Programmed cell death in colorectal carcinogenesis

A. M. Valentini, M. L. Caruso, R. Armentano, M. Pirrelli, E. Rizzi, F. Lapenna, L. Renna

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish
Pages (from-to)3019-3024
Number of pages6
JournalAnticancer Research
Volume19
Issue number4 B
Publication statusPublished - 1999

Keywords

  • Apoptosis
  • bcl-2
  • Cell proliferation
  • Colorectal cancer
  • p53

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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