Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/10038
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Type: Journal article
Title: Deregulation of apoptosis in colorectal carcinoma: theoretical and therapeutic implications
Author: Butler, L.
Hewett, P.
Fitridge, R.
Cowled, P.
Citation: Australian and New Zealand Journal of Surgery, 1999; 69(2):88-94
Publisher: Blackwell Science
Issue Date: 1999
ISSN: 0004-8682
1445-2197
Statement of
Responsibility: 
Lisa M. Butler, Peter J. Hewett, Robert A. Fitridge and Prudence A. Cowled
Abstract: Apoptosis, or programmed cell death, maintains the structure of the colonic crypts by providing a balance to the rate of cell proliferation. Colorectal carcinoma arises partly from a disruption in this balance in the favour of uncontrolled growth. Until recently, most research into colon cancer has focused on the molecular regulators of cell-cycle progression and proliferation, but it is now evident that apoptosis is also defective. A failure of cells to die in response to premalignant damage may allow the progression of the disease and maintain the resistance of cancer cells to cytotoxic therapy. This review outlines the importance of apoptosis in the normal colon and presents recent studies that demonstrate that induction of apoptosis is defective in colonic tumours. When the molecular regulation of apoptosis is better understood, this knowledge may lead to the earlier detection of patients at greater risk of developing colorectal carcinoma, and also to the development of more effective therapies.
Keywords: apoptosis; Bcl-2; colorectal carcinoma; p53; programmed cell death; terminal deoxynucleotidyl transferase-dUTP nick end labelling (TUNEL)
Description: Article first published online: 6 APR 2002
RMID: 0030004719
DOI: 10.1046/j.1440-1622.1999.01498.x
Appears in Collections:Surgery publications

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