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PubMed · 10652586

Programmed cell death in colorectal carcinogenesis.

A M Valentini·M L Caruso·R Armentano·M Pirrelli·E Rizzi·F Lapenna·L Renna
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Abstract

The most studied mechanism of malignant transformation has been cell proliferation. The relationship between programmed cell death (apoptosis), cell proliferation, and apoptosis regulatory genes (p53 and bcl-2), was studied in normal colonic epithelium, 26 sporadic adenomas both early and late, 25 FAP adenomas, and 34 carcinomas. We showed a decrease in programmed cell death and an increase in cell proliferation during the transition from adenoma to carcinoma. The increase of expression of p53 from early (10%) to late adenomas (87%) contrasted with the decrease of bcl-2 staining. Sixty-two per cent and 23% of carcinomas were reactive for p53 and bcl-2 respectively. Abnormal early activation of the bcl-2 gene, rather than late p53 gene mutation appears to be responsible for inhibition of apoptosis in colorectal carcinogenesis. bcl-2 was higher in FAP adenomas than in sporadic cases, and in carcinomas favouring the accumulation of long-living cells, which are more subject to mutation and thus cancerization.

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ApoptosisColorectal NeoplasmsHumansImmunohistochemistryMutationProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-bcl-2Tumor Suppressor Protein p53Journal Article

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A M Valentini, M L Caruso, R Armentano, M Pirrelli, E Rizzi, F Lapenna, L Renna. Programmed cell death in colorectal carcinogenesis.. https://pubmed.ncbi.nlm.nih.gov/10652586/

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