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PubMed1977

[Effect of estrogens on the concentration of carcinoembryonal antigen in the serum of rats with intestinal neoplasms and in the presence of non-specific injuries to its mucous membrane].

Carcinoembryonal antigen (CEA) was shown to be present in 70% of rats with tumours of the large intestine induced with 1,2-dimethyl-hydrazine and in rats with posttraumatic mucosa regeneration of the same organ. After treatment with estrogen--diethyl stilbestrol propionate (0.57 microgram/day for 6 days) the incidence of CEA finding in the serum of these rats was increased. In rats with an injured mucosa of the large intestine estrogen treatment prevented the natural decrease of CEA during the decline of regeneration.

Animals↗
PubMed1988

Growth factors and intestinal neoplasms.

Signals that control normal and neoplastic epithelial proliferation are not completely understood. We have reviewed the importance of the possible roles of the following control mechanisms: polyamine biosynthesis, intraluminal nutrients, gastrointestinal hormones and growth factors, bowel resection, carcinogens, and oncogenes. The mechanisms by which these agents act and the precise roles they play in normal and abnormal proliferation of intestinal mucosa have not yet been clearly defined. Peptide hormones and growth factors exert their mitogenic effects by first interacting with specific receptors in the cell membrane. Oncogenes induce production of growth factors or replace growth factors and, by themselves, stimulate growth. We believe that no single agent is likely to be responsible; rather, multiple agents are involved in stimulation of growth of normal and neoplastic intestinal epithelial cells. A clear understanding of the factors responsible for regulation of normal and abnormal intestinal cell growth will greatly facilitate the development of therapeutic strategies for the prevention and treatment of gastrointestinal cancers.

Animals↗
PubMed1985

Demonstration of vincristine resistance in primary intestinal neoplasms in the rat by the 'post-metaphase index'.

A method is described enabling the direct measurement of vincristine resistance in intact tissues in vivo by morphological study. Using the metaphase arresting properties of the drug, counts were made of escaping anaphase and telophase mitotic figures at a range of doses. The proportion of post-metaphase mitotic figures is called the post-metaphase index (PMI). In 95 primary intestinal tumours induced by dimethylhydrazine (DMH) in rats, an increase in resistance to vincristine was shown over normal mucosa (P less than 0.001). The data were analysed by computer modelling and a linear relationship is demonstrated between the logit of the post-metaphase index, and log dose of vincristine. To achieve a PMI of 1% the fitted lines show an enhanced vincristine dose requirement over normal mucosa of 6 times in colonic tumours, and 8 times in small intestinal tumours. Non-neoplastic mucosa from the DMH-treated animals requires an enhanced dose of vincristine of 1.5 times, compared with normal mucosa, to achieve a PMI of 1%. Given current interest in the mechanism of vincristine resistance in cell lines this new approach provides a technique for assessing the resistance of solid tumours, both in vivo and in vitro, and for subsequent experimental manipulation.

Animals↗
PubMedDate not supplied

[Entero-uterine fistual as the first symptom of intestinal neoplasms. Description of a case].

Vaginal elimination of stool due to sigmoid-uterine fistula was the first symptom in a case of neoplasia of the sigma. Few instances of a similar fistula appear in the literature. Bouskela, Chérisié, Yourde and Taieb observed one case starting from the uterus. McGregor & Bacon have described a fistula starting from the colon due to diverticulitis, as have Colceck & Staumann, Smalley et al., and Johnston & Stubbs. No previous example of tumour of the large intestine as the cause of a fistula with the corpus uteri could be found. On examination, the patient presented losss of stool via the vagina and a sigmoid-uterine fistula. Her condition was poor. Blood glucose was high, the protein picture was altered with a los of albumin, and infection was present. Radical management was impossible. Left colostomy reduce the causes of infection and permitted devitalisation of the fistula. Subjective and objective improvement followed, though further enlargement of the tumour engulfing the sigma and uterus led to death some months later due to the onset of renal block.

Adenocarcinoma, Mucinous↗
PubMed1991

Intestinal neoplasm mimicking a Meckel's diverticulum on scintigraphic imaging.

A 33-year-old man presented with colicky, intermittent, midabdominal pain with nausea and vomiting. A Tc-99m pertechnetate abdominal scan was performed and revealed a focal area of increased uptake in the midabdomen associated with dilated proximal loops of small bowel. Surgery revealed a high-grade partial obstruction of the midportion of the jejunum secondary to an annular adenocarcinoma of the jejunum. This is the first known report of abnormal Tc-99m pertechnetate accumulation in an adenocarcinoma of the small bowel.

Adenocarcinoma↗
PubMed1992

Naturally occurring intestinal epithelial neoplasms in aged Crl:CD BR rats.

Spontaneous primary epithelial neoplasms of the intestinal tract occurred in 6/682 (0.9%) male and 1/694 (0.1%) female Sprague-Dawley rats. Six of 7 neoplasms were adenocarcinomas, and 1 of 7 was an adenoma. Metastasis to the liver or lung occurred in 3 of the rats with adenocarcinoma. These findings are consistent with those reported for female Sprague-Dawley rats and for males and females of other strains over the past 25 years. The intestinal neoplasm incidence in males exceeded that reported for other Sprague-Dawley males with one exception, reported 30 years ago.

Adenocarcinoma↗
PubMed1979

Enhanced colonic carcinogenesis with azoxymethane in rats after pancreaticobiliary diversion to mid small bowel.

Since biliary excretion of metabolites might determine the pattern of intestinal neoplasms induced by azoxymethane, the number and distribution of tumors were studied in rats after pancreaticobiliary diversion to the mid small bowel. Pancreaticobiliary diversion was performed either immediately before the first of 16 weekly injections of azoxymethane or 10 days after the last. Seven months after pancreaticobiliary diversion, persistent ileal hyperplasia was manifested by higher levels of mucosal RNA and DNA compared with controls (34--102%: P less than 0.001), while there was little residual adaptation in the colon. Qualitative and quantitative analysis of fecal bile acids 6--26 wk after pancreaticobiliary diversion showed few differences. Pancreaticobiliary diversion doubled the incidence of colonic tumors, whether operation preceded (P less than 0.005) or followed (P less than 0.02) the course of azoxymethane. Suture-line tumors were common in the small bowel, particularly in the transposed duodenal stump. Despite intense ileal hyperplasia as a consequence of pancreaticobiliary diversion, the ileum remained resistant to chemical carcinogenesis. The potentiation of colonic neoplasms by pancreaticobiliary diversion probably depends on the stimulation of colonic mucosal proliferation.

Adenocarcinoma↗
PubMed1992

[The mucin profile in the mucosa of the large intestine in neoplasms].

Qualitative and quantitative changes in secretion of goblet cells of large bowel mucosa in adenomatous polyps (60), adenocarcinoma (30) and bioptates of adjacent transitional mucosa (30) were studied. As neoplasia progressed, mucin profile appeared to follow a certain pattern: it reached its peak in moderate dysplasia in polyps containing predominantly sulphomucins; subsequently both sulphomucin and sialomucin levels decreased. Adenocarcinomas showed a sharp drop in glycoprotein level, and an insignificant build-up of sialomucins was registered in some cases only. Enhanced abnormal secretion was observed in mucinous carcinoma and adenocarcinoma characterized by the presence of large mucinous areas. Also, qualitative changes were identified in transitional mucosa adjacent to tumor.

Adenocarcinoma↗
PubMed1992

[An immunohistochemical and ultrastructural survey on smooth muscle tumors of the alimentary tract].

33 cases of smooth muscle tumors of the alimentary tract were analysed. Among them, 18 cases showed positive reaction to desmin, including one out of two cases of esophageal neoplasms, 6 out of 11 cases of gastric neoplasms, 5 from 12 cases of small intestinal neoplasms, 6 from 8 cases of large intestinal neoplasms, 14 out of 21 cases of benign tumors as well as sarcomas in grade I, and 4 from 12 cases of sarcomas in grade II and III (only mild positive result obtained in grade II and III-sarcomas). S-100 protein staining was performed in 27 cases and positive reaction was obtained only in five. Among them, 2 cases showed prominent positive reaction. 20 cases were studied by electron microscopy, and cytoplasmic myofilaments as well as dense bodies were demonstrated in 7 cases. All of them were the benign neoplasm or sarcoma in grade I. The conclusion is that most stromal tumors of the digestive system are originating from the smooth muscle, except very few cases are neurogenic in origin.

Desmin↗