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1. 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.
  • Gains of CTNNB1 due to trisomy 3 occurred in each tumor with acinar cell carcinoma but in none of the other tumors in this study.
  • CONCLUSION: FISH abnormalities of CTNNB1 due to trisomy 3 were observed only in acinar cell carcinoma.

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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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2. Denève E, Ramos J, Aufort S, Marchand JP, Rousset T, Perrochia H, Domergue J, Navarro F: [Endocrine tumor arising in heterotopic gastric pancreas]. Gastroenterol Clin Biol; 2008 Feb;32(2):195-201
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  • [Title] [Endocrine tumor arising in heterotopic gastric pancreas].
  • We report the case of a 49-year-old caucasian woman, in whom an endocrine tumor arising in gastric heterotopic pancreas was diagnosed.
  • Heterotopic pancreas is a benign anatomic condition, probably widely underdiagnosed because usually asymptomatic.
  • The malignant transformation of aberrant pancreas is very rare and almost always in adenocarcinoma.
  • The endocrine tumors developed in heterotopic pancreas are exceedingly rare.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Choristoma / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology. Stomach Diseases / pathology
  • [MeSH-minor] Carcinoma, Islet Cell / pathology. Female. Follow-Up Studies. Gastrins / analysis. Humans. Islets of Langerhans / pathology. Middle Aged. Somatostatin / analysis

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  • (PMID = 18387430.001).
  • [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
  • [Chemical-registry-number] 0 / Gastrins; 51110-01-1 / Somatostatin
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3. Mortelé KJ, Peters HE, Odze RD, Glickman JN, Jajoo K, Banks PA: An unusual mixed tumor of the pancreas: sonographic and MDCT features. JOP; 2009;10(2):204-8
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  • [Title] An unusual mixed tumor of the pancreas: sonographic and MDCT features.
  • CONTEXT: Mixed tumors of the pancreas are exceedingly rare.
  • CASE REPORT: We herein report on a 54-year-old female who presented with an enlarging cystic lesion in the head of the pancreas.
  • Right upper quadrant ultrasound and multidetector-row CT scan showed a well-defined unilocular cystic tumor located in the head of the pancreas and surrounded, in part, by a hypervascular solid mass.
  • [MeSH-minor] Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Mucinous / pathology. Carcinoma, Islet Cell / metabolism. Carcinoma, Islet Cell / pathology. Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Papillary / metabolism. Carcinoma, Papillary / pathology. Female. Humans. Immunohistochemistry. Middle Aged. Mucin-2 / analysis. Pancreas / radiography. Pancreas / ultrasonography. Synaptophysin / analysis. Tomography, X-Ray Computed / methods. Ultrasonography / methods

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  • (PMID = 19287120.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / MUC2 protein, human; 0 / Mucin-2; 0 / Synaptophysin
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4. Chiang KC, Hsu JT, Chen HY, Jwo SC, Hwang TL, Jan YY, Yeh CN: Multifocal intraductal papillary mucinous neoplasm of the pancreas--a case report. World J Gastroenterol; 2009 Feb 7;15(5):628-32

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  • [Title] Multifocal intraductal papillary mucinous neoplasm of the pancreas--a case report.
  • Cystic neoplasms of the pancreas are relatively rare, comprising 10 percent of pancreatic cysts and only 1 percent of pancreatic cancers.
  • Cystic neoplasms include mucinous cystic neoplasms, serous cystadenomas, papillary cystic tumors, cystic islet cell tumors and intraductal papillary mucinous neoplasms of the pancreas (IPMNs).
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Carcinoma, Pancreatic Ductal / pathology

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  • (PMID = 19195068.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2653357
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5. Nakakura EK, Bergsland EK: Islet cell carcinoma: neuroendocrine tumors of the pancreas and periampullary region. Hematol Oncol Clin North Am; 2007 Jun;21(3):457-73; viii
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  • [Title] Islet cell carcinoma: neuroendocrine tumors of the pancreas and periampullary region.
  • Most patients who have islet cell tumors, except those who have insulinomas, present with locally advanced or metastatic disease.
  • In contrast with patients who have adenocarcinoma of the pancreas, those who have islet cell carcinomas can achieve long-term survival even if their disease is advanced.
  • [MeSH-major] Carcinoma, Islet Cell. Common Bile Duct Neoplasms. Neuroendocrine Tumors. Pancreatic Neoplasms

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  • (PMID = 17548034.001).
  • [ISSN] 0889-8588
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 57
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6. Kubota K, Kita J, Rokkaku K, Iwasaki Y, Sawada T, Imura J, Fujimori T: Ectopic hepatocellular carcinoma arising from pancreas: a case report and review of the literature. World J Gastroenterol; 2007 Aug 21;13(31):4270-3
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  • [Title] Ectopic hepatocellular carcinoma arising from pancreas: a case report and review of the literature.
  • With a tentative diagnosis of non-functional islet-cell tumor, the patient underwent resection of the pancreatic body and tail with splenectomy.
  • These results supported a diagnosis of HCC without any adenocarcinoma component.
  • The patient is currently doing well without any signs of recurrence in either the remaining pancreas or liver three years after surgery.
  • We report the rare case with ectopic HCC in the pancreas with a review of the literature.

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  • (PMID = 17696261.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers; 0 / CAM 5.2 antigen; 0 / Keratin-18; 68238-35-7 / Keratins
  • [Number-of-references] 33
  • [Other-IDs] NLM/ PMC4250631
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7. Klimstra DS: Nonductal neoplasms of the pancreas. Mod Pathol; 2007 Feb;20 Suppl 1:S94-112
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  • [Title] Nonductal neoplasms of the pancreas.
  • The most common and best-characterized nonductal neoplasms are pancreatic endocrine neoplasm, acinar cell carcinoma, pancreatoblastoma, and solid pseudopapillary neoplasm.
  • [MeSH-major] Adenocarcinoma, Papillary / pathology. Adenoma, Islet Cell / pathology. Carcinoma, Acinar Cell / pathology. Carcinoma, Islet Cell / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 17486055.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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8. Hav M, Lem D, Chhut SV, Kong R, Pauwels P, Cuvelier C, Piet P: Clear-cell variant of solid-pseudopapillary neoplasm of the pancreas: a case report and review of the literature. Malays J Pathol; 2009 Dec;31(2):137-41
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  • [Title] Clear-cell variant of solid-pseudopapillary neoplasm of the pancreas: a case report and review of the literature.
  • Solid-pseudopapillary neoplasm (SPN) of the pancreas is a rare neoplasm reported to have a favourable prognosis because of its slow-growing behaviour.
  • Its clear cell variant creates challenges in distinction from other clear cell tumours in the pancreas.
  • Exploratory laparotomy revealed a 5.2 cm well-demarcated tumour in the head of the pancreas, which was treated with Whipple procedure.
  • Microscopically, the tumour showed an extensive solid growth pattern consisting of cells with abundant clear cytoplasm, and papillary areas containing cells with eosinophilic cytoplasm, indicating a clear-cell solid-papillary neoplasm.
  • Difficulties are recognized in differentiating clear-cell SPN from "sugar" tumours, metastatic renal cell carcinoma, clear-cell variant of pancreatic endocrine neoplasm and ductal adenocarcinoma.
  • When facing such difficulties, nuclear and cytoplamic beta-catenin, nuclear E-cadherin expressions and absence of membranous E-cadherin staining are useful in differentiating clear-cell SPN from other clear cell tumours in the pancreas.
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Carcinoma, Islet Cell / diagnosis. Carcinoma, Pancreatic Ductal / diagnosis. Carcinoma, Renal Cell / diagnosis. Carcinoma, Renal Cell / secondary. Cell Nucleus / chemistry. Cell Nucleus / pathology. Cytoplasm / chemistry. Cytoplasm / pathology. Diagnosis, Differential. Female. Humans. Perivascular Epithelioid Cell Neoplasms / diagnosis


9. Iwamuro M, Kubota J, Saito S, Goubaru M, Ohta T, Ogata M, Takuma Y, Tanaka S, Makino Y, Murakami I: [A case of mixed duct-islet cell tumor of the pancreas]. Nihon Shokakibyo Gakkai Zasshi; 2007 Jun;104(6):829-36
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  • [Title] [A case of mixed duct-islet cell tumor of the pancreas].
  • Surgical resection was performed, but curative resection was impossible because the component of adenocarcinoma infiltrating into surrounding tissue coexisted with insulinoma.
  • Postoperatively, we make a diagnosis of combined tumor of the pancreas, i.e. mixed duct-islet cell carcinoma.
  • [MeSH-major] Carcinoma, Islet Cell / diagnosis. Carcinoma, Pancreatic Ductal / diagnosis. Insulinoma / diagnosis. Neoplasms, Multiple Primary. Pancreatic Neoplasms / diagnosis

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  • (PMID = 17548951.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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10. Prichett W, Milman P, Gagnon J, Munoz DG, Woulfe J: Intranuclear rodlets in human pancreatic islet cells. Pancreas; 2007 Oct;35(3):207-11
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  • [Title] Intranuclear rodlets in human pancreatic islet cells.
  • We recently identified these structures in pancreatic islet cells.
  • The objectives of this study are to describe the light microscopic features and cellular pattern of distribution of INRs in human pancreatic islet cells.
  • Promyelocytic leukemia staining within the nuclei of B cells was confined to INRs and was not present in the typical PML bodies present in other cell types.
  • Spatially, PML and C3T staining of islet cell INRs appeared to be mutually exclusive within individual INRs.
  • CONCLUSIONS: Intranuclear rodlets are present within the nuclei of pancreatic islet cells, where they reside predominantly but not exclusively in B cells.
  • Immunoreactivity of B-cell INRs for PML suggests that the functional significance of INRs may be related to that of PML and/or PML bodies.
  • The mutually exclusive pattern of PML and C3T staining suggests dynamic interactions between these 2 proteins in B-cell INRs.
  • [MeSH-major] Adenocarcinoma / ultrastructure. Intranuclear Inclusion Bodies / ultrastructure. Islets of Langerhans / ultrastructure. Pancreatic Neoplasms / ultrastructure

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  • (PMID = 17895839.001).
  • [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 / Tubulin
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11. Deng H, Shi J, Wilkerson M, Meschter S, Dupree W, Lin F: Usefulness of S100P in diagnosis of adenocarcinoma of pancreas on fine-needle aspiration biopsy specimens. Am J Clin Pathol; 2008 Jan;129(1):81-8
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  • [Title] Usefulness of S100P in diagnosis of adenocarcinoma of pancreas on fine-needle aspiration biopsy specimens.
  • Even though the cytologic criteria for pancreatic ductal adenocarcinoma (PDA) on fine-needle aspiration biopsy (FNAB) specimens have been well defined, a diagnostic challenge is still present.
  • We immunohistochemically evaluated the diagnostic value of S100P on cell-block and/or smear preparations in 58 cases of FNAB specimens of the pancreas.
  • S100P is a sensitive and specific marker for the detection of PDA on FNAB specimens on cell-block and smear preparations.
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / metabolism. Biopsy, Fine-Needle. Carcinoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / metabolism. Diagnosis, Differential. Epithelial Cells / metabolism. Epithelial Cells / pathology. Humans. Immunoenzyme Techniques. Islets of Langerhans / metabolism. Islets of Langerhans / pathology. Pancreatic Ducts / metabolism. Pancreatic Ducts / pathology

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  • (PMID = 18089492.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / Nuclear Proteins; 0 / S100PBP protein, human
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12. Yang W, Chen MH, Yan K, Wu W, Dai Y, Zhang H: Differential diagnosis of non-functional islet cell tumor and pancreatic carcinoma with sonography. Eur J Radiol; 2007 Jun;62(3):342-51
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  • [Title] Differential diagnosis of non-functional islet cell tumor and pancreatic carcinoma with sonography.
  • OBJECTIVE: To investigate the differential diagnosis of non-functional islet cell tumor (NFICT) and pancreatic ductal adenocarcinoma (pancreatic carcinoma) with clinical presentation and sonographic features.
  • [MeSH-major] Adenoma, Islet Cell / diagnosis. Carcinoma, Pancreatic Ductal / diagnosis. Pancreas / ultrasonography. Pancreatic Neoplasms / diagnosis. Ultrasonography / methods

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  • (PMID = 17412543.001).
  • [ISSN] 0720-048X
  • [Journal-full-title] European journal of radiology
  • [ISO-abbreviation] Eur J Radiol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Phospholipids; 0 / contrast agent BR1; WS7LR3I1D6 / Sulfur Hexafluoride
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13. Shimada K, Sakamoto Y, Esaki M, Kosuge T, Hiraoka N: Role of medial pancreatectomy in the management of intraductal papillary mucinous neoplasms and islet cell tumors of the pancreatic neck and body. Dig Surg; 2008;25(1):46-51
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  • [Title] Role of medial pancreatectomy in the management of intraductal papillary mucinous neoplasms and islet cell tumors of the pancreatic neck and body.
  • RESULTS: Among 10 patients with intraductal papillary mucinous neoplasms, 3 patients had minimally invasive adenocarcinoma, and 3 had adenocarcinoma in situ.
  • A medial pancreatectomy was converted to a distal pancreatectomy in 1 patient with adenocarcinoma in situ.
  • Three patients with islet cell tumor and 1 patient with solid pseudopapillary tumor had no malignant disease.
  • CONCLUSIONS: A medial pancreatectomy is a safe and effective alternative for the treatment of intraductal papillary mucinous neoplasm, islet cell tumor, or solid pseudopapillary tumor located in the neck or body of the pancreas.
  • [MeSH-major] Adenocarcinoma, Mucinous / surgery. Adenocarcinoma, Papillary / surgery. Adenoma, Islet Cell / surgery. Carcinoma, Intraductal, Noninfiltrating / surgery. Pancreatectomy. Pancreatic Neoplasms / surgery

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  • (PMID = 18292661.001).
  • [ISSN] 1421-9883
  • [Journal-full-title] Digestive surgery
  • [ISO-abbreviation] Dig Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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14. Esni F, Miyamoto Y, Leach SD, Ghosh B: Primary explant cultures of adult and embryonic pancreas. Methods Mol Med; 2005;103:259-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary explant cultures of adult and embryonic pancreas.
  • The developmental plasticity of adult pancreas is evidenced by the ability to undergo conversion between different epithelial cell types.
  • Specific examples of such conversions include acinar to ductal metaplasia, ductal to islet metaplasia, and generation of ductal structures within islets.
  • Although 90% of human pancreatic cancers are classified as ductal adenocarcinoma, markers of all pancreatic epithelial cell types (acini, ductal, and endocrine) as well as markers of gastric and intestinal lineages can be detected in these tumors.
  • In recent years considerable knowledge has been gained regarding regulation of cellular differentiation and various signaling pathways involved in normal and neoplastic pancreas through studies of pancreatic cancer and immortalized ductal cell lines.
  • Here we have described a detailed method for preparation, maintenance, and manipulation of adult and embryonic mouse pancreas.
  • [MeSH-minor] Animals. Cell Culture Techniques / methods. Epithelial Cells / cytology. Immunohistochemistry. Male. Mice. Pancreas / cytology. Pancreas / embryology. Rats

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  • (PMID = 15542912.001).
  • [ISSN] 1543-1894
  • [Journal-full-title] Methods in molecular medicine
  • [ISO-abbreviation] Methods Mol. Med.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK56211-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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15. de Juan C, Sanchez M, Miquel R, Pages M, Ayuso JR, Ayuso C: Uncommon tumors and pseudotumoral lesions of the pancreas. Curr Probl Diagn Radiol; 2008 Jul-Aug;37(4):145-64
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  • [Title] Uncommon tumors and pseudotumoral lesions of the pancreas.
  • Ductal adenocarcinoma is the most common tumor of the pancreas, accounting for about 80% of all pancreatic tumors.
  • The other 20% of pancreatic tumors is represented by a heterogeneous group of pancreatic neoplasms that includes cystic pancreatic neoplasms, islet cell tumors, and the so-called rare pancreatic tumors.
  • Some of these lesions may show an appearance similar to ductal adenocarcinoma being radiologically indistinguishable.
  • Many of these uncommon tumors and pseudotumoral lesions have a different approach, therapy, and prognosis than ductal adenocarcinoma.
  • In the present article, we review the radiological features of uncommon pancreatic tumors, atypical manifestations of ductal adenocarcinoma, and pseudotumoral masses, focusing on those features that can be helpful for the differential diagnosis.

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  • (PMID = 18502323.001).
  • [ISSN] 1535-6302
  • [Journal-full-title] Current problems in diagnostic radiology
  • [ISO-abbreviation] Curr Probl Diagn Radiol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
  • [Number-of-references] 42
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16. Nijs E, Callahan MJ, Taylor GA: Disorders of the pediatric pancreas: imaging features. Pediatr Radiol; 2005 Apr;35(4):358-73; quiz 457
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  • [Title] Disorders of the pediatric pancreas: imaging features.
  • The purpose of this manuscript is to provide an overview of the normal development of the pancreas as well as pancreatic pathology in children.
  • Diagnostic imaging plays a major role in the evaluation of the pancreas in infants and children.
  • These include pancreas divisum, annular pancreas, agenesis of the dorsal pancreatic anlagen and ectopic pancreatic tissue.
  • Primary pancreatic neoplasms are rare in children and are divided into exocrine tumors such as pancreatoblastoma and adenocarcinoma and into endocrine or islet cell tumors.
  • Islet cell tumors are classified as functioning (insulinoma, gastrinoma, VIPoma and glucagonoma) and nonfunctioning tumors.
  • Although quite rare, secondary tumors of the pancreas can be associated with certain primary malignancies.
  • [MeSH-minor] Adult. Child. Humans. Infant. Pancreas / abnormalities. Pancreas / anatomy & histology. Pancreatic Neoplasms / diagnosis

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  • (PMID = 15536562.001).
  • [ISSN] 0301-0449
  • [Journal-full-title] Pediatric radiology
  • [ISO-abbreviation] Pediatr Radiol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 50
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17. Jiang X, Abiatari I, Kong B, Erkan M, De Oliveira T, Giese NA, Michalski CW, Friess H, Kleeff J: Pancreatic islet and stellate cells are the main sources of endocrine gland-derived vascular endothelial growth factor/prokineticin-1 in pancreatic cancer. Pancreatology; 2009;9(1-2):165-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic islet and stellate cells are the main sources of endocrine gland-derived vascular endothelial growth factor/prokineticin-1 in pancreatic cancer.
  • METHODS: mRNA levels of EG-VEGF/prokineticin 1 (PK1), prokineticin 2 (PK2) and their receptors 1 (PKR1) and 2 (PKR2) were measured in pancreatic tissues, pancreatic cancer cell lines and PSCs by quantitative reverse-transcriptase polymerase chain reaction (QRT-PCR).
  • RESULTS: QRT-PCR analysis in bulk tissues of normal pancreas, chronic pancreatitis and pancreatic ductal adenocarcinoma showed no significant difference of PK1 mRNA levels, whereas PK2 mRNA was barely detectable.
  • High PK1 mRNA levels were observed only in cultured PSCs and microdissected islet cells, but not in cancer cells, and PK1 protein was localized mainly in islets and cancer-associated stromal cells.
  • CONCLUSIONS: Islet and/or PSC-derived PK1 might act through its receptors on endothelial cells to increase angiogenesis in pancreatic diseases.
  • [MeSH-major] Islets of Langerhans / metabolism. Pancreas / metabolism. Pancreatic Neoplasms / metabolism. Vascular Endothelial Growth Factor, Endocrine-Gland-Derived / biosynthesis
  • [MeSH-minor] Cell Line, Tumor. Cells, Cultured. Gastrointestinal Hormones / biosynthesis. Humans. Neuropeptides / biosynthesis. Pancreatitis, Chronic / metabolism. RNA, Messenger / metabolism. Receptors, G-Protein-Coupled / biosynthesis. Receptors, Peptide / biosynthesis

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  • [Copyright] Copyright 2008 S. Karger AG, Basel and IAP.
  • (PMID = 19077468.001).
  • [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
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Gastrointestinal Hormones; 0 / Neuropeptides; 0 / PROK2 protein, human; 0 / PROKR1 protein, human; 0 / PROKR2 protein, human; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Peptide; 0 / Vascular Endothelial Growth Factor, Endocrine-Gland-Derived
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18. 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.
  • We hypothesized that Polycomb might play a role in preneoplastic states in the pancreas and in tumour development/progression.
  • 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.
  • [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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19. Pamuklar E, Semelka RC: MR imaging of the pancreas. Magn Reson Imaging Clin N Am; 2005 May;13(2):313-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MR imaging of the pancreas.
  • (1) TI-weighted fat-suppressed and dynamic gadolinium-enhanced SGE imaging for the detection of chronic pancreatitis, ductal adeno-carcinoma, and islet-cell tumors;.
  • (2) T2-weighted fat-suppressed imaging and T2-weighted breath-hold imaging for the detection of islet-cell tumors;and (3) precontrast breath-hold SGE imaging for the detection of acute pancreatitis.
  • Relatively specific morphologic and signal intensity features permit characterization of acute pancreatitis,chronic pancreatitis, ductal adenocarcinoma, insulinoma, gastrinoma, glucagonoma, microcystic cystadenoma, macrocystic cystadenoma, and solid and papillary epithelial neoplasm.
  • MR imaging is effective as a problem-solving modality because it distinguishes chronic pancreatitis from normal pancreas and chronic pancreatitis with focal enlargement from pancreatic cancer in the majority of cases.MR imaging studies should be considered in the following settings:.
  • (2) in patients with prior CT imaging who have focal enlargement of the pancreas with no definable mass;.
  • Patients with biochemical evidence of islet-cell tumors should be examined by MR imaging as the first-line imaging modality because of the high sensitivity of MR imaging for detecting the presence of islet-cell tumors and determining the presence of metastatic disease.

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  • (PMID = 15935314.001).
  • [ISSN] 1064-9689
  • [Journal-full-title] Magnetic resonance imaging clinics of North America
  • [ISO-abbreviation] Magn Reson Imaging Clin N Am
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
  • [Number-of-references] 56
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20. 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.
  • 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.
  • After this initial period, the resulting tissues were cultured in DM without cholera toxin, supplemented with gastrin (50 nmol/L) and hepatocyte growth factor (HGF; 10 ng/mL), with islet neogenesis-associated protein (INGAP; 167 nmol/L) or with gastrin + HGF + INGAP for 6 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.
  • 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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21. Hashimoto Y, Murakami Y, Uemura K, Hayashidani Y, Sudo T, Ohge H, Sueda T, Shimamoto F, Hiyama E: Mixed ductal-endocrine carcinoma derived from intraductal papillary mucinous neoplasm (IPMN) of the pancreas identified by human telomerase reverse transcriptase (hTERT) expression. J Surg Oncol; 2008 Apr 1;97(5):469-75
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  • [Title] Mixed ductal-endocrine carcinoma derived from intraductal papillary mucinous neoplasm (IPMN) of the pancreas identified by human telomerase reverse transcriptase (hTERT) expression.
  • We report a case of mixed ductal-endocrine carcinoma derived from intraductal papillary mucinous neoplasm (IPMN) of the pancreas.
  • This pathologically unique tumor is the first case of mixed ductal-endocrine carcinoma derived from pancreatic IPMN and telomerase activation could play a potential role in the neoplastic progression of mixed ductal-endocrine carcinomas of the pancreas.
  • [MeSH-major] Adenocarcinoma, Mucinous / metabolism. Carcinoma, Islet Cell / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Papillary / metabolism. Neoplasms, Second Primary / metabolism. Pancreatic Neoplasms / metabolism. Telomerase / metabolism

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  • [Copyright] (Copyright) 2008 Wiley-Liss, Inc.
  • (PMID = 18161862.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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22. 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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  • [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.
  • 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 conclusion, YAP65 is expressed mainly in centroacinar and small ductal cells in the normal pancreas.
  • 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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23. Kayed H, Kleeff J, Esposito I, Giese T, Keleg S, Giese N, Büchler MW, Friess H: Localization of the human hedgehog-interacting protein (Hip) in the normal and diseased pancreas. Mol Carcinog; 2005 Apr;42(4):183-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Localization of the human hedgehog-interacting protein (Hip) in the normal and diseased pancreas.
  • Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a poor prognosis.
  • In the current study we analyzed the expression, distribution, and function of another component of this signaling pathway, the human hedgehog-interacting protein (Hip), in the normal pancreas, CP and PDAC utilizing real-time quantitative reverse transcription-polymerase chain reaction (QRT-PCR), immunohistochemistry, immunofluorescence, Hip siRNA transfection, cell growth assays, and cell cycle analysis.
  • Only SU-8686 and BxPC-3 pancreatic cancer cells expressed Hip mRNA, whereas expression was below the level of detection in the other six pancreatic cancer cell lines tested.
  • As shown by immunohistochemistry, Hip was expressed in normal pancreatic tissues mainly in the cytoplasm of islet cells and in smooth muscle cells of blood vessels.
  • Incubation of pancreatic cancer cell lines with recombinant Hip revealed a growth inhibitory effect in SU-8686 and Capan-1 pancreatic cancer cells and no effect on cell growth in the other tested cell lines.
  • In conclusion, Hip is expressed in the normal pancreas, CP and PDAC tissues.
  • The different pattern of Hip expression and abnormal localization in the diseased pancreas suggest that the enhanced activation of hedgehog signaling in CP and PDAC is-at least in part-due to the aberrant responsiveness and expression of Hip in these diseases.
  • [MeSH-major] Adenocarcinoma / genetics. Carcinoma, Pancreatic Ductal / genetics. Carrier Proteins / genetics. Membrane Glycoproteins / genetics. Pancreatic Ducts / pathology

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15754313.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA Primers; 0 / HHIP protein, human; 0 / Membrane Glycoproteins; 0 / RNA, Messenger
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24. Xu X, Ehdaie B, Ohara N, Yoshino T, Deng CX: Synergistic action of Smad4 and Pten in suppressing pancreatic ductal adenocarcinoma formation in mice. Oncogene; 2010 Feb 4;29(5):674-86
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  • [Title] Synergistic action of Smad4 and Pten in suppressing pancreatic ductal adenocarcinoma formation in mice.
  • 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.
  • [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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25. Oue N, Mitani Y, Aung PP, Sakakura C, Takeshima Y, Kaneko M, Noguchi T, Nakayama H, Yasui W: Expression and localization of Reg IV in human neoplastic and non-neoplastic tissues: Reg IV expression is associated with intestinal and neuroendocrine differentiation in gastric adenocarcinoma. J Pathol; 2005 Oct;207(2):185-98
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  • [Title] Expression and localization of Reg IV in human neoplastic and non-neoplastic tissues: Reg IV expression is associated with intestinal and neuroendocrine differentiation in gastric adenocarcinoma.
  • Regenerating islet-derived family, member 4 (Reg IV) is a candidate marker for cancer and inflammatory bowel disease.
  • Insulin-producing beta cells of the endocrine pancreas were positive for Reg IV.
  • Reg IV expression was also detected in 5 (21.7%) of 23 ductal adenocarcinomas of the pancreas.
  • [MeSH-major] Adenocarcinoma / chemistry. Lectins, C-Type / analysis. Neoplasm Proteins / analysis. Stomach Neoplasms / chemistry
  • [MeSH-minor] Adenoma / chemistry. Biomarkers, Tumor / analysis. Blotting, Western / methods. Breast Neoplasms / chemistry. Carcinoid Tumor / chemistry. Cell Differentiation / physiology. Cell Line, Tumor. Colon / metabolism. Colorectal Neoplasms / chemistry. Female. Humans. Immunohistochemistry / methods. Intestine, Small / metabolism. Lung Neoplasms / chemistry. Pancreas / metabolism. Pancreatic Neoplasms / chemistry. Phenotype. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Stomach / metabolism

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  • [Copyright] Copyright (c) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 16086444.001).
  • [ISSN] 0022-3417
  • [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 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / Neoplasm Proteins; 0 / REG4 protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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26. Buscaglia JM, Giday SA, Kantsevoy SV, Jagannath SB, Magno P, Wolfgang CL, Daniels JA, Canto MI, Okolo Iii PI: Patient- and cyst-related factors for improved prediction of malignancy within cystic lesions of the pancreas. Pancreatology; 2009;9(5):631-8
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  • [Title] Patient- and cyst-related factors for improved prediction of malignancy within cystic lesions of the pancreas.
  • Final pathological diagnoses were branch-duct IPMN (n = 118, 50% malignant), serous cystadenoma (n = 71), pseudocyst (n = 37), mucinous cyst adenoma/adenocarcinoma (n = 36), islet cell tumor (n = 4), simple cyst (n = 3), and ductal adenocarcinoma with cystic degeneration (n = 1).
  • [MeSH-major] Pancreas / ultrasonography. Pancreatic Cyst / ultrasonography

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19657218.001).
  • [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
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Carcinoembryonic Antigen
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27. Zhong L: Magnetic resonance imaging in the detection of pancreatic neoplasms. J Dig Dis; 2007 Aug;8(3):128-32
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  • Primary tumors of the pancreas may be mainly classified as ductal adenocarcinomas, cystic tumors and islet cell tumors (ICT).
  • The combined MRI features of a focal pancreatic mass, pancreatic duct dilatation and parenchymal atrophy are highly suggestive of a ductal adenocarcinoma.
  • Most cystic neoplasms of the pancreas are either microcystic adenomas or mucinous cystic neoplasms.
  • ICT are rare neoplasms arising from neuroendocrine cells in the pancreas or the periampullary region.
  • The most frequent tumors to metastasize to the pancreas are cancers of the breast, lung, kidney and melanoma.
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / pathology. Humans. Neoplasms, Cystic, Mucinous, and Serous / diagnosis. Neoplasms, Cystic, Mucinous, and Serous / pathology. Pancreas / pathology

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  • (PMID = 17650223.001).
  • [ISSN] 1751-2972
  • [Journal-full-title] Journal of digestive diseases
  • [ISO-abbreviation] J Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Australia
  • [Number-of-references] 10
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28. Takahashi K, Hirano F, Matsumoto K, Aso K, Haneda M: Homeobox gene CDX2 inhibits human pancreatic cancer cell proliferation by down-regulating cyclin D1 transcriptional activity. Pancreas; 2009 Jan;38(1):49-57
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  • [Title] Homeobox gene CDX2 inhibits human pancreatic cancer cell proliferation by down-regulating cyclin D1 transcriptional activity.
  • This study is intended to investigate the effect of CDX2 expression on cell proliferation and cyclin D1 expression in pancreatic cancer cells.
  • METHODS: Four pancreatic ductal adenocarcinoma cell lines (PancQGO-1, BxPC-3, MIAPaCa-2, CFPAC-1), 1 islet carcinoma cell line (QGP-1), and 1 adenosquamous carcinoma cell line (KP-3) were analyzed for CDX1 and CDX2 expression using real-time reverse transcription-polymerase chain reaction and Western blot analysis.
  • Moreover, CDX2 was expressed at a middle level in 4 pancreatic ductal adenocarcinoma cells.
  • Cell proliferation and cyclin D1 mRNA level were inhibited significantly after CDX2 transfection in pancreatic cancer cells.
  • CONCLUSIONS: CDX2 might play a role in inhibiting cell proliferation and repressing cyclin D1 transcriptional activity through the proximal nuclear factor kappaB binding site in pancreatic cancer cells.
  • [MeSH-major] Cell Proliferation. Cyclin D1 / genetics. Gene Expression Regulation, Neoplastic. Homeodomain Proteins / genetics. Pancreatic Neoplasms / genetics. Transcription, Genetic
  • [MeSH-minor] Carcinoma, Adenosquamous / genetics. Carcinoma, Adenosquamous / pathology. Carcinoma, Islet Cell / genetics. Carcinoma, Islet Cell / pathology. Carcinoma, Pancreatic Ductal / genetics. Carcinoma, Pancreatic Ductal / pathology. Cell Line, Tumor. Cyclooxygenase 2 / genetics. Down-Regulation. Humans. NF-kappa B / genetics. Promoter Regions, Genetic. RNA, Messenger / metabolism. Time Factors. Transfection

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  • (PMID = 19106744.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCND1 protein, human; 0 / CDX1 protein, human; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / NF-kappa B; 0 / RNA, Messenger; 136601-57-5 / Cyclin D1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
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29. Habbe N, Shi G, Meguid RA, Fendrich V, Esni F, Chen H, Feldmann G, Stoffers DA, Konieczny SF, Leach SD, Maitra A: Spontaneous induction of murine pancreatic intraepithelial neoplasia (mPanIN) by acinar cell targeting of oncogenic Kras in adult mice. Proc Natl Acad Sci U S A; 2008 Dec 2;105(48):18913-8
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  • [Title] Spontaneous induction of murine pancreatic intraepithelial neoplasia (mPanIN) by acinar cell targeting of oncogenic Kras in adult mice.
  • Pancreatic ductal adenocarcinoma (PDAC) is believed to arise through a multistep model comprised of putative precursor lesions known as pancreatic intraepithelial neoplasia (PanIN).
  • 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.
  • 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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30. Hong X, Michalski CW, Kong B, Zhang W, Raggi MC, Sauliunaite D, De Oliveira T, Friess H, Kleeff J: ALCAM is associated with chemoresistance and tumor cell adhesion in pancreatic cancer. J Surg Oncol; 2010 Jun 1;101(7):564-9
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  • [Title] ALCAM is associated with chemoresistance and tumor cell adhesion in pancreatic cancer.
  • AIMS: Cell-cell adhesion is a major factor in integrity of epithelia which is frequently disturbed in cancer leading to local invasion and distant metastasis.
  • METHODS: To define expression and function of activated leukocyte cell adhesion molecule (ALCAM, CD166) in pancreatic cancer and in pancreatic neuroendocrine tumors (PNET), microarray analyses, RT-PCR, immunohistochemistry, RNAi, adhesion, migration, invasion, and chemoresistance assays were used.
  • RESULTS: We demonstrate that expression of ALCAM is altered and its serum levels are increased in pancreatic ductal adenocarcinoma (PDAC).
  • ALCAM was expressed on the membranes of islet cells in the normal pancreas whereas normal pancreatic ducts were ALCAM-negative.
  • PNET were mostly ALCAM-positive with a cytoplasmic staining pattern which was in contrast to the membrane expression observed in non-transformed islet cells.
  • In vitro, ALCAM silencing using RNAi had no effects on growth or invasion of pancreatic cancer cells but reduced cell adhesion and induced chemoresistance.
  • In neuroendocrine tumor cell lines, silencing of ALCAM decreased cell growth.
  • CONCLUSIONS: We propose ALCAM as a novel serum biomarker in human pancreatic tumors which is associated with cell adhesion, growth and chemoresistance.
  • [MeSH-major] Activated-Leukocyte Cell Adhesion Molecule / blood. Biomarkers, Tumor / blood. Carcinoma, Pancreatic Ductal / pathology. Neuroendocrine Tumors / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Case-Control Studies. Cell Adhesion. Cell Line, Tumor. Cell Transformation, Neoplastic. Drug Resistance, Neoplasm. Humans. Middle Aged. Survival Analysis

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  • (PMID = 20461761.001).
  • [ISSN] 1096-9098
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Activated-Leukocyte Cell Adhesion Molecule; 0 / Biomarkers, Tumor
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31. Saruc M, Iki K, Pour PM: Morphometric studies in human pancreatic cancer argues against the etiological role of type 2 diabetes in pancreatic cancer. Histol Histopathol; 2010 04;25(4):423-32
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  • BACKGROUND: To understand the role of islet amyloid polypeptide (IAPP) in type 2 diabetes and pancreatic cancer (PC), we investigated the patterns of its expression and its ratio to insulin, glucagon, somatostatin and pancreatic polypeptide cells by morphometry in tissues from these two diseases in comparison to the normal pancreas.
  • RESULTS: In the normal pancreas, only 50% of the beta-cells while alpha- and delta-cells co-expressed IAPP only sporadically.
  • In zone B, however, significantly more beta-cell and IAPP-expressing cells and a significantly lower number of alpha-cells were found compared to those in zone A.
  • Significant differences were also found between the specimens from type 2 diabetics and pancreatic cancer relative to the ratios of IAPP/beta-cell, IAPP/alpha-cells and beta-cell/delta-cells.
  • [MeSH-major] Adenocarcinoma / pathology. Diabetes Mellitus, Type 2 / pathology. Morphogenesis / physiology. Pancreas / pathology. Pancreatic Neoplasms / pathology. Somatostatin / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Amyloid / metabolism. Biomarkers, Tumor / metabolism. Female. Glucagon / metabolism. Humans. Immunoenzyme Techniques. Insulin / metabolism. Islet Amyloid Polypeptide. Islets of Langerhans / metabolism. Islets of Langerhans / pathology. Male. Middle Aged. Pancreatic Polypeptide / metabolism


32. Lowe AW, Olsen M, Hao Y, Lee SP, Taek Lee K, Chen X, van de Rijn M, Brown PO: Gene expression patterns in pancreatic tumors, cells and tissues. PLoS One; 2007 Mar 28;2(3):e323
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Cancers of the pancreas originate from both the endocrine and exocrine elements of the organ, and represent a major cause of cancer-related death.
  • This study provides a comprehensive assessment of gene expression for pancreatic tumors, the normal pancreas, and nonneoplastic pancreatic disease.
  • METHODS/RESULTS: DNA microarrays were used to assess the gene expression for surgically derived pancreatic adenocarcinomas, islet cell tumors, and mesenchymal tumors.
  • The addition of normal pancreata, isolated islets, isolated pancreatic ducts, and pancreatic adenocarcinoma cell lines enhanced subsequent analysis by increasing the diversity in gene expression profiles obtained.

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  • (PMID = 17389914.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA077097; United States / NCI NIH HHS / CA / CA77097
  • [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 / Axin Protein; 0 / DNA, Neoplasm; 0 / RNA, Neoplasm; 0 / Repressor Proteins
  • [Other-IDs] NLM/ PMC1824711
  • [General-notes] NLM/ Original DateCompleted: 20070726
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33. Larghi A, Stobinski M, Galasso D, Lecca PG, Costamagna G: Concomitant intraductal papillary mucinous neoplasm and pancreatic endocrine tumour: Report of two cases and review of the literature. Dig Liver Dis; 2009 Oct;41(10):759-61
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  • Clinicopathological features of patients with concomitant intraductal papillary mucinous neoplasm of the pancreas and pancreatic endocrine neoplasm.
  • Clinicopathological features of patients with concomitant intraductal papillary mucinous neoplasm of the pancreas and pancreatic endocrine neoplasm.
  • Nesidioblastosis coexisting with islet cell tumor and intraductal papillary mucinous hyperplasia.
  • Endocrine tumor and intraductal papillary mucinous neoplasm of the pancreas: a fortuitous association?
  • Pancreas 2005;31:79-83].
  • [MeSH-major] Adenocarcinoma, Mucinous / diagnosis. Carcinoma, Neuroendocrine / diagnosis. Carcinoma, Papillary / diagnosis. Cholangiopancreatography, Magnetic Resonance / methods. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Carcinoma, Pancreatic Ductal / diagnosis. Endosonography / methods. Female. Gastrointestinal Agents. Humans. Middle Aged. Pancreas / pathology. Secretin

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  • (PMID = 19223252.001).
  • [ISSN] 1878-3562
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Gastrointestinal Agents; 1393-25-5 / Secretin
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34. Kayed H, Bekasi S, Keleg S, Welsch T, Esposito I, Shimamura A, Michalski CW, Friess H, Kleeff J: Expression of the Shwachman-Bodian-Diamond syndrome (SBDS) protein in human pancreatic cancer and chronic pancreatitis. Histol Histopathol; 2008 07;23(7):819-26
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: In this study, the expression and localization of SBDS were investigated in normal human pancreatic tissues, chronic pancreatitis (CP) tissues, primary and metastatic pancreatic ductal adenocarcinoma (PDAC) tissues, as well as in cultured pancreatic cancer cell lines by immunohistochemistry, immunoblotting and immunocytochemistry.
  • RESULTS: In the normal pancreas, SBDS was localized in the cytoplasm of islet cells and ductal cells.
  • Different levels of SBDS protein were detected in cultured pancreatic cancer cell lines.
  • CONCLUSION: SBDS is expressed in normal, CP, and PDAC tissues, as well as in pancreatic cancer cell lines.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Pancreas / metabolism. Pancreatic Neoplasms / metabolism. Pancreatitis, Chronic / metabolism. Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Line, Tumor. Cell Nucleus / metabolism. Cell Nucleus / pathology. Cytoplasm / metabolism. Cytoplasm / pathology. Humans. Middle Aged. Syndrome


35. Vosters O, Beuneu C, Goldman M, Verhasselt V: N-acetylcysteine derivative inhibits CD40-dependent proinflammatory properties of human pancreatic duct cells. Pancreas; 2008 May;36(4):363-8
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  • OBJECTIVES: We recently observed that duct cells constitutively express CD40, a membrane molecule whose engagement results in duct cell activation and proinflammatory cytokine secretion.
  • This observation suggests a potential role of this pathway in the pathogenesis of type 1 diabetes, islet graft rejection, or acute pancreatitis.
  • METHODS: We assessed the effects of Nacystelyn on CD40 expression and function in human caucasian pancreatic adenocarcinoma, ATCC n degrees THB-80 (CAPAN-2) cells, a human pancreatic duct cell line.
  • To assess CAPAN-2 cell responses to CD40 engagement, we looked at nuclear factor-kappaB transcription factor activation using enzyme-linked immunosorbent assay and electrophoretic mobility shift assay and cytokine mRNA levels by quantitative real-time reverse transcriptase polymerase chain reaction.
  • [MeSH-minor] Adenocarcinoma / pathology. Cell Line, Tumor. Gene Expression Regulation, Neoplastic / drug effects. Humans. NF-kappa B / drug effects. NF-kappa B / genetics. Pancreatic Neoplasms / pathology. Transcription, Genetic / drug effects

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  • (PMID = 18437082.001).
  • [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 / Antigens, CD40; 0 / N-acetylcysteine lysinate; 0 / NF-kappa B; K3Z4F929H6 / Lysine; WYQ7N0BPYC / Acetylcysteine
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36. Ishiwata T, Cho K, Kawahara K, Yamamoto T, Fujiwara Y, Uchida E, Tajiri T, Naito Z: Role of lumican in cancer cells and adjacent stromal tissues in human pancreatic cancer. Oncol Rep; 2007 Sep;18(3):537-43
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  • Lumican is a member of a small leucine-rich proteoglycan family and its overexpression has been reported in carcinoid tumor, breast, colorectal, neuroendocrine cell, uterine cervical and pancreatic cancers.
  • Reverse-transcription polymerase chain reaction and Western blot analyses revealed lumican mRNA and protein expression in six pancreatic ductal adenocarcinoma cell lines (i.e.
  • On the basis of its immunoreactivity, lumican was found to be localized in islet cells of normal pancreatic tissues, but not in exocrine cells.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adenocarcinoma / physiopathology. Carcinoma, Pancreatic Ductal / genetics. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Pancreatic Ductal / physiopathology. Cell Line, Tumor. Humans. Islets of Langerhans / physiology. Lymphatic Metastasis. Neoplasm Invasiveness. Pancreas / physiology. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17671699.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Chondroitin Sulfate Proteoglycans; 0 / RNA, Messenger; 0 / lumican; 9056-36-4 / Keratan Sulfate
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37. Peng SY, Hong DF, Liu YB, Tan ZJ, Li JT, Tao F: [Binding pancreaticogastrostomy]. Zhonghua Wai Ke Za Zhi; 2009 Jan 15;47(2):139-42

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  • METHODS: From May 2008 to October 2008, 15 patients were performed with BPG, included pancreatic head cancer in 7 cases, duodenal adenocarcinoma in 2 cases,mass-type chronic pancreatitis with pancreatolithiasis in 1 case, ampullary carcinoma in 1 case, gallbladder cancer in 1 case, islet cell tumor in 1 case and cholangiocarcinoma in 2 cases.
  • The main procedures of BPG included: isolating remnant pancreas; slitting partial posterior wall of stomach and preplaced with seromuscular purse-string suture; cutting gastric anterior wall; performing pancreaticogastrostomy (binding of outer seromuscular and inner mucous layer of stomach).
  • [MeSH-major] Pancreas / surgery. Stomach / surgery

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  • (PMID = 19563012.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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38. Corsini MM, Miller RC, Haddock MG, Donohue JH, Farnell MB, Nagorney DM, Jatoi A, McWilliams RR, Kim GP, Bhatia S, Iott MJ, Gunderson LL: Adjuvant radiotherapy and chemotherapy for pancreatic carcinoma: the Mayo Clinic experience (1975-2005). J Clin Oncol; 2008 Jul 20;26(21):3511-6
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  • PURPOSE: To determine prognostic factors and impact of adjuvant chemotherapy (CT) and radiotherapy (RT) on overall survival (OS) after resection of pancreatic adenocarcinoma.
  • PATIENTS AND METHODS: We performed a retrospective review 472 consecutive patients who underwent complete resection with negative margins (R0) for invasive carcinoma (T1-3N0-1M0) of the pancreas between 1975 and 2005 at the Mayo Clinic in Rochester, MN.
  • Exclusion criteria included metastatic or unresectable disease at surgery, positive surgical margins, and indolent tumor types (islet cell tumors and mucinous cystadenocarcinoma).
  • Tumor extension beyond the pancreas was an adverse prognostic factor by univariate analysis alone (P = .03).
  • CONCLUSION: This study represents one of the largest, single-institution, retrospective reviews of adjuvant therapy in patients after R0 resection of carcinoma of the pancreas.
  • [MeSH-major] Adenocarcinoma / therapy. Chemotherapy, Adjuvant. Pancreatic Neoplasms / therapy. Radiotherapy, Adjuvant

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  • [CommentIn] J Clin Oncol. 2008 Jul 20;26(21):3478-80 [18640927.001]
  • (PMID = 18640932.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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39. Esposito I, Kayed H, Keleg S, Giese T, Sage EH, Schirmacher P, Friess H, Kleeff J: Tumor-suppressor function of SPARC-like protein 1/Hevin in pancreatic cancer. Neoplasia; 2007 Jan;9(1):8-17
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  • Pancreatic ductal adenocarcinoma (PDAC) and other pancreatic neoplasms exhibited increased SPARCL1 mRNA levels compared to those of the normal pancreas.
  • SPARCL1 mRNA levels were low to absent in microdissected and cultured pancreatic cancer cells, and promoter demethylation increased SPARCL1 levels only slightly in three of eight cell lines.
  • SPARCL1 was observed in small capillaries in areas of inflammation/tumor growth and in some islet cells.
  • Recombinant SPARCL1 inhibited pancreatic cancer cell invasion and exerted moderate growth-inhibitory effects.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Pancreatic Ductal / prevention & control. Cell Line, Tumor. Humans. Immunohistochemistry. Middle Aged. Neoplasm Invasiveness. RNA, Messenger / analysis. Transcription, Genetic

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  • (PMID = 17325739.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Extracellular Matrix Proteins; 0 / RNA, Messenger; 0 / SPARCL1 protein, human; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC1803032
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40. Frankel WL: Update on pancreatic endocrine tumors. Arch Pathol Lab Med; 2006 Jul;130(7):963-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • [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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41. Bockman DE: Transition to pancreatic cancer in response to carcinogen. Langenbecks Arch Surg; 2008 Jul;393(4):557-60
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  • 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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42. Dowen SE, Crnogorac-Jurcevic T, Gangeswaran R, Hansen M, Eloranta JJ, Bhakta V, Brentnall TA, Lüttges J, Klöppel G, Lemoine NR: Expression of S100P and its novel binding partner S100PBPR in early pancreatic cancer. Am J Pathol; 2005 Jan;166(1):81-92
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  • S100P is a member of the S100 family of calcium-binding proteins and there have been several recent reports of its overexpression in pancreatic ductal adenocarcinoma (PDAC).
  • S100PBPR was found to localize to cell nuclei where S100P is also present, and the two proteins co-immunoprecipitate.
  • By in situ hybridization, S100PBPR transcript was found in islet cells but not duct cells of the healthy pancreas.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Base Sequence. Calcium / metabolism. Cloning, Molecular. DNA Primers. Disease Progression. Humans. In Situ Hybridization. Magnesium / metabolism. Polymerase Chain Reaction. RNA, Messenger / genetics. Transfection

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  • (PMID = 15632002.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Carrier Proteins; 0 / DNA Primers; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / S100P protein, human; 0 / S100PBP protein, human; I38ZP9992A / Magnesium; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC1602285
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43. Dietrich CF: Comments and illustrations regarding the guidelines and good clinical practice recommendations for contrast-enhanced ultrasound (CEUS)--update 2008. Ultraschall Med; 2008 Sep;29 Suppl 4:S188-202

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Ductal adenocarcinoma as the most common tumor of the pancreas is typically hypoenhanced compared to the adjacent pancreatic tissue in all phases.
  • Neuroendocrine tumors and serous microcystic adenoma of the pancreas are characterized by hypervascularization appearing typically hyperenhanced during CEUS.
  • [MeSH-minor] Adenoma, Islet Cell / ultrasonography. Carcinoma, Pancreatic Ductal / ultrasonography. Endosonography / standards. Humans. Liver Diseases / ultrasonography. Liver Neoplasms / ultrasonography. Neuroendocrine Tumors / ultrasonography. Pancreatic Diseases / ultrasonography. Pancreatic Neoplasms / ultrasonography

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  • (PMID = 18833497.001).
  • [ISSN] 1438-8782
  • [Journal-full-title] Ultraschall in der Medizin (Stuttgart, Germany : 1980)
  • [ISO-abbreviation] Ultraschall Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Contrast Media
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44. Recaldini C, Carrafiello G, Bertolotti E, Angeretti MG, Fugazzola C: Contrast-enhanced ultrasonograpic findings in pancreatic tumors. Int J Med Sci; 2008;5(4):203-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CONCLUSION: As regards hypoechoic lesions at B-mode ultrasound, CEUS often can distinguish among adenocarcinoma, islet cell tumor and serous microcystic adenoma.
  • [MeSH-major] Contrast Media / chemistry. Pancreas / ultrasonography. Pancreatic Neoplasms / diagnosis. Ultrasonography / methods

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  • (PMID = 18645620.001).
  • [ISSN] 1449-1907
  • [Journal-full-title] International journal of medical sciences
  • [ISO-abbreviation] Int J Med Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Contrast Media
  • [Other-IDs] NLM/ PMC2467517
  • [Keywords] NOTNLM ; contrast-enhanced ultrasonography / pancreatic tumors
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45. Bilimoria KY, Tomlinson JS, Merkow RP, Stewart AK, Ko CY, Talamonti MS, Bentrem DJ: Clinicopathologic features and treatment trends of pancreatic neuroendocrine tumors: analysis of 9,821 patients. J Gastrointest Surg; 2007 Nov;11(11):1460-7; discussion 1467-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Patients were less likely to undergo resection if they were > 55 years old, had tumors in the head of the pancreas, tumors > or = 4 cm, or had distant metastases (P < 0.0001).
  • As PNETs have a better prognosis than adenocarcinoma, concerns regarding the morbidity and mortality of pancreatic surgery and neoplasms should not preclude resection.
  • [MeSH-minor] Adenoma, Islet Cell / pathology. Adenoma, Islet Cell / surgery. Adult. Aged. Cell Differentiation. Female. Humans. Male. Middle Aged. Patient Selection. Prognosis. Retrospective Studies

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  • (PMID = 17846854.001).
  • [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] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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46. Inan N, Arslan A, Akansel G, Okay E, Gurbuz Y: Unusual magnetic resonance image of an insulinoma with extensive desmoplastic reaction. JOP; 2008;9(1):61-6
Hazardous Substances Data Bank. GADOLINIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CONTEXT: Unlike other islet-cell tumors, insulinomas are usually benign.
  • However, in rare cases, insulinomas may be hypointense on T2-weighted images and on immediate post-gadolinium images, mimicking a ductal adenocarcinoma.

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  • (PMID = 18182746.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 9007-34-5 / Collagen; AU0V1LM3JT / Gadolinium
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47. Takahashi M, Kitahashi T, Ishigamori R, Mutoh M, Komiya M, Sato H, Kamanaka Y, Naka M, Maruyama T, Sugimura T, Wakabayashi K: Increased expression of inducible nitric oxide synthase (iNOS) in N-nitrosobis(2-oxopropyl)amine-induced hamster pancreatic carcinogenesis and prevention of cancer development by ONO-1714, an iNOS inhibitor. Carcinogenesis; 2008 Aug;29(8):1608-13
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Reverse transcription-polymerase chain reaction analysis demonstrated iNOS expression in a hamster pancreatic cancer cell line as well as in human pancreatic cancer cell lines.
  • Immunohistochemical analysis revealed increased expression of iNOS protein in atypical hyperplasia and ductal adenocarcinomas of the pancreas in BOP-treated hamsters.
  • In addition, iNOS expression was also observed in macrophages and islet cells in pancreatic tissue surrounding tumors.
  • In order to assess the role of iNOS expression in carcinogenesis in the pancreas, the effects of ONO-1714 [(1S, 5S, 6R, 7R)-7-chloro-3-imino-5-methyl-2-azabicyclo[4.1.0]heptane], an iNOS inhibitor, on hamster pancreatic ductal carcinogenesis were investigated.
  • The incidences and multiplicities of atypical hyperplasia and invasive adenocarcinoma and total adenocarcinomas (non-invasive and invasive adenocarcinomas) in the pancreas were significantly lowered by treatment with 200 p.p.m. ONO-1714.
  • [MeSH-minor] Animals. Carcinogens / toxicity. Cell Line, Tumor. Cricetinae. DNA Primers. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Heterocyclic Compounds, 2-Ring / pharmacology. Humans. Mesocricetus. Nitrosamines / toxicity. RNA, Messenger / genetics

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  • (PMID = 18567618.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 7-chloro-3-imino-5-methyl-2-azabicyclo(4.1.0)heptane; 0 / Amidines; 0 / Carcinogens; 0 / DNA Primers; 0 / Heterocyclic Compounds, 2-Ring; 0 / Nitrosamines; 0 / RNA, Messenger; 60599-38-4 / nitrosobis(2-oxopropyl)amine; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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48. King J, Kazanjian K, Matsumoto J, Reber HA, Yeh MW, Hines OJ, Eibl G: Distal pancreatectomy: incidence of postoperative diabetes. J Gastrointest Surg; 2008 Sep;12(9):1548-53
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • INTRODUCTION: Distal pancreatectomy is an accepted and safe procedure for lesions of the body and tail of the pancreas.
  • RESULTS: Of these 125 patients, 27 (21.6%) had an islet cell tumor, 25 (20%) adenocarcinoma, 24 (18.4%) serous cystic neoplasm, 19 (15.2%) mucinous cystic neoplasm, 11 (8.8%) chronic pancreatitis, and eight (6.4%) intraductal papillary mucinous neoplasm.

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  • (PMID = 18543045.001).
  • [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
  • [Grant] United States / NCCIH NIH HHS / AT / P01 AT003960; United States / NCI NIH HHS / CA / R21 CA124609
  • [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 / Blood Glucose
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