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[Late development of colonic neoplasms after uretero-sigmoidostomy].

A case report is given of a patient who developed adenocarcinoma of the colon 20 years after ureterosigmoidostomy, which had been done because of exstrophy of the bladder. A review of the literature is given covering 42 cases showing development of tumors after ureterosigmoidostomy. Possible causal mechanisms are discussed. A careful follow-up of patients with ureterosigmoidostomy is warranted, since malignant disease of the colon may occur as a late complication.

Adenocarcinoma↗

[Determination of bile acids in stools of patients with colonic neoplasms and adenomatous polyps].

Since several years ago, the biliar acids have been incriminated in the etiopathogeny of colon cancer and adenomatous polyps, above all the secondary ones, involved by its aggressive action over the colonic epithelium in these mechanisms. The dietetical habits of developed countries have the high responsibility for this situation, their food pattern being a high animal fat diet, high in refined carbohydrates, animal proteins and low in dietetic fiber (diet type "occidental") unlike to developing countries that have a high natural fiber diet, having a much lower incidence in colon cancer and adenomatous polyps. Dietetic fiber has been studied considering it with a protector effect over the aggressive action of biliar acids on the colon mucous. We have studied 60 patients, 20 of them with colon cancer, 20 with adenomatous and 20 case controls without colonic pathology. All of them had total high biliar acids in stools, a dietetical screening was carried out to determine the intake of animal fat and dietetic fibre during a week. There was a significant correlation in cases of cancer, polyps and biliar acids high in stools. There was also a significant correlation between the undue dietetic habits in colon cancer patients and high bilar acids. In those cases of adenomatous polyps, there was not a significant relation to dietetic habits.

Adenomatous Polyps↗

[The rectal carcinoma. Characteristics of the tumor and its position within the framework of colonic neoplasms].

For the period of 15 years (May 1960 till the end of April 1975) all cases of colon carcinoma (1752) were checked. Of these 851 carcinoma were located in the rectum. Results concerning anamnesis, diagnosis and therapy between these groups are compared and discussed. The necessity of early recognition and the possibilities of practical use are underlined and described.

Adenocarcinoma↗

Cell proliferation of colonic neoplasms in dimethylhydrazine-treated rats.

We have measured mitotic indices and 3H-thymidine-labelling indices for the colonic epithelial tumours induced in rats by the administration of dimethyl-hydrazine (DMH). The fraction-of-labelled-mitoses (FLM) technique has been used to estimate the duration of the cell-cycle phases. In general, mitotic and labelling indices in the tumours are similar to those in the proliferation zone of the normal crypt epithelium; lesions considered to be least well differentiated on histological grounds appear to have the lowest mean labelling index. Benign tumours and the different types of malignant tumours have mean cell-cycle times about half those of the normal mucosa.

Animals↗

Abnormal methylation of the calcitonin gene in human colonic neoplasms.

Earlier studies of the methylation status of total genomic DNA and of specific genes have demonstrated, predominantly, hypomethylation in human neoplasms. However, we have recently documented the presence of new sites of methylation in the calcitonin gene in human lymphomas (100%), small cell lung carcinomas (92%), and acute myeloid leukemias (95%). We now report that these same novel calcitonin gene methylation sites are also a feature of DNA from human colonic adenomas (13 out of 14 studied), colon carcinomas (4/13), and established colon carcinoma cell lines (18/19), despite the presence of overall genomic DNA hypomethylation in these neoplasms. The data provide further evidence that regional increases in DNA methylation, like gene hypomethylation, occur in benign colonic neoplasms prior to malignant transformation. The fact that abnormalities of calcitonin gene methylation are less frequent in DNA from human colonic carcinomas than from adenomas and colon carcinoma cell culture lines is of special interest. This finding suggests that a more heterogeneous population of cells is present in the carcinomas and that the calcitonin gene hypermethylation may be inherent to cells which are initially selected for growth in culture or are capable of prolonged survival under culture conditions.

Adenoma↗