Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Colorectal adenocarcinomas were induced in male Wistar rats, by weekly subcutaneous administration of 1,2-dimethylhydrazine, classified according to the degree of differentiation and submitted to immunocytochemistry for the peptides cholecystokinin (CCK), gastrin, gastric inhibitory polypeptide (GIP), glucagon, neurotensin, pancreatic polypeptide (PP), peptide YY (PYY), somatostatin and vasoactive intestinal polypeptide (VIP) and the biogenic monoamine 5-hydroxytryptamine. Well- or moderately well-differentiated adenocarcinomas comprised 46% of the tumour population, only 4% were poorly-differentiated adenocarcinomas, and the remaining 50% possessed a mixture of these two morphologies. Glucagon, PYY and 5-hydroxytryptamine immunoreactive cells were frequently observed within well- or moderately well-differentiated tumours and within such regions of tumours possessing a mixed morphological pattern. The tumours contained no cells immunoreactive for any of the peptides not normally located within the colorectum, nor did they contain cells immunoreactive for somatostatin and VIP, although known positive controls did stain. Poorly-differentiated tumours and portions of tumours of mixed type, were consistently negative. 5-hydroxytryptamine was the most frequently located of the three antigens, being detected in 87% of the moderately well-differentiated tumours and 32% of the tumours with mixed morphologies. 11% of moderately well-differentiated tumours possessed 5-hydroxytryptamine positive cells in such profusion that they contributed significantly to the tumour mass. The distribution of glucagon- and PYY-immunoreactive cells was similar, although they occurred with a lower frequency, presumably corresponding to their lower numbers within the normal colorectal mucosa. Additionally, these two peptide immunoreactivities were colocalized in the majority of cells, although some cells contained only one antigen.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Neuroendocrine cells within colorectal tumours induced by dimethylhydrazine. An immunocytochemical study. 377

Gut endocrine cells in a total of 122 intestinal-tract adenocarcinomas induced in inbred Wistar rats by 1,2-dimethylhydrazine dihydrochloride were examined histologically, ultrastructurally, and immunohistochemically for gastrin, somatostatin, vasoactive-intestinal polypeptide (VIP), and glicentin (enteroglucagon). Of the 122 tumors, argyrophil cells were detected in 42 tumors (34.3%) comprising 15 tumors of the well differentiated type and 27 tumors of the poorly differentiated type, including signet-ring-cell carcinomas. Of the 27 tumors of the poorly differentiated type, 12 were regarded as endocrine-cell carcinomas composed of numerous argyrophil or argentaffin cells and mucus-containing cells. Immunohistochemically, 7 of the 12 tumors had glicentin and two of these seven tumors also had gastrin and argentaffin cells synchronously. None of the tumors showed immunoreactivity for somatostatin and VIP. Nine of the 12 tumors metastasized to the lung, pancreas, liver, mesenterium, omentum, and lymph nodes. The metastatic foci of these tumors were also shown to have glicentin and argentaffin cells. Ultrastructurally, four types of endocrine granule were found in the tumor cells and amphicrine cells containing endocrine granules and mucous granules were noted. These endocrine-cell tumors were assumed to develop from totipotent immature cells of endodermal origin.
 ...
PMID:Gut endocrine cells in rat intestinal-tract carcinoma induced by 1,2-dimethylhydrazine. 613 77

Colonic carcinoma was induced in male Sprague-Dawley rats by injecting them with 1,2-dimethylhydrazine dihydrochloride. Control rats were injected with EDTA solution. Tissue specimens of colon from four groups of animals: (i) rats without tumour, (ii) with dysplasia and lymphoid hyperplasia, (iii) with colonic adenocarcinoma, and (iv) controls, were investigated. The colonic endocrine cells were detected by immunocytochemistry and quantified by computerised image analysis. Peptide YY (PYY)- and serotonin-immunoreactive cells were found in the colon of all the groups investigated. There were few somatostatin- or enteroglucagon-immunoreactive cells and no pancreatic polypeptide (PP)-immunoreactive cells in the colon of any of the groups studied. The density of PYY-immunoreactive cells increased significantly in rats with dysplasia and lymphoid hyperplasia and in rats with colon carcinoma. There was no statistically significant difference as regards cell secretory index (CSI) or nuclear area of PYY-immunoreactive cells in any of treated groups examined. Nor was there any statistically significant difference between all treated animal groups and controls, as regards cell density, CSI, or nuclear area of serotonin-immunoreactive cells. The present observations in an animal model of human colon carcinoma support the assumption that neuroendocrine peptides in the gut are involved in the carcinogenesis of colorectal carcinoma. However, The nature of the changes in the colonic endocrine cells observed here differed from those in patients with colon carcinoma, possibly due to a difference between the response of young rats to an induced colon carcinoma and a spontaneously developed carcinoma in elderly humans, or due to a species difference.
 ...
PMID:Colonic endocrine cells in rats with chemically induced colon carcinoma. 1151 Sep 74