Carcinoma, Acinar Cell / surgery. Pancreatic Neoplasms / epidemiology. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Aged. Carcinoma, Pancreatic Ductal / epidemiology. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Pancreatic Ductal / surgery. Chi-Square Distribution. Female. Humans. Lymphatic Metastasis. Male. Middle Aged. Pancreatectomy. Prognosis. ROC Curve. Regression Analysis. Statistics, Nonparametric. Survival Rate. Treatment Outcome. United States / epidemiology

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  • (PMID = 18836784.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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12. 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


13. Igarashi H, Shinozaki S, Mukada T: A case of acinar cell carcinoma of the pancreas that formed extensive tumor thrombus of the portal vein. Clin J Gastroenterol; 2009 Apr;2(2):96-102

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  • [Title] A case of acinar cell carcinoma of the pancreas that formed extensive tumor thrombus of the portal vein.
  • Abdominal ultrasonography and computed tomography revealed a large mass in the body and tail of the pancreas, which directly invaded the stomach and the spleen.
  • The specimens obtained from portal tumor thrombus were histologically compatible with acinar cell carcinoma.
  • Portal tumor thrombus is a rare condition in pancreatic tumors; however, it seems to be important to differentiate tumor thrombus from blood thrombus of the portal vein in order to know the true clinical stage and provide a suitable treatment.

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  • (PMID = 26192173.001).
  • [ISSN] 1865-7257
  • [Journal-full-title] Clinical journal of gastroenterology
  • [ISO-abbreviation] Clin J Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Keywords] NOTNLM ; Acinar cell carcinoma / Pancreas / Portal vein / Tumor thrombus
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14. Takanami K, Abe K, Mitamura A, Miyazaki S, Abe K, Ishida K, Yamada S, Takahashi S: Two cases of 18 F-FDG PET/CT findings in acinar cell carcinoma of the pancreas. Clin Nucl Med; 2009 Apr;34(4):209-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Two cases of 18 F-FDG PET/CT findings in acinar cell carcinoma of the pancreas.
  • The patients consisted of a 60-year-old woman and a 72-year-old man with no significant symptoms, who were both referred to the hospital due to the presence of large pancreatic tumors.
  • They underwent F-18 FDG PET/CT and subsequently a pancreaticoduodenectomy and acinar cell carcinoma in the pancreas was proven histopathologically.
  • In one case, the tumor consisted of a solid component presenting intense FDG uptake and necrotic tissue.
  • This report thus documents 2 cases of acinar cell carcinoma that showed contrasting histopathologic and F-18 FDG PET/CT findings.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / radionuclide imaging. Fluorodeoxyglucose F18 / pharmacology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / radionuclide imaging. Positron-Emission Tomography / methods. Tomography, X-Ray Computed / methods

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  • (PMID = 19300048.001).
  • [ISSN] 1536-0229
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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15. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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16. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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17. 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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18. Imamura M, Kimura Y, Ito H, Nobuoka T, Koito K, Sasaki A, Hirata K: Acinar cell carcinoma of the pancreas with intraductal growth: report of a case. Surg Today; 2009;39(11):1006-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinar cell carcinoma of the pancreas with intraductal growth: report of a case.
  • Acinar cell carcinomas (ACCs) of the pancreas are rare neoplasms, accounting for approximately 1% of all exocrine pancreatic tumors.
  • This type of tumor is known to be aggressive, although the survival rates are somewhat better than they are for ductal carcinoma.
  • This report presents a case of ACC of the pancreas with intraductal papillary growth and lymph node metastasis.
  • [MeSH-major] Carcinoma, Acinar Cell / surgery. Neoplasm Invasiveness. Pancreatectomy / methods. Pancreatic Ducts / pathology. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Aged. Cholangiopancreatography, Endoscopic Retrograde. Diagnosis, Differential. Endosonography. Female. Humans

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  • (PMID = 19882327.001).
  • [ISSN] 1436-2813
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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19. 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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20. 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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  • [Cites] J Clin Oncol. 2002 Dec 15;20(24):4673-8 [12488412.001]
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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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21. Tatli S, Mortele KJ, Levy AD, Glickman JN, Ros PR, Banks PA, Silverman SG: CT and MRI features of pure acinar cell carcinoma of the pancreas in adults. AJR Am J Roentgenol; 2005 Feb;184(2):511-9
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  • [Title] CT and MRI features of pure acinar cell carcinoma of the pancreas in adults.
  • OBJECTIVE: We sought to describe the CT and MRI features of pure acinar cell carcinoma of the pancreas in adults.
  • MATERIALS AND METHODS: Eleven patients (six women and five men; mean age, 64 years) with acinar cell carcinoma, documented by pathologic examination of resected specimens, underwent CT (n=9) or MRI (n=2) examinations.
  • In addition, they assessed the presence of calcification, pancreatic or bile duct dilation, and metastases.
  • RESULTS: Masses were distributed throughout the pancreas (head, n=5; body, n=2; and tail, n=4).
  • All masses enhanced less than the surrounding pancreas.
  • Common bile and pancreatic duct dilatation was present in two and three patients, respectively.
  • CONCLUSION: Pure acinar cell carcinoma of the pancreas is usually an exophytic, oval or round, well-marginated, and hypovascular mass on CT and MRI.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Magnetic Resonance Imaging. Pancreatic Neoplasms / pathology. Tomography, X-Ray Computed

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  • (PMID = 15671372.001).
  • [ISSN] 0361-803X
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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22. 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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23. Kebir FZ, Lahmar A, Arfa N, Manai S, El Ouaer MA, Bouraoui S, Gouttalier C, Mezabi-Regaya S: Acinar cell carcinoma of the pancreas in a young patient with chronic pancreatitis. Hepatobiliary Pancreat Dis Int; 2010 Feb;9(1):103-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinar cell carcinoma of the pancreas in a young patient with chronic pancreatitis.
  • BACKGROUND: Acinar cell carcinoma (ACC) is a rare malignancy of the pancreas arising from acinar cells.
  • Unlike ductal adenocarcinoma, this tumor rarely presents with pancreatitis.
  • METHODS: We present a case of ACC associated with chronic calcifying pancreatitis, and a review of the literature focusing on diagnosis and management.
  • CONCLUSIONS: The clinical presentation of ACC of the pancreas is not specific and the tumor can be under-diagnosed when associated with chronic pancreatitis.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Neoplasms / diagnosis. Pancreatitis, Chronic / complications

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  • (PMID = 20133240.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
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24. 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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25. Radhi J, Tse F, Marcaccio M: Papillocystic variant of acinar cell pancreatic carcinoma. J Oncol; 2010;2010:242016

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

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  • [Cites] Gastroenterology. 2004 May;126(5):1330-6 [15131794.001]
  • [Cites] Cancer Imaging. 2006;6:60-71 [16861136.001]
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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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26. 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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27. Wargo JA, Warshaw AL: Surgical approach to pancreatic exocrine neoplasms. Minerva Chir; 2005 Dec;60(6):445-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surgical approach to pancreatic exocrine neoplasms.
  • Pancreatic exocrine neoplasms represent a wide spectrum of pathophysiologic entities that challenge us as surgeons.
  • In this review, we will explore the contemporary clinical management of pancreatic adenocarcinoma, acinar cell carcinoma, and cystic neoplasms of the pancreas.
  • [MeSH-major] Pancreas, Exocrine / surgery. Pancreatectomy. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adenocarcinoma / surgery. Algorithms. Carcinoma, Acinar Cell / surgery. Chemotherapy, Adjuvant. Cystadenocarcinoma / surgery. Cystadenoma / surgery. Decision Trees. Humans. Magnetic Resonance Imaging. Neoadjuvant Therapy / methods. Neoplasm Staging. Radiotherapy, Adjuvant. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 16401999.001).
  • [ISSN] 0026-4733
  • [Journal-full-title] Minerva chirurgica
  • [ISO-abbreviation] Minerva Chir
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 181
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28. Illyés G, Luczay A, Benyó G, Kálmán A, Borka K, Köves K, Rácz K, Tulassay T, Schaff Z: Cushing's syndrome in a child with pancreatic acinar cell carcinoma. Endocr Pathol; 2007;18(2):95-102
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cushing's syndrome in a child with pancreatic acinar cell carcinoma.
  • A case of pancreatic acinar cell tumor (ACC) is presented in a 10-year-old boy.
  • Biopsy of the mass showed a solid, poorly differentiated ACC of the pancreas.
  • [MeSH-major] Carcinoma, Acinar Cell / complications. Cushing Syndrome / etiology. Pancreatic Neoplasms / complications


29. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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30. Seki Y, Okusaka T, Ikeda M, Morizane C, Ueno H: Four cases of pancreatic acinar cell carcinoma treated with gemcitabine or S-1 as a single agent. Jpn J Clin Oncol; 2009 Nov;39(11):751-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Four cases of pancreatic acinar cell carcinoma treated with gemcitabine or S-1 as a single agent.
  • Pancreatic acinar cell carcinoma (ACC) is a comparatively rare tumor and account for approximately 1% of all cases of pancreatic cancer.
  • 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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31. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acinar cell carcinoma of the pancreas: 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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32. Antonello D, Gobbo S, Corbo V, Sipos B, Lemoine NR, Scarpa A: Update on the molecular pathogenesis of pancreatic tumors other than common ductal adenocarcinoma. Pancreatology; 2009;9(1-2):25-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Update on the molecular pathogenesis of pancreatic tumors other than common ductal adenocarcinoma.
  • PURPOSE: Although ductal adenocarcinoma is the most common and well known pancreatic tumor type, other distinct epithelial neoplasms affecting the pancreas that show different symptoms, biological behaviors and outcomes are becoming more frequently recognized and documented.
  • Pancreatic epithelial tumors may be separated into ductal and nonductal neoplasms.
  • The former group includes pancreatic ductal adenocarcinoma, intraductal papillary-mucinous tumor, mucinous cystic tumor and serous cystic tumor.
  • The latter group includes pancreatic endocrine tumor, pancreatic acinar cell carcinoma, pancreatoblastoma and solid-pseudopapillary tumor.
  • The aim of this review is to summarize recently acquired knowledge regarding the molecular characterization of these uncommon pancreatic epithelial neoplasms.
  • RECENT FINDINGS: Molecular studies of uncommon pancreatic epithelial tumors suggest that the different morphological entities are associated with distinct molecular profiles, highlighting the involvement of different molecular pathways leading to the development of each subtype of pancreatic neoplasm.
  • CONCLUSION: The correct classification of rare pancreatic epithelial tumors and the identification of their characteristic molecular aspects is the fundamental starting point in identifying novel diagnostic molecular tools and new targets for innovative therapeutic strategies.
  • [MeSH-major] Pancreatic Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adenocarcinoma, Mucinous / genetics. Adenocarcinoma, Mucinous / pathology. Carcinoma, Acinar Cell / genetics. Carcinoma, Acinar Cell / pathology. Cystadenoma, Mucinous / genetics. Cystadenoma, Mucinous / pathology. Humans

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  • [Copyright] Copyright 2008 S. Karger AG, Basel and IAP.
  • (PMID = 19077452.001).
  • [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] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 120
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33. Lee JH, Lee KG, Park HK, Lee KS: [Acinar cell carcinoma of the pancreas in Korea--clinicopathologic analysis of 27 patients from korean literature and 2 cases from our hospital--]. Korean J Gastroenterol; 2010 Apr;55(4):245-51
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  • [Title] [Acinar cell carcinoma of the pancreas in Korea--clinicopathologic analysis of 27 patients from korean literature and 2 cases from our hospital--].
  • BACKGROUND/AIMS: Acinar cell carcinoma (ACC) of the pancreas is a rare malignancy.
  • ACC has been considered a cancer with poor prognosis due to frequent metastasis, a high recurrence rate, and low resectability.
  • RESULTS: ACC was more common in male, and age at diagnosis ranged from 25 to 68 years (median 54).
  • Liver was most common organ of metastasis at diagnosis and recurrence after operation.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 20389178.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 22
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34. Sanati S, Watson MA, Salavaggione AL, Humphrey PA: Gene expression profiles of ductal versus acinar adenocarcinoma of the prostate. Mod Pathol; 2009 Oct;22(10):1273-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression profiles of ductal versus acinar adenocarcinoma of the prostate.
  • Ductal adenocarcinoma is an uncommon variant of prostatic adenocarcinoma with a generally more aggressive clinical course than usual acinar adenocarcinoma.
  • However, the molecular distinction between ductal and acinar adenocarcinomas is not well characterized.
  • The aim of this investigation was to evaluate the relatedness of ductal versus acinar prostatic adenocarcinoma by comparative gene expression profiling.
  • Archived, de-identified, snap frozen tumor tissue from 5 ductal adenocarcinomas, 3 mixed ductal-acinar adenocarcinomas, and 11 acinar adenocarcinomas cases were analyzed.
  • All cases of acinar and ductal adenocarcinomas were matched by Gleason grade.
  • RNA from whole tissue sections of the 5 ductal and 11 acinar adenocarcinomas cases were subjected to gene expression profiling on Affymetrix U133Plus2 microarrays.
  • Independently, laser-capture microdissection was also performed on the three mixed ductal-acinar cases and five pure acinar cases to isolate homogeneous populations of ductal and acinar carcinoma cells from the same tumor.
  • Seven of these laser-capture microdissected samples (three ductal and four acinar cell populations) were similarly analyzed on U133Plus2 arrays.
  • Analysis of data from whole sections of ductal and acinar carcinomas identified only 25 gene transcripts whose expression was significantly and at least two-fold different between ductal and acinar adenocarcinomas.
  • A similar analysis of microdissected cell populations identified 10 transcripts, including the prolactin receptor, with more significant differences in expression of 5- to 27-fold between ductal and acinar adenocarcinomas cells.
  • Overexpression of prolactin receptor protein in ductal versus acinar adenocarcinoma was confirmed by immunohistochemistry in an independent set of tumors.
  • We conclude that ductal and acinar adenocarcinomas of the prostate are strikingly similar at the level of gene expression.
  • However, several of the genes identified in this study, including the prolactin receptor, represent targets for further investigations on the molecular basis for histomorphological and clinical behavioral differences between acinar and ductal adenocarcinomas.
  • [MeSH-major] Biomarkers, Tumor / genetics. Carcinoma, Acinar Cell / genetics. Carcinoma, Ductal / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Pancreatic Neoplasms / genetics

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  • (PMID = 19633648.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / Receptors, Prolactin
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35. 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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36. Poelman SM, Nguyen K: Pancreatic panniculitis associated with acinar cell pancreatic carcinoma. J Cutan Med Surg; 2008 Jan-Feb;12(1):38-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic panniculitis associated with acinar cell pancreatic carcinoma.
  • BACKGROUND: Pancreatic panniculitis is a rare entity, occurring in less than 2% of patients with pancreatic disorders.
  • Skin manifestations may precede the diagnosis of a pancreatic disease by many months.
  • When treatable, correction of the underlying pancreatic disorder may lead to prompt resolution of the panniculitis.
  • OBJECTIVE: We present the case of a 74-year-old-man with a history of chronic pancreatitis who presented with an acute onset of tender, nonulcerating nodules.
  • The clinical and histologic features of pancreatic panniculitis are discussed, with a brief review of the differential diagnosis and clinical approach to panniculitis.
  • CONCLUSIONS: Pancreatic panniculitis is a recognizable clinical entity with characteristic histologic features that may resolve with treatment of the underlying pancreatic disorder.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Diseases / diagnosis. Pancreatic Neoplasms / diagnosis. Panniculitis / diagnosis
  • [MeSH-minor] Aged. Algorithms. Diagnosis, Differential. Fatal Outcome. Humans. Leg. Male

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  • (PMID = 18258147.001).
  • [ISSN] 1203-4754
  • [Journal-full-title] Journal of cutaneous medicine and surgery
  • [ISO-abbreviation] J Cutan Med Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 31
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37. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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38. 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


39. Habbe N, Shi G, Meguid RA, Fendrich V, Esni F, Chen H, Feldmann G, Stoffers DA, Konieczny SF, Leach SD, Maitra A: Spontaneous induction of murine pancreatic intraepithelial neoplasia (mPanIN) by acinar cell targeting of oncogenic Kras in adult mice. Proc Natl Acad Sci U S A; 2008 Dec 2;105(48):18913-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spontaneous induction of murine pancreatic intraepithelial neoplasia (mPanIN) by acinar cell targeting of oncogenic Kras in adult mice.
  • Pancreatic ductal adenocarcinoma (PDAC) is believed to arise through a multistep model comprised of putative precursor lesions known as pancreatic intraepithelial neoplasia (PanIN).
  • The most faithful genetic models activate an oncogenic Kras(G12D) knockin allele within the pdx1- or ptf1a/p48-expression domain of the entire pancreatic anlage during development, thus obscuring the putative cell(s)-of-origin from which subsequent mPanIN lesions arise.
  • In our study, activation of this knockin Kras(G12D) allele in the Elastase- and Mist1-expressing mature acinar compartment of adult mice resulted in the spontaneous induction of mPanIN lesions of all histological grades, although invasive carcinomas per se were not seen.
  • We observed no requirement for concomitant chronic exocrine injury in the induction of mPanIN lesions from the mature acinar cell compartment.
  • The acinar cell derivation of the mPanINs was established through lineage tracing in reporter mice, and by microdissection of lesional tissue demonstrating Cre-mediated recombination events.
  • In contrast to the uniformly penetrant mPanIN phenotype observed following developmental activation of Kras(G12D) in the Pdx1-expressing progenitor cells, the Pdx1-expressing population in the mature pancreas (predominantly islet beta cells) appears to be relatively resistant to the effects of oncogenic Kras.
  • We conclude that in the appropriate genetic context, the differentiated acinar cell compartment in adult mice retains its susceptibility for spontaneous transformation into mPanIN lesions, a finding with potential relevance vis-à-vis the origins of PDAC.

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  • (PMID = 19028870.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK56211; United States / NIDDK NIH HHS / DK / R21 DK072532-01; United States / NCI NIH HHS / CA / R01 CA113669-02; United States / NIDDK NIH HHS / DK / R21 DK072532-02; United States / NCI NIH HHS / CA / R01 CA113669-01; United States / NCI NIH HHS / CA / CA113669-02; United States / NCI NIH HHS / CA / CA113669-04; United States / NIDDK NIH HHS / DK / DK072532-01; United States / NCI NIH HHS / CA / CA113669-03; United States / NCI NIH HHS / CA / CA113669; United States / NIDDK NIH HHS / DK / DK55489; United States / NIDDK NIH HHS / DK / DK072532; United States / NIDDK NIH HHS / DK / R01 DK055489-11A1; United States / NIDDK NIH HHS / DK / R01 DK055489; United States / NCI NIH HHS / CA / R01 CA124586-04; United States / NCI NIH HHS / CA / R01 CA113669-05; United States / NIDDK NIH HHS / DK / DK61215; United States / NIDDK NIH HHS / DK / R21 DK072532; United States / NIDDK NIH HHS / DK / R01 DK061215; United States / NCI NIH HHS / CA / R01 CA113669-03; United States / NCI NIH HHS / CA / CA124586-04; United States / NIDDK NIH HHS / DK / T32 DK007713; United States / NCI NIH HHS / CA / R01 CA124586; United States / NIDDK NIH HHS / DK / T32DK007713; United States / NCI NIH HHS / CA / CA124586; United States / NIDDK NIH HHS / DK / DK055489-11A1; United States / NCI NIH HHS / CA / R01 CA113669; United States / NIDDK NIH HHS / DK / R01 DK056211; United States / NCI NIH HHS / CA / R01 CA113669-04; United States / NCI NIH HHS / CA / CA113669-05; United States / NIDDK NIH HHS / DK / DK072532-02; United States / NCI NIH HHS / CA / CA113669-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Notch; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ PMC2596215
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40. 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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41. Shi G, Zhu L, Sun Y, Bettencourt R, Damsz B, Hruban RH, Konieczny SF: Loss of the acinar-restricted transcription factor Mist1 accelerates Kras-induced pancreatic intraepithelial neoplasia. Gastroenterology; 2009 Apr;136(4):1368-78
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  • [Title] Loss of the acinar-restricted transcription factor Mist1 accelerates Kras-induced pancreatic intraepithelial neoplasia.
  • BACKGROUND & AIMS: Invasive pancreatic ductal adenocarcinoma is thought to originate from duct-like lesions called pancreatic intraepithelial neoplasia (PanIN).
  • METHODS: In this study, we examined the importance of the acinar-restricted transcription factor Mist1 to KrasG12D-induced mouse PanIN (mPanIN) formation in 3 different mouse models of pancreatic cancer.
  • RESULTS: In the absence of Mist1 (Mist1KO), KrasG12D-expressing mice exhibited severe exocrine pancreatic defects that were rescued by ectopic expression of Mist1 in acinar cells. mPanIN development was greatly accelerated in Mist1KO/KrasG12D/+ pancreata, and in vitro assays revealed that Mist1KO acinar cells were predisposed to convert to a ductal phenotype and activate epidermal growth factor receptor (EGFR) and Notch-signaling pathways.
  • CONCLUSIONS: We propose that convergence of EGFR, Notch, and Kras pathways in acinar cells lacking Mist1 leads to enhanced mPanIN formation.

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  • (PMID = 19249398.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK055489-10; United States / NCI NIH HHS / CA / P50CA62924; United States / NCI NIH HHS / CA / R01 CA124586-02; United States / NCI NIH HHS / CA / P50 CA062924; United States / NIDDK NIH HHS / DK / DK055489-10; United States / NCI NIH HHS / CA / CA124586-02; United States / NIDDK NIH HHS / DK / DK55489; United States / NIDDK NIH HHS / DK / R01 DK055489; United States / NCI NIH HHS / CA / R01 CA124586; United States / NCI NIH HHS / CA / CA124586
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Mist1 protein, mouse; 0 / Receptors, Notch; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ NIHMS182460; NLM/ PMC2845927
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42. La Rosa S, Franzi F, Marchet S, Finzi G, Clerici M, Vigetti D, Chiaravalli AM, Sessa F, Capella C: The monoclonal anti-BCL10 antibody (clone 331.1) is a sensitive and specific marker of pancreatic acinar cell carcinoma and pancreatic metaplasia. Virchows Arch; 2009 Feb;454(2):133-42
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  • [Title] The monoclonal anti-BCL10 antibody (clone 331.1) is a sensitive and specific marker of pancreatic acinar cell carcinoma and pancreatic metaplasia.
  • Acinar cell carcinoma (ACC) is a rare pancreatic cancer which may be difficult to distinguish from other solid nonadenocarcinoma tumors.
  • The diagnosis depends on the demonstration of acinar differentiation, obtained with antibodies recognizing various pancreatic enzymes that, although specific, show different sensitivity.
  • The C-terminal portion of the BCL10 protein shows homology with carboxyl ester hydrolase (CEH), an enzyme produced by pancreatic acinar cells.
  • We investigated the usefulness of a C-terminal BCL10 monoclonal antibody in the diagnosis of ACCs.
  • We examined normal pancreases and different pancreatic tumors including ACCs, mixed acinar-endocrine carcinomas, ductal adenocarcinomas, mucinous, serous, solid pseudopapillary, and endocrine neoplasms.
  • In addition, various normal tissues and cases of pancreatic metaplasia of the gastroesophageal mucosa, cases of ectopic pancreas, gastrointestinal endocrine tumors, salivary and breast acinic cell carcinomas, gastric adenocarcinomas with and without acinar differentiation, and hepatocellular carcinomas were studied.
  • BCL10 immunoreactivity paralleled that of CEH and was restricted to acinar cells of normal and ectopic pancreas, of pancreatic metaplasia, and of ACCs.
  • The anti-BCL10 antibody was more sensitive in detecting ACCs and pancreatic metaplasia than antibodies directed against other pancreatic enzymes.
  • We suggest using BCL10 antibody for diagnosing pancreatic tumors and whenever an acinar differentiation is suspected in gastrointestinal neoplastic and metaplastic lesions.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / analysis. Antibodies, Monoclonal / immunology. Biomarkers, Tumor / analysis. Carcinoma, Acinar Cell / diagnosis. Pancreas / pathology. Pancreatic Neoplasms / diagnosis

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  • (PMID = 19066953.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antibodies, Monoclonal; 0 / BCL10 protein, human; 0 / Biomarkers, Tumor; EC 3.1.1.1 / Carboxylesterase
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43. Sorscher SM: Metastatic acinar cell carcinoma of the pancreas responding to gemcitabine, 5-fluorouracil and leucovorin therapy: a case report. Eur J Cancer Care (Engl); 2009 May;18(3):318-9
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  • [Title] Metastatic acinar cell carcinoma of the pancreas responding to gemcitabine, 5-fluorouracil and leucovorin therapy: a case report.
  • Acinar cell carcinoma of the pancreas is rare tumour with a generally poor prognosis.
  • In this case report, a patient with metastatic acinar cell carcinoma in the liver developed progressive disease after cisplatin/etoposide and then had progressive disease after weekly paclitaxel chemotherapy.
  • This case represents the first reported metastatic acinar cell carcinoma responding to this regimen.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Liver Neoplasms / drug therapy. Pancreatic Neoplasms

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  • (PMID = 19445023.001).
  • [ISSN] 1365-2354
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; 12001-76-2 / Vitamin B Complex; B76N6SBZ8R / gemcitabine; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
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44. Shi C, Hong SM, Lim P, Kamiyama H, Khan M, Anders RA, Goggins M, Hruban RH, Eshleman JR: KRAS2 mutations in human pancreatic acinar-ductal metaplastic lesions are limited to those with PanIN: implications for the human pancreatic cancer cell of origin. Mol Cancer Res; 2009 Feb;7(2):230-6
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  • [Title] KRAS2 mutations in human pancreatic acinar-ductal metaplastic lesions are limited to those with PanIN: implications for the human pancreatic cancer cell of origin.
  • Pancreatic intraepithelial neoplasia (PanIN) is a precursor to invasive ductal adenocarcinoma of the pancreas.
  • Observations made in genetically engineered mouse models suggest that the acinar/centroacinar compartment can give rise to ductal neoplasia.
  • To integrate findings in mice and men, we examined human acinar cells, acinar-ductal metaplasia (ADM) lesions, and PanINs for KRAS2 gene mutations.
  • Stromal cells, acinar cells, ADMs, and PanINs were separately isolated using laser capture microdissection.
  • Twelve of these 31 foci of ADM occurred in isolation, whereas 19 were in the same lobules as a PanIN lesion.
  • All 31 microdissected foci of acinar cells were KRAS2 gene wild-type, as were all 12 isolated ADM lesions lacking an associated PanIN.
  • Ductal neoplasms of the human pancreas, as defined by KRAS2 gene mutations, do not appear to arise from acinar cells.

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  • (PMID = 19208745.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / P50 CA062924-15; United States / NCI NIH HHS / CA / CA62924
  • [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 / DNA, Neoplasm; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS89589; NLM/ PMC2708114
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45. Logsdon CD, Ji B: Ras activity in acinar cells links chronic pancreatitis and pancreatic cancer. Clin Gastroenterol Hepatol; 2009 Nov;7(11 Suppl):S40-3
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  • [Title] Ras activity in acinar cells links chronic pancreatitis and pancreatic cancer.
  • The relationship between chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC) is unclear.
  • However, we have recently found that excessive activity within the Ras signaling pathway can lead to acinar cell death or metaplasia and is associated with the development of fibrosis resembling CP and the development of PDAC from acinar cells through the full complement of preneoplastic (pancreatic intraepithelial neoplasia) lesions.

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  • (PMID = 19896097.001).
  • [ISSN] 1542-7714
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK052067-11; United States / NCI NIH HHS / CA / P30 CA016672; United States / NIDDK NIH HHS / DK / R21 DK068414; United States / NCI NIH HHS / CA / CA16672; United States / NIDDK NIH HHS / DK / R01 DK052067; United States / NIDDK NIH HHS / DK / R01 DK052067-11; United States / NIDDK NIH HHS / DK / 5R21DK068414; United States / NCI NIH HHS / CA / P20 CA101936; United States / NIAAA NIH HHS / AA / R01 AA020822; United States / NIDDK NIH HHS / DK / DK052067
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 46
  • [Other-IDs] NLM/ NIHMS268542; NLM/ PMC3050544
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46. Dewald GW, Smyrk TC, Thorland EC, McWilliams RR, Van Dyke DL, Keefe JG, Belongie KJ, Smoley SA, Knutson DL, Fink SR, Wiktor AE, Petersen GM: Fluorescence in situ hybridization to visualize genetic abnormalities in interphase cells of acinar cell carcinoma, ductal adenocarcinoma, and islet cell carcinoma of the pancreas. Mayo Clin Proc; 2009 Sep;84(9):801-10
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  • [Title] Fluorescence in situ hybridization to visualize genetic abnormalities in interphase cells of acinar cell carcinoma, ductal adenocarcinoma, and islet cell carcinoma of the pancreas.
  • OBJECTIVE: To use fluorescence in situ hybridization (FISH) to visualize genetic abnormalities in interphase cell nuclei (interphase FISH) of acinar cell carcinoma, ductal adenocarcinoma, and islet cell carcinoma of the pancreas.
  • PATIENTS AND METHODS: Between April 4, 2007, and December 4, 2008, interphase FISH was used to study paraffin-embedded preparations of tissue obtained from 18 patients listed in the Mayo Clinic Biospecimen Resource for Pancreas Research with a confirmed diagnosis of acinar cell carcinoma, ductal adenocarcinoma, islet cell carcinoma, or pancreas without evidence of neoplasia.
  • RESULTS: FISH abnormalities were observed in 12 (80%) of 15 patients with pancreatic cancer: 5 of 5 patients with acinar cell carcinoma, 5 of 5 patients with ductal adenocarcinoma, and 2 (40%) of 5 patients with islet cell carcinoma.
  • All 3 specimens of pancreatic tissue without neoplasia had normal FISH results.
  • Gains of CTNNB1 due to trisomy 3 occurred in each tumor with acinar cell carcinoma but in none of the other tumors in this study.
  • FISH abnormalities of all other cancer genes studied were observed in all forms of pancreatic tumors in this investigation.
  • CONCLUSION: FISH abnormalities of CTNNB1 due to trisomy 3 were observed only in acinar cell carcinoma.
  • FISH abnormalities of genes implicated in familial cancer, tumor progression, and the 5-fluorouracil pathway were common but were not associated with specific types of pancreatic cancer.

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  • (PMID = 19720778.001).
  • [ISSN] 1942-5546
  • [Journal-full-title] Mayo Clinic proceedings
  • [ISO-abbreviation] Mayo Clin. Proc.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA102701; United States / NCI NIH HHS / CA / P50 CA102701-07; United States / NCI NIH HHS / CA / R01 CA097075; United States / NCI NIH HHS / CA / R01 CA97075
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2735430
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47. Cao D, Maitra A, Saavedra JA, Klimstra DS, Adsay NV, Hruban RH: Expression of novel markers of pancreatic ductal adenocarcinoma in pancreatic nonductal neoplasms: additional evidence of different genetic pathways. Mod Pathol; 2005 Jun;18(6):752-61
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  • [Title] Expression of novel markers of pancreatic ductal adenocarcinoma in pancreatic nonductal neoplasms: additional evidence of different genetic pathways.
  • Solid pseudopapillary tumor, pancreatoblastoma, undifferentiated carcinoma with osteoclastic-like giant cells, and acinar cell carcinomas are rare pancreatic nonductal neoplasms.
  • Compared to the significant advances in our understanding of the pathogenesis of pancreatic ductal adenocarcinomas in the last decades, the molecular mechanisms underlying pancreatic nonductal neoplasms are poorly understood.
  • In order to elucidate their molecular pathogenesis, we constructed tissue microarrays to study the expression of some novel pancreatic ductal adenocarcinoma-associated tumor markers in these nonductal pancreatic neoplasms.
  • We analyzed nine markers including tumor suppressor gene (14-3-3 sigma), proliferation marker (topoisomerase II alpha), epithelial markers (prostate stem cell antigen, mesothelin and cytokeratin 19), stromal markers (fascin, hsp47 and fibronectin), and gamma-synuclein whose function is not delineated.
  • In addition, we included tumor suppressor gene DPC4 and oncogene Beta-catenin to further confirm their expression in pancreatic nonductal tumors.
  • Our results showed that in contrast to pancreatic ductal adenocarcinomas that show loss of Dpc4 protein in 55% of cases, loss of Dpc4 expression is absent in pancreatic nonductal neoplasms.
  • Expression of 14-3-3 sigma is frequently seen in both pancreatic nonductal neoplasms (25-100%) and ductal adenocarcinomas (89%).
  • Aberrant nuclear expression of beta-catenin is common in pancreatic nonductal neoplasms, specifically in solid pseudopapillary tumors (88%) and pancreatoblastomas (100%) but is rarely seen in pancreatic ductal adenocarcinomas (<5%).
  • Expression of topoisomerase II alpha is not seen in solid pseudopapillary tumors and undifferentiated carcinomas with osteoclastic-like giant cells but is focally seen in pancreatoblastomas (50%) and acinar cell carcinomas (85%).
  • Expression of PSCA and mesothelin was observed in pancreatic nonductal neoplasms but their expression was seen less frequently (0-50%) and weaker than that in pancreatic ductal adenocarcinomas (60-100%).
  • CK19, a marker of pancreatic ductal adenocarcinomas, is not expressed in pancreatic nonductal neoplasms.
  • Our findings indicate pancreatic nonductal neoplasms have distinctive patterns of protein expression relative to pancreatic ductal adenocarcinomas and suggest that pancreatic nonductal neoplasms have different genetic pathways from the more common pancreatic ductal adenocarcinomas.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] 14-3-3 Proteins. Antigens, Neoplasm. Carcinoma, Acinar Cell / metabolism. Carcinoma, Acinar Cell / pathology. Carrier Proteins / analysis. Cytoskeletal Proteins / analysis. DNA-Binding Proteins / analysis. Exonucleases / analysis. Exoribonucleases. Fibronectins / analysis. GPI-Linked Proteins. HSP47 Heat-Shock Proteins. Heat-Shock Proteins / analysis. Humans. Immunohistochemistry. Keratins / analysis. Membrane Glycoproteins / analysis. Microfilament Proteins / analysis. Neoplasm Proteins / analysis. Nerve Tissue Proteins / analysis. Serpins / analysis. Smad4 Protein. Synucleins. Trans-Activators / analysis. beta Catenin. gamma-Synuclein

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  • (PMID = 15696124.001).
  • [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
  • [Grant] 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; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 14-3-3 Proteins; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Carrier Proteins; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Fibronectins; 0 / GPI-Linked Proteins; 0 / HSP47 Heat-Shock Proteins; 0 / Heat-Shock Proteins; 0 / Membrane Glycoproteins; 0 / Microfilament Proteins; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / PSCA protein, human; 0 / SERPINH1 protein, human; 0 / SMAD4 protein, human; 0 / Serpins; 0 / Smad4 Protein; 0 / Synucleins; 0 / Trans-Activators; 0 / beta Catenin; 0 / gamma-Synuclein; 0 / mesothelin; 146808-54-0 / fascin; 68238-35-7 / Keratins; EC 3.1.- / Exonucleases; EC 3.1.- / Exoribonucleases; EC 3.1.- / SFN protein, human
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48. 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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49. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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50. Wang Y, Xie SL, Wang CF, Liu SM, Shan Y, Zhao DB, Liu Q, Luo W, Zhao P: [Clinical and pathological analysis of 114 cases with non-ductal pancreatic adenocarcinoma occupying lesions]. Zhonghua Yi Xue Za Zhi; 2010 Apr 27;90(16):1089-92
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  • [Title] [Clinical and pathological analysis of 114 cases with non-ductal pancreatic adenocarcinoma occupying lesions].
  • OBJECTIVE: To improve the diagnosis and treatment of non-ductal pancreatic adenocarcinoma-occupying lesions.
  • METHODS: A retrospective analysis was made for 114 cases of pancreatic non-ductal adenocarcinoma-occupying pathologically confirmed lesions. RESULTS:.
  • (4) pancreaticoduodenectomy was performed in 26 patients, distal pancreatectomy in 53, tumor enucleation in 15, segmental pancreatectomy in 9, partial resection in 3, duodenum-preserving pancreatic head resection in 1 and palliative surgery (either cholecystojejunostomy anastomosis or gastrojejunostomy) in 7;.
  • (5) pathologic analysis revealed 35 solid pseudopapillary neoplasm of pancreas, 28 pancreatic endocrine tumors, 18 focal chronic pancreatitis, 11 serous cystic neoplasms, 9 mucinous cystic neoplasms, 4 pancreatic cysts, 3 acinar cell carcinomas, 2 pancreatic cavernous hemangiomas, 1 sarcoma of pancreas, 1 sarcomatoid carcinoma of pancreas, 1 pancreatic schwannoma and 1 pancreatic neuroblastoma.
  • CONCLUSION: The non-ductal pancreatic adenocarcinoma-occupying lesions have no specific clinical presentation or serum tumor marker.
  • [MeSH-major] Pancreatic Neoplasms / pathology

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  • (PMID = 20646423.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen
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51. Fukushima N, Koopmann J, Sato N, Prasad N, Carvalho R, Leach SD, Hruban RH, Goggins M: Gene expression alterations in the non-neoplastic parenchyma adjacent to infiltrating pancreatic ductal adenocarcinoma. Mod Pathol; 2005 Jun;18(6):779-87
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  • [Title] Gene expression alterations in the non-neoplastic parenchyma adjacent to infiltrating pancreatic ductal adenocarcinoma.
  • The non-neoplastic pancreatic parenchyma adjacent to infiltrating ductal adenocarcinoma demonstrates inflammation, fibrosis, acinar cell loss and small duct-like metaplasia of acinar cells.
  • To better understand the pancreatic acinar responses to infiltrating pancreatic ductal adenocarcinoma, we characterized gene expression patterns of pancreatic acinar tissue adjacent to infiltrating pancreatic ductal adenocarcinomas and compared them to gene expression patterns of acinar tissue affected by chronic pancreatitis as well as to those of normal pancreatic acini.
  • Fresh-frozen pancreatic acinar tissue was microdissected from nine patients (three with pancreatic cancer, three with chronic pancreatitis, three with normal pancreata) using laser capture microdissection, and extracted RNA from each microdissection was subjected to two rounds of linear amplification and hybridized to oligonucleotide microarrays.
  • A total of 20 genes was found to be overexpressed in peritumoral acinar tissue compared to normal acinar tissue and to acini affected by chronic pancreatitis.
  • These 20 genes included pancreatitis-associated protein (HIP/PAP), a gene known to be overexpressed in acini adjacent to infiltrating pancreatic cancer, and the gene cartilage glycoprotein-39 (HC gp-39 or TKL-40).
  • Serum HC gp-39 protein levels were significantly higher in patients with pancreatic cancer and in those with chronic pancreatitis than in controls without pancreatic disease.
  • There was no significant difference in the levels of serum HC gp-39 in patients with pancreatic cancer and those with chronic pancreatitis.
  • Our results demonstrate some of the molecular alterations in acinar cells that occur in response to adjacent infiltrating pancreatic ductal adenocarcinoma and reveal that such alterations can provide a rich source of markers of pancreatic cancer.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / pathology. Gene Expression Profiling. Pancreas / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 15791284.001).
  • [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
  • [Grant] 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; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adipokines; 0 / CHI3L1 protein, human; 0 / Glycoproteins; 0 / Lectins; 0 / RNA, Neoplasm
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52. 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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53. 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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54. Tanaka H, Fukamachi K, Futakuchi M, Alexander DB, Long N, Tamamushi S, Minami K, Seino S, Ohara H, Joh T, Tsuda H: Mature acinar cells are refractory to carcinoma development by targeted activation of Ras oncogene in adult rats. Cancer Sci; 2010 Feb;101(2):341-6
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  • [Title] Mature acinar cells are refractory to carcinoma development by targeted activation of Ras oncogene in adult rats.
  • Pancreatic ductal adenocarcinoma (PDA) is one of the most debilitating malignancies in humans.
  • When adenovirus with Cre recombinase under the control of the CMV enhancer/chicken beta-actin (CAG) promoter (Ad-CAG-Cre) is injected into the pancreatic duct of these animals, pancreatic neoplasias develop.
  • Pathologically, the origin of these lesions is duct, intercalated duct, and centroacinar cells, but not acinar cells.
  • The present study was undertaken to test the effect of acinar cell-specific oncogenic ras expression.
  • Adult transgenic rats were injected with adenovirus with Cre recombinase under the control of the acinar cell-specific promoters amylase (Ad-Amy-Cre) and elastase-1 (Ad-Ela-Cre) or under the control of the non-specific CAG promoter.
  • Injection of either Ad-Amy-Cre or Ad-Ela-Cre into the pancreatic ducts of transgenic animals in which oncogenic Kras is tagged with hemagglutinin (HA), HA-Kras(G12V) rats resulted in expression of oncogenic ras in acinar cells but not in duct, intercalated duct, or centroacinar cells.
  • In marked contrast, injection of Ad-CAG-Cre resulted in pancreatic cancer development within 4 weeks.
  • These results indicate that adult acinar cells are refractory to Ras oncogene activation and do not develop neoplasia in this model.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / etiology. Genes, ras. Pancreas, Exocrine / pathology. Pancreatic Neoplasms / etiology

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  • (PMID = 19917056.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
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55. Vakiani E, Young RH, Carcangiu ML, Klimstra DS: Acinar cell carcinoma of the pancreas metastatic to the ovary: a report of 4 cases. Am J Surg Pathol; 2008 Oct;32(10):1540-5
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  • [Title] Acinar cell carcinoma of the pancreas metastatic to the ovary: a report of 4 cases.
  • We report 4 cases of acinar cell carcinoma of the pancreas, 3 presenting as metastases in the ovary, the first report of this circumstance, which may pose a broad differential diagnosis and caused significant diagnostic difficulty in all the cases.
  • In 3 cases, the ovarian tumors were detected before the pancreatic tumor; in 1 case, a large abdominal mass and ovarian tumors were discovered synchronously.
  • Two cases had a predominant acinar growth pattern of cells with brightly eosinophilic, granular cytoplasm.
  • The main differential diagnostic consideration was well-differentiated neuroendocrine neoplasm (carcinoid tumor); positive immunostaining with antibodies against chymotrypsin and trypsin and negative immunostaining with antibodies against synaptophysin and chromogranin helped exclude this diagnosis.
  • We observed focal alpha-inhibin immunostaining in 2 cases, which may represent a potential diagnostic pitfall, as a Sertoli cell tumor or unusual granulosa cell tumor may also enter the differential diagnosis.
  • Inclusion of antibodies against the pancreatic enzymes chymotrypsin and trypsin in the immunohistochemical panel is critical in establishing the correct diagnosis and should be considered when evaluating ovarian tumors with architectural (mainly acinar) and cytologic (granular eosinophilic cytoplasm) characteristics that should bring a metastatic acinar cell carcinoma into consideration.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Ovarian Neoplasms / secondary. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Middle Aged

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  • (PMID = 18724247.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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56. Lipsett MA, Castellarin ML, Rosenberg L: Acinar plasticity: development of a novel in vitro model to study human acinar-to-duct-to-islet differentiation. Pancreas; 2007 May;34(4):452-7
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  • [Title] Acinar plasticity: development of a novel in vitro model to study human acinar-to-duct-to-islet differentiation.
  • OBJECTIVES: The plasticity of pancreatic tissue is demonstrated in many pancreatic diseases.
  • It has previously been shown that pancreatic islet-to-duct transformation and acinoductal metaplasia have been associated with both pancreatic regeneration and adenocarcinoma in various in vivo and in vitro settings.
  • Understanding this inherent morphogenetic plasticity of the adult pancreas could lead to new therapeutic approaches to pancreatic disease.
  • METHODS: Cadaveric human pancreases (n = 7) were digested, and purified acinar tissue, which was approximately 85% immunoreactive for amylase and approximately 15% immunoreactive for CK-19, was embedded in a type 1 collagen matrix and cultured in a differentiation medium (DM) consisting of Dulbecco modified Eagle/F12 medium supplemented with cholera toxin (100 ng/mL), epidermal growth factor (10 ng/mL), and insulin (24 mU/mL) for 8 days.
  • Tissue samples were then analyzed for amylase, cytokeratin 19, pancreas duodenum homeobox 1, and endocrine hormone immunoreactivity as well as dithizione positivity.
  • Addition of INGAP led to an approximately 18-fold increase in pancreas duodenum homeobox 1 immunoreactivity, although without an observed increase in insulin production as measured by dithizone positivity.
  • However, when acinar-derived ductlike structures were cultured with gastrin + HGF + INGAP, the total incidence of dithizone-positive structures increased approximately 6-fold (10.9 +/- 2.9% vs 1.7 +/- 0.4%, P = 0.037).
  • CONCLUSIONS: We have developed a novel in vitro model of adult human acinoductal metaplasia that will aid not only in developing new methods of expanding beta-cell mass but also provide insights into pancreatic carcinogenesis.
  • [MeSH-major] Cell Differentiation. Islets of Langerhans / pathology. Pancreatic Ducts / pathology. Regeneration
  • [MeSH-minor] Adult. Amylases / metabolism. C-Peptide / metabolism. Cell Proliferation. Cells, Cultured. Cytokines / pharmacology. Gastrins / pharmacology. Hepatocyte Growth Factor / pharmacology. Homeodomain Proteins / biosynthesis. Humans. Insulin-Secreting Cells / pathology. Keratin-19 / metabolism. Metaplasia. Pancreas / pathology. Pancreas / physiopathology. Peptide Fragments / pharmacology. Phenotype. Time Factors. Trans-Activators / biosynthesis. Up-Regulation

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  • (PMID = 17446845.001).
  • [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 / C-Peptide; 0 / Cytokines; 0 / Gastrins; 0 / Homeodomain Proteins; 0 / INGAP peptide; 0 / Keratin-19; 0 / Peptide Fragments; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein; 67256-21-7 / Hepatocyte Growth Factor; EC 3.2.1.- / Amylases
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57. Guerra C, Schuhmacher AJ, Cañamero M, Grippo PJ, Verdaguer L, Pérez-Gallego L, Dubus P, Sandgren EP, Barbacid M: Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice. Cancer Cell; 2007 Mar;11(3):291-302
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  • [Title] Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice.
  • Pancreatic ductal adenocarcinoma (PDA), one of the deadliest human cancers, often involves somatic activation of K-Ras oncogenes.
  • We report that selective expression of an endogenous K-Ras(G12V) oncogene in embryonic cells of acinar/centroacinar lineage results in pancreatic intraepithelial neoplasias (PanINs) and invasive PDA, suggesting that PDA originates by differentiation of acinar/centroacinar cells or their precursors into ductal-like cells.
  • [MeSH-major] Carcinoma in Situ / pathology. Carcinoma, Pancreatic Ductal / pathology. Genes, ras. Pancreatic Neoplasms / pathology. Pancreatitis, Chronic / pathology
  • [MeSH-minor] Animals. Cell Lineage. Cell Transformation, Neoplastic. Ceruletide. Doxycycline / pharmacology. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Mice. Mice, Mutant Strains. Mutation. Neoplasm Invasiveness. Pancreas / pathology. Signal Transduction


58. Guo J, Kleeff J, Zhao Y, Li J, Giese T, Esposito I, Büchler MW, Korc M, Friess H: Yes-associated protein (YAP65) in relation to Smad7 expression in human pancreatic ductal adenocarcinoma. Int J Mol Med; 2006 May;17(5):761-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Yes-associated protein (YAP65) in relation to Smad7 expression in human pancreatic ductal adenocarcinoma.
  • Pancreatic ductal adenocarcinoma (PDAC) is characterized by multiple alterations in the TGF-beta signaling pathway.
  • In the present study, the expression of YAP65 in PDAC was analyzed in order to elucidate the potential role of this molecule in the pathogenesis of pancreatic cancer.
  • YAP65 mRNA expression levels in human pancreatic tissue samples and cell lines were analyzed by Northern blotting and quantitative RT-PCR.
  • Enhanced expression of YAP65 mRNA was identified by Northern blotting and quantitative RT-PCR in PDAC in comparison to the normal pancreas (2.5-fold increase) and to chronic pancreatitis (1.3-fold increase).
  • In the normal pancreas, YAP65 was absent in acinar cells, large ducts and islet cells, but exhibited moderate to strong immunoreactivity in centroacinar cells and ductules.
  • In contrast, weak to moderate YAP65 immunoreactivity was present in the cancer cells.
  • There was no correlation between YAP65 immunostaining and Smad7 staining or Smad4 mutations in the cancer samples.
  • In conclusion, YAP65 is expressed mainly in centroacinar and small ductal cells in the normal pancreas.
  • In PDAC, YAP65 is present in tubular complexes and to a lesser extent in cancer cells.
  • Together with the known function of YAP65 in different growth and differentiation regulating pathways, it is suggested that this gene plays a role in the normal and diseased pancreas.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Adenocarcinoma / pathology. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / pathology. Phosphoproteins / genetics. Smad7 Protein / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Blotting, Northern. Blotting, Western. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunohistochemistry. Male. Middle Aged. Mutation. RNA, Messenger / genetics. RNA, Messenger / metabolism. Smad4 Protein / genetics. Transforming Growth Factor beta / pharmacology

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  • (PMID = 16596258.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-75059
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / SMAD4 protein, human; 0 / SMAD7 protein, human; 0 / Smad4 Protein; 0 / Smad7 Protein; 0 / Transforming Growth Factor beta; 0 / YAP1 (Yes-associated) protein, human
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59. Cavallari I, Silic-Benussi M, Rende F, Martines A, Fogar P, Basso D, Vella MD, Pedrazzoli S, Herman JG, Chieco-Bianchi L, Esposito G, Ciminale V, D'Agostino DM: Decreased expression and promoter methylation of the menin tumor suppressor in pancreatic ductal adenocarcinoma. Genes Chromosomes Cancer; 2009 May;48(5):383-96
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  • [Title] Decreased expression and promoter methylation of the menin tumor suppressor in pancreatic ductal adenocarcinoma.
  • Loss of menin, a tumor suppressor coded by the MEN1 gene, is a key factor in the pathogenesis of multiple endocrine neoplasia type I and in a percentage of sporadic endocrine tumors of the pancreas and parathyroid glands.
  • This study investigated expression of the menin protein in the normal exocrine pancreas and in pancreatic ductal adenocarcinoma (PDAC), the most common pancreatic tumor.
  • Immunofluorescence (IF) analyses showed that menin is expressed at high levels in normal acinar and duct cells.
  • IF analyses also revealed low to undetectable menin expression in the PDAC cell lines MiaPaCa-2 and Panc-1.
  • Ectopic expression of menin in these cells resulted in a marked alteration of the cell cycle, with an increase in the G1/S+G2 ratio.
  • These findings represent the first evidence that the MEN1 gene is a target of mutation and methylation in PDAC and that menin influences the cell cycle profile of duct cells.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic. Pancreatic Neoplasms / genetics. Promoter Regions, Genetic. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Aged. Base Sequence. Cell Cycle. Cell Line, Tumor. Epigenesis, Genetic. Female. Fluorescent Antibody Technique. Humans. Loss of Heterozygosity. Male. Middle Aged. Molecular Sequence Data. Multivariate Analysis. Pancreas, Exocrine / cytology. Pancreas, Exocrine / metabolism. Pancreatic Ducts / cytology. Pancreatic Ducts / metabolism. Polymerase Chain Reaction. Proportional Hazards Models

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  • [Copyright] Copyright 2009 Wiley-Liss,Inc.
  • (PMID = 19170121.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins
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60. 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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61. Xu X, Ehdaie B, Ohara N, Yoshino T, Deng CX: Synergistic action of Smad4 and Pten in suppressing pancreatic ductal adenocarcinoma formation in mice. Oncogene; 2010 Feb 4;29(5):674-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synergistic action of Smad4 and Pten in suppressing pancreatic ductal adenocarcinoma formation in mice.
  • Mutations of SMAD4/DPC4 are found in about 60% of human invasive pancreatic ductal adenocarcinomas (PDACs); yet, the manner in which SMAD4 deficiency enhances tumorigenesis remains elusive.
  • Using a Cre-LoxP approach, we generated a mutant mouse carrying a targeted deletion of Smad4 in the pancreas.
  • We showed that the absence of Smad4 alone did not trigger pancreas tumor formation; however, it increased the expression of an inactivated form of Pten, suggesting a role of Pten in preventing Smad4-/- cells from undergoing malignancy.
  • The absence of Smad4 in a Pten-mutant background enhanced cell proliferation and triggered transdifferentiation from acinar, centroacinar and islet cells, accompanied by activation of Notch1 signaling.
  • We showed that all tumors developed in the Smad4/Pten-mutant pancreas exhibited high levels of pAKT and mTOR, and that about 50 and 83% of human pancreatic cancers examined showed increased pAKT and pmTOR, respectively.
  • Besides the similarity in gene expression, the pAKT and/or pmTOR-positive human PDACs and mouse pancreatic tumors also shared some histopathological similarities.
  • These observations indicate that Smad4/Pten-mutant mice mimic the tumor progression of human pancreatic cancers that are driven by activation of the AKT-mTOR pathway, and uncovered a synergistic action of Smad4 and Pten in repressing pancreatic tumorigenesis.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. PTEN Phosphohydrolase / metabolism. Pancreatic Neoplasms / metabolism. Signal Transduction / physiology. Smad4 Protein / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Cell Transdifferentiation / physiology. Gene Expression. Genotype. Humans. Immunohistochemistry. Intracellular Signaling Peptides and Proteins / metabolism. Mice. Mice, Knockout. Phenotype. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. TOR Serine-Threonine Kinases

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  • (PMID = 19901970.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Smad4 Protein; 0 / Smad4 protein, mouse; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
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62. Wang W, Reiser-Erkan C, Michalski CW, Raggi MC, Quan L, Yupei Z, Friess H, Erkan M, Kleeff J: Hypoxia inducible BHLHB2 is a novel and independent prognostic marker in pancreatic ductal adenocarcinoma. Biochem Biophys Res Commun; 2010 Oct 22;401(3):422-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypoxia inducible BHLHB2 is a novel and independent prognostic marker in pancreatic ductal adenocarcinoma.
  • In the present study, the expression, regulation, functions and prognostic impact of BHLHB2 in pancreatic cancer were investigated.
  • METHODS: Expression analyses were carried out in tissues of the normal pancreas (n=10) and pancreatic ductal adenocarcinoma (n=77) as well as in eight pancreatic cancer cell lines using quantitative RT-PCR, semiquantitative immunohistochemistry, and immunoblot analyses.
  • RESULTS: BHLHB2 mRNA and protein expressions were strongly induced by hypoxia and by serum starvation in pancreatic cancer cell lines.
  • Ex vivo, the weak/absent nuclear staining in normal pancreatic ducts and acinar cells was replaced by moderate to strong nuclear/cytoplasmic staining in PanIN lesions and pancreatic cancer cells.
  • CONCLUSIONS: Hypoxia-inducible BHLHB2 expression is a novel independent prognostic marker in pancreatic cancer patients and indicates increased chemosensitivity towards gemcitabine.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Basic Helix-Loop-Helix Transcription Factors / metabolism. Biomarkers, Tumor / metabolism. Carcinoma, Pancreatic Ductal / mortality. Deoxycytidine / analogs & derivatives. Drug Resistance, Neoplasm. Homeodomain Proteins / metabolism. Pancreatic Neoplasms / mortality
  • [MeSH-minor] Aged. Cell Hypoxia. Female. Humans. Male. Pancreas / metabolism. Pancreas / pathology. Prognosis. RNA Interference

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20863812.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / BHLHE40 protein, human; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / Homeodomain Proteins; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
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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. 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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65. 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

  • [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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66. 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.

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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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67. Reuss R, Aberle S, Klingel K, Sauter M, Greschniok A, Franke FE, Padberg W, Blin N: The expression of the carboxyl ester lipase gene in pancreas and pancreatic adenocarcinomas. Int J Oncol; 2006 Sep;29(3):649-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expression of the carboxyl ester lipase gene in pancreas and pancreatic adenocarcinomas.
  • Since pancreatic cancer is an aggressive and often incurable malignancy, we investigated if the carboxyl ester lipase gene (CEL) is specifically expressed in pancreatic tissues and its promoter can be used for a specific suicide gene approach.
  • Twenty-five tumor samples, 24 samples of normal pancreatic tissue and control tissues from other organs were examined by radioactive in situ hybridization (ISH) to localize CEL mRNA.
  • Two carcinoma samples and 6 permanent cell lines were examined by reverse transcriptase-polymerase chain reaction (RT-PCR).
  • By ISH, we verified a strong CEL gene expression in acinar cells of the normal pancreas.
  • A minor expression was noted in a single sample of acinar cell carcinoma and adenocarcinomas did not show any expression.
  • In summary, these results show that, contrary to notable expression of carboxyl ester lipase in acinar cells of normal pancreatic tissue, this lipase is not significantly active in pancreatic adenocarcinomas and thus not an apt genetic marker for diagnostic or therapeutic approaches.
  • [MeSH-major] Biomarkers, Tumor / genetics. Gene Expression Regulation, Enzymologic / physiology. Lipase / genetics. Pancreas / enzymology. Pancreatic Neoplasms / enzymology
  • [MeSH-minor] Adenocarcinoma / enzymology. Adenocarcinoma / genetics. Adenocarcinoma, Mucinous / enzymology. Adenocarcinoma, Mucinous / genetics. Carcinoma, Acinar Cell / enzymology. Carcinoma, Acinar Cell / genetics. Carcinoma, Pancreatic Ductal / enzymology. Carcinoma, Pancreatic Ductal / genetics. Humans. In Situ Hybridization. Liver Neoplasms / enzymology. Liver Neoplasms / genetics. Liver Neoplasms / secondary. Pancreatitis / enzymology. Pancreatitis / genetics. RNA Probes. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16865281.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA Probes; 0 / RNA, Messenger; EC 3.1.1.3 / CEL protein, human; EC 3.1.1.3 / Lipase
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68. Fitzgerald TL, Hickner ZJ, Schmitz M, Kort EJ: Changing incidence of pancreatic neoplasms: a 16-year review of statewide tumor registry. Pancreas; 2008 Aug;37(2):134-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Changing incidence of pancreatic neoplasms: a 16-year review of statewide tumor registry.
  • OBJECTIVES: Although most pancreatic neoplasms are adenocarcinoma, there are many other histological types, some of which may be increasing in frequency.
  • METHODS: Using the State of Michigan tumor registry, all patients with primary pancreatic cancers from 1986 to 2002 were identified, and patients were excluded if there were insufficient data or the histological subtype was not clearly defined in the literature.
  • RESULTS: There were 17,610 pancreatic neoplasms identified, and 2425 were excluded, leaving a final population of 15,185.
  • Twenty-five types of primary pancreatic neoplasms were identified.
  • The most common were adenocarcinoma, mucinous cystadenocarcinoma, nonfunctional neuroendocrine, adenosquamous, anaplastic, intraductal papillary mucinous, and acinar cell (8.37, 0.43, 0.18, 0.05, 0.04, 0.04, and 0.02 per 100,000 per year, respectively).
  • CONCLUSIONS: The incidence of most pancreatic neoplasms has changed a little; however, nonfunctional neuroendocrine neoplasms increased greater than 2-fold.
  • [MeSH-major] Pancreatic Neoplasms / epidemiology
  • [MeSH-minor] Adenocarcinoma / epidemiology. Aged. Carcinoma, Acinar Cell / epidemiology. Carcinoma, Adenosquamous / epidemiology. Carcinoma, Pancreatic Ductal / epidemiology. Cystadenocarcinoma, Mucinous / epidemiology. Female. Humans. Male. Michigan / epidemiology. Middle Aged. Neuroendocrine Tumors / epidemiology. Registries. Time Factors

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  • (PMID = 18665072.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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69. Hruban RH, Maitra A, Goggins M: Update on pancreatic intraepithelial neoplasia. Int J Clin Exp Pathol; 2008;1(4):306-16
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  • [Title] Update on pancreatic intraepithelial neoplasia.
  • Pancreatic intraepithelial neoplasia (PanIN) is a histologically well-defined precursor to invasive ductal adenocarcinoma of the pancreas.
  • Molecular studies have helped establish the progression of PanIN to invasive cancer, and recently genetically engineered mouse models have been generated that recapitulate the entire spectrum of lesions from precursor to invasive pancreatic cancer.
  • Some PanIN lesions produce lobulocentric atrophy of the pancreatic parenchyma, and, when multifocal, this lobulocentric atrophy may be detectable using currently available imaging techniques such as endoscopic ultrasound.
  • The association of acinar-ductal metaplasia with PanIN lesions has led some to hypothesize that PanINs develop from acinar cells that undergo acinar-ductal metaplasia.

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  • (PMID = 18787611.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2480542
  • [Keywords] NOTNLM ; Pancreatic cancer / epigenetics / genetics / intraepithelial neoplasm / metaplasia
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70. 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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71. 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. Cell Differentiation. Fatal Outcome. Female. Homeodomain Proteins / metabolism. Humans. Immunohistochemistry. Keratin-20 / metabolism. Lymphatic Metastasis. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19908063.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Keratin-20; 0 / Tumor Suppressor Protein p53
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72. Seretis EC, Gavriil AN, Golematis VC, Voloudakis-Baltatzis IE: Immunoelectron study of pancreatic carcinomas using antibodies to gastrointestinal hormones. Ultrastruct Pathol; 2007 Jul-Aug;31(4):303-14
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  • [Title] Immunoelectron study of pancreatic carcinomas using antibodies to gastrointestinal hormones.
  • The aim of this study was to investigate the ultrastructural appearance of pancreatic adenocarcinoma combined with glucagon and gastrin/cholecystokinin (CCK) expression.
  • The authors investigated the ultrastructure and the immunocytochemistry of 12 human pancreatic cancer specimens and used 3 chronic pancreatitis samples and 6 adjacent histological normal pancreatic tissues (away from the tumor) as controls.
  • Glucagon appeared to be located not only in islet alpha cells but also in intermediate alpha acinar cells.
  • The changes were more significant in adenocarcinoma cases.
  • Abnormality in the immunoreaction of the peptides was indicated not only in the tumor area but also in the islets near the cancer.
  • Cells immunoreactive with antibodies were found in all 12 adenocarcinoma cases.
  • Abnormal co-location of both hormones in the same type of endocrine cell was also found.
  • Increased and ectopic gastrin/CCK expression was correlated with pancreatic adenocarcinomas exhibiting poor histological grade and neoplastic endocrine cells, providing a potential marker for pancreatic adenocarcinomas with aggressive behavior.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / ultrastructure. Antibodies, Monoclonal. Gastrointestinal Hormones / biosynthesis. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / ultrastructure

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  • (PMID = 17786831.001).
  • [ISSN] 1521-0758
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Gastrointestinal Hormones; 9007-92-5 / Glucagon; 9011-97-6 / Cholecystokinin
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73. Perez EA, Gutierrez JC, Koniaris LG, Neville HL, Thompson WR, Sola JE: Malignant pancreatic tumors: incidence and outcome in 58 pediatric patients. J Pediatr Surg; 2009 Jan;44(1):197-203
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  • [Title] Malignant pancreatic tumors: incidence and outcome in 58 pediatric patients.
  • OBJECTIVE: The purpose of the study was to examine current incidence trends and outcomes for children with pancreatic malignancies.
  • METHODS: The Surveillance, Epidemiology, and End Results registry (1973-2004) was examined for pediatric patients with pancreatic malignancies (up to 19 years of age).
  • RESULTS: Malignant pancreatic neoplasms were identified in 58 patients.
  • Exocrine tumors included pancreatoblastoma (n = 10), solid-cystic tumor (SCT) (n = 10), ductal adenocarcinoma (DA) (n = 7), and acinar cell carcinoma (ACC) (n = 4).
  • Ductal adenocarcinoma, SCT, acinar cell carcinoma, sarcomas, and endocrine tumors were more common in children older than 10 years, whereas pancreatoblastoma was more common in younger children (P = .045).
  • CONCLUSIONS: Pediatric pancreatic neoplasms are uncommon and carry a variable prognosis.
  • [MeSH-major] Pancreatic Neoplasms / epidemiology. Pancreatic Neoplasms / surgery

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  • (PMID = 19159743.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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74. Lin J, Jing X: Fine-needle aspiration of intrapancreatic accessory spleen, mimic of pancreatic neoplasms. Arch Pathol Lab Med; 2010 Oct;134(10):1474-8
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  • [Title] Fine-needle aspiration of intrapancreatic accessory spleen, mimic of pancreatic neoplasms.
  • Distinguishing IPAS from pancreatic neoplasm/malignancy is extremely important from a treatment perspective.
  • We report the case of a 67-year-old asymptomatic man who had a 1.3-cm, incidentally detected, pancreatic tail mass.
  • The image findings were highly suggestive of a pancreatic endocrine neoplasm.
  • Hematoxylin-eosin–stained cell block sections showed conspicuous thin-walled blood vessels in addition to inflammatory cells.
  • By correlating the cytologic findings with the result of immunostaining, we rendered the diagnosis of IPAS.
  • Our experience supports the view that endoscopic ultrasound-guided fine-needle aspiration may enable a reliable, preoperative diagnosis of IPAS and thus prevent unnecessary surgery.
  • [MeSH-major] Biopsy, Fine-Needle / methods. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology. Spleen / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / ultrasonography. Aged. Animals. Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / ultrasonography. Coloring Agents. Diagnosis, Differential. Humans. Inflammation / pathology. Inflammation / ultrasonography. Lymphocytes / pathology. Lymphocytes / ultrasonography. Male. Pancreas / anatomy & histology. Pancreas / ultrasonography

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  • (PMID = 20923303.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Coloring Agents
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75. 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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76. Kitoh H, Ryozawa S, Harada T, Kondoh S, Furuya T, Kawauchi S, Oga A, Okita K, Sasaki K: Comparative genomic hybridization analysis for pancreatic cancer specimens obtained by endoscopic ultrasonography-guided fine-needle aspiration. J Gastroenterol; 2005 May;40(5):511-7
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  • [Title] Comparative genomic hybridization analysis for pancreatic cancer specimens obtained by endoscopic ultrasonography-guided fine-needle aspiration.
  • BACKGROUND: Comparative genomic hybridization (CGH) analysis of pancreatic cancer has been done exclusively for surgical and autopsy specimens, because of the difficulty of tissue sampling without surgery.
  • METHODS: In the present study, we performed EUS-FNA for 17 patients with pancreatic cancer before surgery.
  • RESULTS: In the 15 patients with tubular adenocarcinoma, the most common loci of gains (including amplification) were 5p, 8q, and 20q (60% of the patients); and 1q, 7p, and 12p (27%).
  • Both of the patients with acinar cell carcinoma showed gains of 2q and 5p, and losses of 1p, 9p, 9q, 11p, 11q, 14q, 17p, 17q, and 18q.
  • This analytical strategy will enable us to evaluate the biological characteristics of pancreatic cancer before treatment.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / ultrasonography. Biopsy, Fine-Needle / methods. Nucleic Acid Hybridization. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / ultrasonography

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  • (PMID = 15942717.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
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77. 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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78. Jiang X, Zhang W, Kayed H, Zheng P, Giese NA, Friess H, Kleeff J: Loss of ONECUT1 expression in human pancreatic cancer cells. Oncol Rep; 2008 Jan;19(1):157-63
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  • [Title] Loss of ONECUT1 expression in human pancreatic cancer cells.
  • ONECUT1 (HNF-6) is the prototype of a new class of homeodomain transcription factors, that controls the development of pancreatic ducts during mouse development.
  • In the present study, the role of ONECUT1 and its targeted genes TCF2, PKHD1 and CYS1 was analyzed in human pancreatic ductal adenocarcinoma (PDAC).
  • mRNA levels of ONECUT1, TCF2, PKHD1 and CYS1 were measured in pancreatic tissues and pancreatic cancer cell lines by quantitative reverse-transcriptase polymerase chain reaction (QRT-PCR).
  • Protein expression of ONECUT1 and TCF2 was assessed in pancreatic tissues by immunohistochemistry.
  • ONECUT1 was transfected into Panc-1 and T3M4 pancreatic cancer cells and its effects on anchorage-dependent and -independent growth as well as invasion and adhesion were analyzed.
  • ONECUT1 protein was expressed in normal acinar and ductal cells, but neither in the cancer cells of PDAC tissues nor in 7 of 8 cultured pancreatic cancer cell lines.
  • Transfection of ONECUT1 into pancreatic cancer cells resulted in up-regulation of the target gene TCF2, a reduction in invasiveness, but no change in adhesion or growth.
  • In conclusion, ONECUT1 expression is lost in pancreatic cancer cells, suggesting a tumor suppressor function in this malignancy.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Hepatocyte Nuclear Factor 6 / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Movement / physiology. Gene Expression. Hepatocyte Nuclear Factor 1-beta / metabolism. Humans. Immunoblotting. Immunohistochemistry. Lasers. Membrane Proteins / metabolism. Microdissection. Oligonucleotide Array Sequence Analysis. RNA, Messenger / analysis. Receptors, Cell Surface / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 18097590.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / CYS1 protein, human; 0 / HNF1B protein, human; 0 / Hepatocyte Nuclear Factor 6; 0 / Membrane Proteins; 0 / ONECUT1 protein, human; 0 / PKHD1 protein, human; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 138674-15-4 / Hepatocyte Nuclear Factor 1-beta
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79. Torrisani J, Bournet B, du Rieu MC, Bouisson M, Souque A, Escourrou J, Buscail L, Cordelier P: let-7 MicroRNA transfer in pancreatic cancer-derived cells inhibits in vitro cell proliferation but fails to alter tumor progression. Hum Gene Ther; 2009 Aug;20(8):831-44
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  • [Title] let-7 MicroRNA transfer in pancreatic cancer-derived cells inhibits in vitro cell proliferation but fails to alter tumor progression.
  • Pancreatic ductal adenocarcinoma (PDAC) is still the fourth leading cause of cancer-related deaths in Western countries, with increasing incidence.
  • Neither effective prognostic markers nor therapies exist for this cancer.
  • Because let-7 microRNA targets the K-ras oncogene, we aimed to characterize let-7 expression and function in PDAC in vitro and in vivo.
  • Let-7 is present in normal acinar pancreatic cells, and lost in poorly differentiated cancer samples.
  • Restoring let-7 levels in cancer-derived cell lines strongly inhibits cell proliferation, K-ras expression, and mitogen-activated protein kinase activation, but fails to impede tumor growth progression after intratumoral gene transfer or after implantation of Capan-1 cells stably overexpressing let-7 microRNA.
  • In addition, this study provides the initial steps for a microRNA replacement therapy for this cancer.
  • [MeSH-major] MicroRNAs / genetics. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Animals. Biopsy, Fine-Needle. Cell Line, Tumor. Cell Proliferation. Disease Progression. Enzyme Activation. Female. Gene Expression Regulation, Neoplastic. Genes, ras. Humans. Male. Mice. Middle Aged. Mitogen-Activated Protein Kinases / metabolism. Transfection

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  • (PMID = 19323605.001).
  • [ISSN] 1557-7422
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / mirnlet7 microRNA, human; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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80. Heller A, Zörnig I, Müller T, Giorgadze K, Frei C, Giese T, Bergmann F, Schmidt J, Werner J, Buchler MW, Jaeger D, Giese NA: Immunogenicity of SEREX-identified antigens and disease outcome in pancreatic cancer. Cancer Immunol Immunother; 2010 Sep;59(9):1389-400
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  • [Title] Immunogenicity of SEREX-identified antigens and disease outcome in pancreatic cancer.
  • Despite spontaneous or vaccination-induced immune responses, pancreatic cancer remains one of the most deadly immunotherapy-resistant malignancies.
  • We sought to comprehend the spectrum of pancreatic tumor-associated antigens (pTAAs) and to assess the clinical relevance of their immunogenicity.
  • An autologous SEREX-based screening of a cDNA library constructed from a pancreatic T3N0M0/GIII specimen belonging to a long-term survivor (36 months) revealed 18 immunogenic pTAA.
  • PNLIPRP2 and MIA demonstrated the most distinct pancreatic cancer-specific patterns.
  • ELISA-based screening of sera for corresponding autoantibodies revealed that although significantly increased, the immunogenicity of these molecules was not a common feature in pancreatic cancer.
  • QRT-PCR and immunohistochemistry characterized PNLIPRP2 as a robust acinar cell-specific marker whose decreased expression mirrored the disappearance of parenchyma in the diseased organ, but was not related to the presence of PNLIPRP2 autoantibodies.
  • The observed pTAA spectrum comprised molecules associated with acinar, stromal and malignant structures, thus presenting novel targets for tumor cell-specific therapies as well as for approaches based on the bystander effects.
  • Applying the concept of cancer immunoediting to interpret relationships between gene expression, antitumor immune responses, and clinical outcome might better discriminate between past and ongoing immune responses, consequently enabling prognostic stratification of patients and individual adjustment of immunotherapy.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / immunology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / immunology
  • [MeSH-minor] Aged. Antigens, Tumor-Associated, Carbohydrate / genetics. Antigens, Tumor-Associated, Carbohydrate / immunology. Antigens, Tumor-Associated, Carbohydrate / metabolism. Autoantibodies / blood. Cloning, Molecular. Enzyme-Linked Immunosorbent Assay. Female. Gene Library. Humans. Immunochemistry. Lipase / genetics. Lipase / immunology. Lipase / metabolism. Male. Middle Aged. Neoplasm Staging. Pancreas / metabolism. Pancreas / pathology. Prognosis

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  • (PMID = 20514540.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Tumor-Associated, Carbohydrate; 0 / Autoantibodies; 0 / MIA antigen, human; EC 3.1.1.- / pancreatic lipase related protein 2; EC 3.1.1.3 / Lipase
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81. Stelow EB, Adams RB, Moskaluk CA: The prevalence of pancreatic intraepithelial neoplasia in pancreata with uncommon types of primary neoplasms. Am J Surg Pathol; 2006 Jan;30(1):36-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The prevalence of pancreatic intraepithelial neoplasia in pancreata with uncommon types of primary neoplasms.
  • Pancreatic ductal adenocarcinoma is thought to develop through a series of genetic events through its purported precursor lesion, pancreatic intraepithelial neoplasia (PanIN).
  • Little, however, is known regarding the role of possible precursor lesions in the development of other primary neoplasms of the pancreas.
  • All pancreata resected at the University of Virginia from June 1, 1991 to March 1, 2005 for neoplasia not diagnosed as conventional ductal adenocarcinoma were reviewed and classified according to the World Health Organization's classification schema for tumors of the exocrine and endocrine pancreas.
  • Three acinar cell carcinomas (ACCs), 18 mucinous cystic neoplasms (MCNs), 24 pancreatic endocrine tumors (PETs), 12 serous cystadenomas (SCs), and 3 solid-pseudopapillary tumors (SPTs) were identified.
  • Although the high prevalence of PanIN in pancreata concomitantly harboring certain uncommon neoplasms of the pancreas could signify its role as a precursor lesion for those neoplasms, its high prevalence throughout our series may simply be the result of a coincidental, prevalent finding seen in all pancreata, especially with aging.
  • Because of the ubiquitous nature of PanIN, it should not be used histologically to assist in the diagnosis and subclassification of pancreatic neoplasia.
  • [MeSH-major] Carcinoma in Situ / pathology. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Age Factors. Aged. Cystadenocarcinoma, Mucinous / pathology. Cystadenocarcinoma, Serous / pathology. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Prevalence

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  • (PMID = 16330940.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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82. Bockman DE: Transition to pancreatic cancer in response to carcinogen. Langenbecks Arch Surg; 2008 Jul;393(4):557-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transition to pancreatic cancer in response to carcinogen.
  • BACKGROUND: It has become obvious that the traditional assumptions about the transition from normal pancreas to pancreatic cancer are incomplete.
  • Experimental studies reveal that the earliest changes during transition to pancreatic adenocarcinoma involve premalignant lesions that are derived from acinar, islet, and ductal cells.
  • As part of redifferentiation and transformation to adenocarcinoma, cells regain the characteristics of developing pancreas.
  • Elements significant in identifying precursor cell types include Pdx1, hedgehog signaling, notch signaling, and nestin, an intermediate filament expressed by precursor cell types.
  • CONCLUSIONS: Thus pancreatic carcinogenesis is not simply a matter of transition of ductal cells to cancer cells months after insult by the carcinogen; ductal cells are not the sole source transitioning to cancer, and PanINs are not the sole route to adenocarcinoma.
  • Tubular complexes, derived from multiple cell sources, are included in routes to pancreatic cancer.
  • Markers characteristic of developing pancreas are consistent with this transition.

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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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83. Chetty R, Serra S, Asa SL, Volkan Adsay N: Pancreatic endocrine tumour with ductules: further observations of an unusual histological subtype. Pathology; 2006 Feb;38(1):5-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic endocrine tumour with ductules: further observations of an unusual histological subtype.
  • AIMS: Pancreatic endocrine tumours (PET) containing ductules are an uncommon histological variant.
  • A study of 21 cases of this variant was undertaken with particular attention paid to the distribution and morphology of the ductules, the presence of entrapped acinar tissue and the surrounding uninvolved pancreatic tissue.
  • CONCLUSIONS: It is likely that in some cases the ductules are entrapped as the tumour grows into surrounding normal pancreatic tissue and the ductular proliferation is a secondary phenomenon.
  • In a proportion of cases, the ductules are likely to be a part of the tumour arising as part of focal chronic inflammation or as a result of the growth factor effects of insulin, in cases associated with insulin production.
  • However, some cases may have a dominant tubular component, which could present problems at frozen section where the association with fibrosis may invoke a mistaken diagnosis of pancreatic ductal adenocarcinoma or chronic pancreatitis.
  • [MeSH-major] Carcinoma, Islet Cell / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Biomarkers / analysis. Carcinoma, Pancreatic Ductal / chemistry. Carcinoma, Pancreatic Ductal / pathology. Diagnosis, Differential. Female. Fibrosis / pathology. Humans. Immunohistochemistry. Insulin / analysis. Islets of Langerhans / chemistry. Islets of Langerhans / pathology. Keratins / analysis. Male. Middle Aged. Pancreatitis, Chronic / pathology

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  • (PMID = 16484000.001).
  • [ISSN] 0031-3025
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / CAM 5.2 antigen; 0 / Insulin; 68238-35-7 / Keratins
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84. 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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85. De La O JP, Murtaugh LC: Notch and Kras in pancreatic cancer: at the crossroads of mutation, differentiation and signaling. Cell Cycle; 2009 Jun 15;8(12):1860-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Notch and Kras in pancreatic cancer: at the crossroads of mutation, differentiation and signaling.
  • Activating mutations in the KRAS proto-oncogene occur almost ubiquitously in pancreatic ductal adenocarcinoma (PDAC) and in its putative precursor lesions, pancreatic intraepithelial neoplasia (PanIN).
  • Conditional expression of an activated Kras allele in the mouse pancreas produces a model that faithfully recapitulates PanIN formation and progression to PDAC.
  • Importantly, although nearly every cell in the pancreata of these mice express activated Kras, only a very small minority of cells give rise to PanINs.
  • How the transforming activity of Kras is constrained in the pancreas remains unknown, and the cell types from which PanINs and PDAC arise are similarly unknown.
  • Here, we describe our recent results demonstrating that acinar cells are competent to form Kras-induced PanINs, and that active Notch signaling can synergize with Kras in PanIN initiation and progression.
  • Further efforts to understand how Notch and Kras synergize, as well as experiments to determine how other pancreatic cell types contribute to PDAC development, should aid in the development of new therapies and early detection techniques that are desperately needed for this cancer.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins p21(ras) / metabolism. Receptors, Notch / metabolism
  • [MeSH-minor] Animals. Cell Differentiation. Disease Models, Animal. Humans. Mice. Mice, Transgenic. Mutation / genetics. Mutation / physiology. Signal Transduction / physiology

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  • (PMID = 19440048.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R21-CA123066; United States / NCI NIH HHS / CA / R21 CA123066-02; United States / NICHD NIH HHS / HD / 5T32-HD07491; United States / NCI NIH HHS / CA / R21 CA123066; United States / NICHD NIH HHS / HD / T32 HD007491
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Notch; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ NIHMS118588; NLM/ PMC2719432
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86. Ji B, Tsou L, Wang H, Gaiser S, Chang DZ, Daniluk J, Bi Y, Grote T, Longnecker DS, Logsdon CD: Ras activity levels control the development of pancreatic diseases. Gastroenterology; 2009 Sep;137(3):1072-82, 1082.e1-6
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  • [Title] Ras activity levels control the development of pancreatic diseases.
  • BACKGROUND & AIMS: Differentiated pancreatic acinar cells expressing endogenous levels of mutant K-Ras do not spontaneously develop pancreatic ductal adenocarcinoma (PDAC).
  • However, we hypothesized that acinar cells would develop PDAC in the presence of Ras activity levels mimicking those of human tumor cells.
  • We compared the effects of acinar cell expression of mutant K-Ras at endogenous and elevated levels on Ras activity and on the development of PDAC.
  • Expression of endogenous levels of mutant K-Ras in differentiated acinar cells resulted in moderately elevated Ras activity and in sparse murine pancreatic intraepithelial neoplasias (mPanINs) that did not spontaneously advance to PDAC unless the tumor suppressor p53 was simultaneously deleted.
  • High Ras activity mimicking levels in PDAC led to acinar cell senescence and generated inflammation and fibrosis resembling the histologic features of chronic pancreatitis.
  • With higher Ras activity in acinar cells, abundant mPanINs formed and spontaneously progressed to both cystic papillary carcinoma and metastatic PDAC.
  • Sufficient Ras activity in pancreatic acinar induces several important pancreatic disease manifestations not previously reported and supports a potential direct linkage between chronic pancreatitis, cystic papillary carcinoma, and PDAC.

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  • (PMID = 19501586.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK052067-11; United States / NCI NIH HHS / CA / P30 CA016672; United States / NIDDK NIH HHS / DK / R21 DK068414; United States / NCI NIH HHS / CA / CA16672; United States / NIDDK NIH HHS / DK / R01 DK052067; United States / NIDDK NIH HHS / DK / R01 DK052067-11; United States / NIDDK NIH HHS / DK / 5R21DK068414; United States / NCI NIH HHS / CA / P20 CA101936; United States / NIAAA NIH HHS / AA / R01 AA020822; United States / NIDDK NIH HHS / DK / R01 DK052067-10; United States / NIDDK NIH HHS / DK / DK052067; United States / NIDDK NIH HHS / DK / DK052067-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS122586; NLM/ PMC2789008
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87. Ohike N, Sato M, Hisayuki T, Imataka H, Sato S, Wada Y, Saito K, Takahashi M, Tajiri T, Kunimura T, Morohoshi T: Immunohistochemical analysis of nestin and c-kit and their significance in pancreatic tumors. Pathol Int; 2007 Sep;57(9):589-93
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  • [Title] Immunohistochemical analysis of nestin and c-kit and their significance in pancreatic tumors.
  • The purpose of the present study was to clarify the difference of expression of two stem cell markers, nestin and c-kit, among various pancreatic epithelial tumors and evaluate their utility.
  • Immunohistochemistry was done for 99 surgically resected pancreatic tumor specimens, including 20 ductal adenocarcinoma (DAC), two undifferentiated carcinomas (UC), 31 intraductal papillary-mucinous neoplasms (IPMN), six mucinous cystic neoplasms (MCN), five serous cystadenomas (SCA), six acinar cell carcinomas, two pancreatoblastoma (PB), eight solid-pseudopapillary neoplasms (SPN), and 19 endocrine neoplasms (EN).
  • Additionally, partial (scattered) expression of c-kit was observed in ductal elements of 16 DAC, eight IPMN, five MCN, and one UC, one SCA, and three EN.
  • These indicate that expression of two stem cell markers is different by tumor type, but the utility of judging direction or degree of differentiation and malignant grade on the basis of their expression status is suggested.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Immunoenzyme Techniques / methods. Intermediate Filament Proteins / analysis. Neoplasm Proteins / metabolism. Nerve Tissue Proteins / analysis. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins c-kit / metabolism
  • [MeSH-minor] Humans. Nestin. Pancreas / metabolism. Pancreas / pathology. Stem Cells / metabolism. Stem Cells / pathology

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  • (PMID = 17685930.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / Nestin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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88. Morris JP 4th, Cano DA, Sekine S, Wang SC, Hebrok M: Beta-catenin blocks Kras-dependent reprogramming of acini into pancreatic cancer precursor lesions in mice. J Clin Invest; 2010 Feb;120(2):508-20
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  • [Title] Beta-catenin blocks Kras-dependent reprogramming of acini into pancreatic cancer precursor lesions in mice.
  • WT mouse acinar cells rapidly regenerate following injury that mimics acute pancreatitis, a process characterized by transient reactivation of pathways involved in embryonic pancreatic development.
  • In contrast, such injury promotes the development of pancreatic ductal adenocarcinoma (PDA) precursor lesions in mice expressing a constitutively active form of the GTPase, Kras, in the exocrine pancreas.
  • The molecular environment that mediates acinar regeneration versus the development of PDA precursor lesions is poorly understood.
  • Here, we used genetically engineered mice to demonstrate that mutant Kras promotes acinar-to-ductal metaplasia (ADM) and pancreatic cancer precursor lesion formation by blocking acinar regeneration following acute pancreatitis.
  • Our results indicate that beta-catenin is required for efficient acinar regeneration.
  • In addition, canonical beta-catenin signaling, a pathway known to regulate embryonic acinar development, is activated following acute pancreatitis.
  • This regeneration-associated activation of beta-catenin signaling was not observed during the initiation of Kras-induced acinar-to-ductal reprogramming.
  • Therefore, these results suggest that beta-catenin signaling is a critical determinant of acinar plasticity and that it is inhibited during Kras-induced fate decisions that specify PDA precursors, highlighting the importance of temporal regulation of embryonic signaling pathways in the development of neoplastic cell fates.


89. Yoshida T, Shiraki N, Baba H, Goto M, Fujiwara S, Kume K, Kume S: Expression patterns of epiplakin1 in pancreas, pancreatic cancer and regenerating pancreas. Genes Cells; 2008 Jul;13(7):667-78
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression patterns of epiplakin1 in pancreas, pancreatic cancer and regenerating pancreas.
  • Here we analyzed the expression patterns of Eppk1 in the developing and adult pancreas in the mice.
  • In the embryonic pancreas, Eppk1+/Pdx1+ and Eppk1+/Sox9+ pancreatic progenitor cells were observed in early pancreatic epithelium.
  • In the adult pancreas, Eppk1 is expressed in centroacinar cells (CACs) and in duct cells.
  • Eppk1 is observed in pancreatic intraepithelial neoplasia (PanIN), previously identified as pancreatic ductal adenocarcinoma (PDAC) precursor lesions.
  • In addition, the expansion of Eppk1-positive cells occurs in a caerulein-induced acute pancreatitis, an acinar cell regeneration model.
  • These results suggest that Eppk1 serves as a useful marker for detecting pancreatic progenitor cells in developing and regenerating pancreas.
  • [MeSH-major] Autoantigens / biosynthesis. Autoantigens / genetics. Gene Expression Regulation / physiology. Pancreas / metabolism. Pancreatic Neoplasms / metabolism. Regeneration / physiology
  • [MeSH-minor] Animals. Biomarkers / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Pancreatic Ductal / pathology. Gene Expression Regulation, Neoplastic / physiology. Mice. Mice, Knockout. Mice, Transgenic. Stem Cells / cytology. Stem Cells / metabolism


90. 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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91. Lee KM, Yasuda H, Hollingsworth MA, Ouellette MM: Notch 2-positive progenitors with the intrinsic ability to give rise to pancreatic ductal cells. Lab Invest; 2005 Aug;85(8):1003-12
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  • [Title] Notch 2-positive progenitors with the intrinsic ability to give rise to pancreatic ductal cells.
  • Pancreatic adenocarcinomas display foci of duct-like structures that are positive for markers of pancreatic ductal cells.
  • The development of these tumors is promoted by conditions leading to acinar-to-ductal metaplasia, a process by which acinar cells are replaced by ductal cells.
  • Acinar-to-ductal metaplasia has recently been shown to proceed through intermediary cells expressing Nestin.
  • To create an in vitro system to study pancreatic adenocarcinomas, we had used an hTERT cDNA to immortalize primary cells of the human pancreas.
  • In this report, we show that the immortalized cells, termed hTERT-HPNE cells, have the ability to differentiate to pancreatic ductal cells.
  • Exposing hTERT-HPNE cells to sodium butyrate and 5-aza-2'-deoxycytidine lead to the formation of pancreatic ductal cells marked by the expression of MDR-1, carbonic anhydrase II, and the cytokeratins 7, 8, and 19. hTERT-HPNE cells were found to have properties of the intermediary cells formed during acinar-to-ductal metaplasia, which included their undifferentiated phenotype, expression of Nestin, evidence of active Notch signaling, and ability to differentiate to pancreatic ductal cells.
  • These results provide further evidence for the presence in the adult pancreas of a precursor of ductal cells. hTERT-HPNE cells should provide a useful model to study acinar-to-ductal metaplasia and the role played by this process in pancreatic cancer development.
  • [MeSH-major] Adenocarcinoma / pathology. Cell Differentiation / physiology. Pancreas / cytology. Pancreatic Neoplasms / pathology. Receptors, Cell Surface / physiology. Stem Cells / metabolism
  • [MeSH-minor] Base Sequence. Blotting, Western. Cell Line, Transformed. DNA Primers. Fluorescent Antibody Technique. Humans. Receptor, Notch2. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction

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  • (PMID = 15924149.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / NOTCH2 protein, human; 0 / Receptor, Notch2; 0 / Receptors, Cell Surface
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92. Erkan M, Kleeff J, Esposito I, Giese T, Ketterer K, Büchler MW, Giese NA, Friess H: Loss of BNIP3 expression is a late event in pancreatic cancer contributing to chemoresistance and worsened prognosis. Oncogene; 2005 Jun 23;24(27):4421-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of BNIP3 expression is a late event in pancreatic cancer contributing to chemoresistance and worsened prognosis.
  • Altered expression of apoptosis-regulating genes plays an important role in the aggressive growth behavior and chemoresistance of pancreatic ductal adenocarcinoma.
  • In the present study, the hypoxia-inducible proapoptotic gene, BNIP3, was analysed in terms of expression, effect on patient survival, and chemo-responsiveness in pancreatic cancer cell lines. cDNA microarray, real-time light cycler quantitative polymerase chain reaction, laser-capture microdissection, and immunohistochemistry analyses were used to evaluate BNIP3 expression in normal and diseased pancreatic specimens.
  • The effect of chemotherapeutic agents on pancreatic cancer cells was assessed utilizing 3-(4,5-methylthiazol-2-yl)-2,5-diphenyl-tetrazolium-bromide assays.
  • BNIP3 mRNA levels were 3.0- and 6.3-fold lower in chronic pancreatitis and pancreatic cancer compared to the normal pancreas, respectively.
  • Microdissection analysis confirmed the reduction of BNIP3 expression in pancreatic cancer cells compared to normal duct cells.
  • By immunohistochemistry, BNIP3 was predominantly expressed in the acinar cells of the normal and diseased pancreas.
  • Interestingly, while BNIP3 was undetectable in the cancer cells of 59% of the cases, 75-100% of PanIN2/3 lesions displayed BNIP3 immunoreactivity.
  • Hypoxia induced BNIP3 expression in four out of eight pancreatic cancer cell lines, while it was absent under normoxic and hypoxic conditions in the remaining four.
  • In conclusion, loss of BNIP3 expression occurs late in pancreatic cancer, contributes to resistance to chemotherapy, and correlates with a worsened prognosis.
  • [MeSH-major] Deoxycytidine / analogs & derivatives. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Membrane Proteins / deficiency. Membrane Proteins / genetics. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology. Proto-Oncogene Proteins / deficiency. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Cell Line, Tumor. Fluorouracil / pharmacology. Humans. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Survival Rate

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  • (PMID = 15856026.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BNIP3 protein, human; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; U3P01618RT / Fluorouracil
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93. Weichert W, Schmidt M, Jacob J, Gekeler V, Langrehr J, Neuhaus P, Bahra M, Denkert C, Dietel M, Kristiansen G: Overexpression of Polo-like kinase 1 is a common and early event in pancreatic cancer. Pancreatology; 2005;5(2-3):259-65
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  • [Title] Overexpression of Polo-like kinase 1 is a common and early event in pancreatic cancer.
  • Therefore, PLK1 has been proposed as a new target for antineoplastic treatment strategies.
  • METHODS: We conducted an immunohistochemical expression study for PLK1 on 86 cases of pancreatic adenocarcinoma as well as on 5 cases of chronic pancreatitis.
  • RESULTS: PLK1 was found overexpressed in pancreatic neoplasia as early as in pancreatic intraepithelial neoplasia III lesions, whereas benign acinar pancreatic parenchyma and ductal epithelia showed only focal PLK1 positivity.
  • Invasive pancreatic adenocarcinomas were PLK1 positive in 47.7% of cases.
  • CONCLUSIONS: The fact that half of the invasive pancreatic carcinomas strongly overexpressed PLK1 indicates that inhibition of this mitotic key regulator might represent a rewarding approach in the treatment of early and late pancreatic carcinoma.
  • [MeSH-major] Carcinoma in Situ / metabolism. Cell Cycle Proteins / metabolism. Pancreatic Neoplasms / metabolism. Protein Kinases / metabolism. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / mortality. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Humans. Immunohistochemistry. Middle Aged. Prognosis. Protein-Serine-Threonine Kinases. Survival Analysis

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  • (PMID = 15855824.001).
  • [ISSN] 1424-3903
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Proto-Oncogene Proteins; EC 2.7.- / Protein Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / polo-like kinase 1
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94. Chang F, Chandra A, Culora G, Mahadeva U, Meenan J, Herbert A: Cytologic diagnosis of pancreatic endocrine tumors by endoscopic ultrasound-guided fine-needle aspiration: a review. Diagn Cytopathol; 2006 Sep;34(9):649-58
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  • [Title] Cytologic diagnosis of pancreatic endocrine tumors by endoscopic ultrasound-guided fine-needle aspiration: a review.
  • Precise localization and diagnosis of pancreatic endocrine tumors (PETs) is important, because pancreatic PETs have different clinical and biological behavior and treatment modalities than do exocrine pancreatic tumors.
  • In contrast to the much more common exocrine adenocarcinomas, cytologic studies of PET are relatively rare and many cytopathologists lack experience with the cytomorphologic features of these tumors.During the last 10 yr, endoscopic ultrasound (EUS)-guided fine-needle aspiration (FNA) has matured into an accurate, highly sensitive, and cost-effective modality for the preoperative localization of pancreatic PETs.
  • This manuscript focuses on the cytomorphologic features most suggestive of pancreatic PETs, differential diagnosis, and diagnostic pitfalls of PETs.
  • The technical development of EUS-guided FNA and the ancillary studies for pancreatic PETs are also reviewed.
  • The data summarized in this review indicate that EUS-FNA is a valuable method in the recognition of pancreatic PETs and in most cases cytopathologists could reach a correct diagnosis of these tumors, including their hormone producing capability on aspirated cytologic material.
  • [MeSH-major] Biopsy, Fine-Needle / methods. Carcinoma, Islet Cell / pathology. Endoscopy, Digestive System / methods. Insulinoma / pathology. Pancreatic Neoplasms / pathology. Ultrasonography / methods
  • [MeSH-minor] Adenocarcinoma, Papillary / pathology. Biomarkers, Tumor / analysis. Carcinoma, Acinar Cell / pathology. Carcinoma, Pancreatic Ductal / pathology. Diagnosis, Differential. Gastrinoma / chemistry. Gastrinoma / pathology. Glucagonoma / chemistry. Glucagonoma / pathology. Humans. Immunohistochemistry. Lymphoma / pathology

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16900463.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 74
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95. Khanna AK, Yadav SK, Dixit VK, Kumar M: AgNOR count and subjective AgNOR pattern assessment (SAPA) score in carcinoma of the pancreatic head including periampullary tumors. JOP; 2005 Nov;6(6):575-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AgNOR count and subjective AgNOR pattern assessment (SAPA) score in carcinoma of the pancreatic head including periampullary tumors.
  • CONTEXT: Only a few studies are available in the literature regarding the AgNOR (argyrophilic nucleolar organizer region) count in pancreatic adenocarcinoma but studies on the SAPA (subjective AgNOR pattern assessment) score are completely lacking.
  • OBJECTIVE: We attempted to estimate the AgNOR count and the SAPA score in carcinoma of the pancreatic head including periampullary tumors and to correlate them with other various clinico-histological parameters.
  • SETTING: Patients undergoing pancreatic resection at the University Hospital, Banaras Hindu University, Varanasi, India.
  • PATIENTS: Twenty-four cases of carcinoma of the pancreatic head including periampullary tumors.
  • In addition, on the resected specimen of the pancreas, the area which was normal was chosen and, in that normal tissue, the AgNOR was also studied.
  • RESULTS: The values of the AgNOR count and the SAPA score were significantly higher in cases of pancreatic cancer than in the healthy pancreas.
  • The AgNOR count was 1.6+/-0.1 in the healthy pancreas while it was 2.8+/-0.5 in cases of pancreatic carcinoma (P<0.001).
  • The SAPA score was 5.6+/-0.2 in the healthy pancreas while it was 8.0+/-1.4 in pancreatic carcinoma (P<0.001).
  • Periampullary tumors had a significantly lower (P<0.001) AgNOR count (2.7+/-0.06) and SAPA score (7.8+/-0.2) as compared to carcinoma of the head of the pancreas (AgNOR count 3.3+/-0.03 and SAPA score 9.2+/-0.7).
  • Well-differentiated carcinomas had significantly lower AgNOR counts as compared to other tumors except acinar cell carcinomas since acinar cell carcinomas are also well-differentiated tumors.
  • The SAPA score was also higher in moderately-differentiated tumors and the difference between moderately-differentiated tumor and other types of tumors was significant although there was no significant difference between cystadenocarcinomas and unclassified tumors, and between acinar cell carcinomas and well-differentiated tumors on SAPA scoring.
  • [MeSH-major] Antigens, Nuclear. Nuclear Proteins. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Cell Count. Female. Humans. Male. Middle Aged. Pancreatectomy

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  • (PMID = 16286708.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Nuclear Proteins; 0 / nucleolar organizer region associated proteins
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96. 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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97. Mansfield A, Tafur A, Smithedajkul P, Corsini M, Quevedo F, Miller R: Mayo Clinic experience with very rare exocrine pancreatic neoplasms. Pancreas; 2010 Oct;39(7):972-5
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  • [Title] Mayo Clinic experience with very rare exocrine pancreatic neoplasms.
  • OBJECTIVES: Limited data are available to guide the management of very rare exocrine neoplasms of the pancreas (VREP).
  • 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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98. Bhatia P, Srinivasan R, Rajwanshi A, Nijhawan R, Khandelwal N, Wig J, Vasishtha RK: 5-year review and reappraisal of ultrasound-guided percutaneous transabdominal fine needle aspiration of pancreatic lesions. Acta Cytol; 2008 Sep-Oct;52(5):523-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 5-year review and reappraisal of ultrasound-guided percutaneous transabdominal fine needle aspiration of pancreatic lesions.
  • OBJECTIVE: To reevaluate the efficacy and safety offine needle aspiration cytology (FNAC) of pancreatic lesions performed by transabdominal approach.
  • STUDY DESIGN: Retrospective 5-year (2001-2006) audit of all pancreatic FNA samples.
  • Seven cases (2.6%) yielded insufficient material for diagnosis; 260 cases were classified as benign (n=118) and malignant (n=142) lesions.
  • Of the 142 malignant aspirates, the cytodiagnosis was adenocarcinoma in 126, neuroendocrine/carcinoid tumor in 7, papillary solid epithelial neoplasm in 2, mucinous cystadenocarcinoma in 2, acinar cell carcinoma in 1 and metastatic small cell carcinoma in lung in 4 cases.
  • CONCLUSION: A spectrum of pancreatic lesions can be accurately diagnosed by the technique.
  • [MeSH-major] Pancreatic Neoplasms / pathology

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  • [CommentIn] Acta Cytol. 2008 Sep-Oct;52(5):521-2 [18833811.001]
  • (PMID = 18833812.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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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
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [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.

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  • [Copyright] ©2010 AACR.
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  • (PMID = 20959479.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA076361; United States / NCI NIH HHS / CA / P01 CA022484; United States / NCI NIH HHS / CA / P01CA022484; United States / NCI NIH HHS / CA / R01CA076361; United States / NCI NIH HHS / CA / T32 CA009135
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS305961; NLM/ PMC3141286
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100. Pujal J, Huch M, José A, Abasolo I, Rodolosse A, Duch A, Sánchez-Palazón L, Smith FJ, McLean WH, Fillat C, Real FX: Keratin 7 promoter selectively targets transgene expression to normal and neoplastic pancreatic ductal cells in vitro and in vivo. FASEB J; 2009 May;23(5):1366-75
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Keratin 7 promoter selectively targets transgene expression to normal and neoplastic pancreatic ductal cells in vitro and in vivo.
  • In the pancreas, it is present in ductal but not in acinar cells.
  • K7 mRNA is overexpressed in pancreatic cancers.
  • All elements required for appropriate cell and tissue specificity in reporter assays are present within the Krt7 -234 bp sequence.
  • This fragment appears more selective to pancreatic ductal cells than the Krt19 promoter.
  • Sequences located 1.5 or 0.25 kb upstream of the transcription initiation site drive reporter expression to ductal, but not acinar, cells in transgenic mice.
  • LacZ mRNA was detected in the pancreas as well as in additional epithelial tissues--such as the intestine and the lung--using both promoter constructs.
  • An AdK7Luc adenovirus was generated to assess targeting selectivity in vivo by intravenous injection to immunocompetent mice and in a xenograft model of pancreatic cancer.
  • The -0.25 kb region showed pancreatic selectivity, high activity in pancreatic cancers, and sustained transgene expression in xenografts.
  • In conclusion, the krt7 promoter is useful to target pancreatic ductal adenocarcinoma cells in vitro and in vivo.

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  • (PMID = 19124560.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / / 104151; United Kingdom / Medical Research Council / / G0700314; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Keratin-7; 0 / Krt2-7 protein, mouse; 0 / Sp1 Transcription Factor
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