Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty exocrine pancreatic adenocarcinomas and 57 benign tumors induced in Syrian hamsters by N-nitrosobis(2-oxopropyl)amine (BOP) were examined for the presence of argyrophil cells antiinsulin, -glucagon, -somatostatin, -pancreatic polypeptide (PP), -gastrin/CCK, -vasoactive intestinal polypeptide (VIP), and - neuron-specific enolase (NSE) reactive cells. Argyrophil - and antihormone-reactive cells were found in the normal pancreatic ducts and in the acini, as well as in hyperplastic and atypical ducts/ductules, tubular complexes, benign lesions, and in 80% of ductal adenocarcinomas. Insulin and antiNSE-reactive cells were the most common, followed in decreasing frequency by glucagon, somatostatin, and PP cells. Antigastrin-/CCK-and -VIP-reactive cells were found in two cases. Argyrophil cells were present in about 60% of the tumors with Grimelius staining and in 55% of those with Churukian-Schenk staining. Insulin cells were seen in ductal cancer that had grown into a lymph node and in the lymph node metastases of another cancer. A novel finding was the presence of argyrophil and insulin cells within the lumen of some malignant glandular structures. Coexistence of several peptide cells was found in 52% of the cancers. The presence of argyrophil and hormone-producing cells in induced pancreatic ductal/ductular lesions further strengthens the existence of a close developmental relationship between exocrine and endocrine cells of the pancreas.
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PMID:Immunohistochemical characterization of endocrine cells in experimental exocrine pancreatic cancer in the Syrian golden hamster. 135 11

The effects of treatment with the somatostatin analogue Sandostatin, separately and in combination with surgical castration, on the development of azaserine-induced lesions in rat pancreas and N-nitrosobis(2-oxopropyl)amine (BOP)-induced lesions in hamster pancreas were investigated. The animals were divided in 4 groups and treated as follows: (a) controls, injected s.c. with saline solution (0.9% NaCl); (b) orchiectomy directly after the last treatment with carcinogen; (c) Sandostatin (SMS 201-995) subcutaneously; (d) orchiectomy followed by treatment with Sandostatin. No significant suppressive effects on plasma EGF or IGF-I concentrations were noted after Sandostatin treatment, but plasma gastrin levels decreased slightly in the rats, not in the hamsters. In rats, Sandostatin treatment enhanced rather than inhibited growth of acidophilic atypical acinar cell nodules. In hamster pancreas, by contrast, Sandostatin inhibited the development of putative pre-neoplastic ductular lesions. There was no interaction between treatment with Sandostatin and surgical castration. It was concluded that Sandostatin, when administered prophylactically, has an inhibitory effect on the growth of putative pre-neoplastic ductular, but not acinar, lesions.
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PMID:Effects of sandostatin and castration on pancreatic carcinogenesis in rats and hamsters. 173 May 18

ILA cells were established from tumors induced by the pancreatic carcinogen N-nitrosobis(2-oxopropyl)amine (BOP) in hamster islets. The proliferation, morphology, karyotype, immunoreactivity with certain antibodies and growth factor secretion of these tumor cells were compared with the same parameters in tumor cells induced by BOP in hamster ductal cells (TAKA-1-BOP) established in a previous study. Minor differences were found in the morphology and ultrastructure of the 2 cell lines. Contrary to TAKA-1-BOP cells, ILA cells did not express cytokeratins 8.13, 13 or 18 but did express DU-PAN-2 and TAG-72, 2 known human pancreatic cancer-associated antigens. No endocrine cell markers were expressed. A significant difference also was found in the chromosomal pattern in that there were more abnormalities and marker chromosomes in ILA cells than in TAKA-1-BOP cells and the Y or X chromosomes were missing in ILA cells. ILA cells produced TGF-alpha, IGF-I, bombesin and gastrin and expressed specific binding sites for hEGF. TGF-alpha secretion from ILA cells was much greater than that from TAKA-1-BOP cells. Our results indicate that pancreatic cancer cells grown in vitro are not a single clone. We conclude that there are some genetic and biological differences between tumors arising from pancreatic duct and islets and that pancreatic ductal adenocarcinomas originating from islets have a profound malignant potential.
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PMID:Establishment of tumor cell culture (ILA) derived from hamster pancreatic islets treated with BOP. 980 35

Pancreatic carcinogenesis is still not well characterized and no specific carcinogen has been isolated in humans. Pancreatic adenocarcinoma acquires genetic abnormalities with successive modification of genes involved in the regulation of cell proliferation and differentiation. The kinetic of genetic alterations in pancreatic cancer is not totally elucidated but experimental pancreatic cancer induced by BOP in Syrian golden hamster attempts to approach this problematic. The activating mutation of the K-ras oncogene on codon 12 seems to occur early in pancreatic carcinogenesis regarding the detection of this mutation in preneoplastic dysplastic lesions and tumors such as intraductal mucinous papillary tumors. Tumor suppressor genes are also inactivated leading commonly to the loss of an inhibitory function on cell proliferation. This inactivation occurs with gene mutation, deletion or methylation on one chromosome arm associated with a loss of heterozygosity: it concerns p53, p16/MTS-1, DPC-4/SMAD4. We recently characterized the somatostatin receptor SST2 gene as a potential suppressor gene for pancreatic carcinoma. The kinetic of these gene alterations is unknown in human. At a late stage of tumor development, an increase of telomerase activity, an over expression of growth factors and/or their receptors (EGF, NGF, gastrin, bombesin), of proangiogenic factors (VEGF, FGF, PDGF), of invasiveness factors (metalloproteinases, E-cadherin, urokinase and tissue plasminogen activators) occur. All these molecular events contribute to the progression and to the metastatic potential of this carcinoma. Recently, the identification of human genome and the large scale analysis of transcriptoma will certainly authorize a better knowledge of pancreatic carcinogenesis as well as the identification of new genetic alterations and new clinical markers.
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PMID:[Molecular pathways of pancreatic carcinogenesis]. 1248 52