PubMed HealthSearch

PubMed · 131424

Susceptibility of the resected stomach to experimental carcinogenesis.

Abstract

The purpose of this study was to find whether gastric resection enhances the incidence of carcinoma in the remaining part of the stomach. 66 male Wistar rats were subjected to stomach resection according to the Billroth I or the Billroth II method. These rats, as well as control animals with intact stomachs, were fed the carcinogen N-Methyl-N'-nitro-N-nitrosoguanidine (NG). -- 25 of 66 animals developed carcinomas in the gastric remnant. Precancerous lesions were seen in 18 rats. The tumours were characterized histologically as adenocarcinomas. They were almost exclusively localized in the region of the gastroenteral anastomosis. The process of tumour formation in the resected stomach was completed within 17-31 weeks on continuous administration of NG in a concentration of 120 mg/l in the drinking water. In contrast to these findings, the development of cancer in the intact stomach required on average 41 weeks under the same conditions of NG administration. However, with regard to the incidence of malignant changes, no significant difference was observed between animals undergoing the Billroth I method and those undergoing the Billroth II method.--The results suggest that the resected stomach of the rat is more susceptible to induction of cancer than the intac one. Exposure of the resected stomach to an oral carcinogen induces carcinogenesis predominantly in the anastomotic region.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

K Dahm, B Werner. 1976-03-19. Susceptibility of the resected stomach to experimental carcinogenesis.. https://doi.org/10.1007/bf00284082

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Interaction of Galpha 12 and Galpha 13 with the cytoplasmic domain of cadherin provides a mechanism for beta -catenin release.

The G12 subfamily of heterotrimeric G proteins, comprised of the alpha-subunits Galpha12 and Galpha13, has been implicated as a signaling component in cellular processes ranging from cytoskeletal changes to cell growth and oncogenesis. In an attempt to elucidate specific roles of this subfamily in cell regulation, we sought to identify molecular targets of Galpha12. Here we show a specific interaction between the G12 subfamily and the cytoplasmic tails of several members of the cadherin family of cell-surface adhesion proteins. Galpha12 or Galpha13 binding causes dissociation of the transcriptional activator beta-catenin from cadherins. Furthermore, in cells lacking the adenomatous polyposis coli protein required for beta-catenin degradation, expression of mutationally activated Galpha12 or Galpha13 causes an increase in beta-catenin-mediated transcriptional activation. These findings provide a potential molecular mechanism for the previously reported cellular transforming ability of the G12 subfamily and reveal a link between heterotrimeric G proteins and cellular processes controlling growth and differentiation.

Adenocarcinoma

Luteinizing hormone-releasing factor-like immunoreactivity in islet cells and insulomas of the human pancreas.

Luteinizing hormone-releasing factor (LRF)-like immunoreactivity was demonstrated by a three-layer immunoperoxidase method in the islet cells of human pancreas and in the neoplastic cells of insulomas. Adenocarcinomas originating in the exocrine pancreas were LRF-negative. The results demonstrate another hypothalamic peptide-like material in the gastrointestinal tract, the biological role of which remains to be clarified.

Adenocarcinoma

[Determination of the lymphocytic and oncofetal antigen subpopulations in patients with adenocarcinomas of the stomach and of the colon and rectum (author's transl)].

The authors present a study of 50 patients with adenocarcinomas of the colon and rectum, patients with gastric adenocarcinomas, and 30 healthy individuals as a control group. In all subjects the following parameters were determined: total number of lymphocytes in the peripheral blood, T lymphocytes, T-active lymphocytes, and B lymphocytes. A study of the test for lymphoblastic transformation (TTL) with phytohemagglutinin (PHA) stimulation and the determination of alpha-fetoprotein (AFP) and carcino-embryonic antigen (CEA) were also carried out. In patients with gastric adenocarcinoma the results revealed a lymphopenia, especially at the expense of T and T-active lymphocytes, as well as a depression (in 73 per cent) of the lymphocytic response to the PHA stimulation. Patients with carcinoma of the colon showed significant results in the T-active lymphocyte population. In both neoplastic situations the determination for alpha-fetoprotein was negative, while the CEA presented a clear correlation with the evolutive stage of the tumor, being more demonstrative in the tumors located in the colon and rectum.

Adenocarcinoma