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[Cancer Research 55, 1811-1816, May 1, 1995]
© 1995 American Association for Cancer Research
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Inhibition of Apoptosis during Development of Colorectal Cancer1

Atul Bedi2, Pankaj J. Pasricha, Adil J. Akhtar, James P. Barber, Gauri C. Bedi, Francis M. Giardiello, Barbara A. Zehnbauer, Stanley R. Hamilton and Richard J. Jones

Johns Hopkins Oncology Center [A. B., A. J. A., J. P. B., S. R. H., R. J. J.], Division of Gastroenterology, Departments of Medicine [P. J. P., F. M. G.], Surgery [G. C. B.], and Pathology [S. R. H.], The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, and Department of Hematology, Molecular Diagnostics Laboratory, Washington University School of Medicine, St. Louis, Missouri 63110 [B. A. Z.]

Colorectal tumorigenesis proceeds through an accumulation of specific genetic alterations. Studies of the mechanism by which these genetic changes effect malignant transformation have focused on the deregulation of cell proliferation. However, colorectal epithelial homoeostasis is dependent not only on the rate of cell production but also on apoptosis, a genetically programmed process of autonomous cell death. We investigated whether colorectal tumorigenesis involved an altered susceptibility to apoptosis by examining colorectal epithelium from normal mucosa, adenomas from familial adenomatous polyposis, sporadic adenomas, and carcinomas. The transformation of colorectal epithelium to carcinomas was associated with a progressive inhibition of apoptosis. The inhibition of apoptosis in colorectal cancers may contribute to tumor growth, promote neoplastic progression, and confer resistance to cytotoxic anticancer agents.

1 This work was supported by funds from NIH Grant P30 CA06973.

2 To whom requests for reprints should be addressed, at Johns Hopkins Oncology Center, 600 N. Wolfe Street, Baltimore, MD 21287.

Received 12/13/94. Accepted 3/17/95.




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