bcl-2 and p53 Oncoprotein Expression during Colorectal Tumorigenesis

Frank A. Sinicrope, Karen R. Cleary, L. Clifton Stephens, J. Jack Lee, Bernard Levin

Research output: Contribution to journalArticlepeer-review

590 Scopus citations


Apoptosis or programmed cell death represents a mechanism by which cells possessing DNA damage can be deleted. The bcl-2 proto-oncogene is a known inhibitor of apoptosis that may allow the accumulation and propagation of cells containing genetic alterations. To determine if and when the bcl-2 gene is activated during colorectal tumorigenesis and its relationship to p53, we analyzed normal mucosa, hyperplastic and dys-plastic epithelial polyps, and carcinomas for the expression of these markers using immunohistocheniistry. Whereas bcl-2 staining was restricted to basal epithelial cells in normal and hyperplastic mucosa, bcl-2 expression was detected in parabasal and superficial regions in dysplastic polyps and carcinomas. An inverse correlation was found between bcl-2 and p53 expression in adenomas, suggesting that these markers may regulate a common cell death pathway. Furthermore, carcinomas with a high percentage of bcl-2-positive cells were significantly more likely to have low rates of spontaneous apoptosis, as determined histologically, than those cancers with low or absent bcl-2 expression. Abnormal activation of the bcl-2 gene appears to be an early event in colorectal tumorigenesis that can inhibit apoptosis in vivo and may facilitate tumor progression.

Original languageEnglish (US)
Pages (from-to)237-241
Number of pages5
JournalCancer research
Issue number2
StatePublished - Jan 15 1995

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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