Bruckheimer E M, Gjertsen B T, McDonnell T J
Department of Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.
Semin Oncol. 1999 Aug;26(4):382-98.
Although the phenomenon of programed cell death, or apoptosis, has been recognized for many years, interest in the clinical implications of apoptotic cell death has not been widely apparent until recently. It is now established that the products of at least some oncogenes and tumor suppressor genes are able to regulate the rates of apoptosis as well as proliferation in tumor cell populations. In fact, it appears that evasion of deletion via apoptotic cell death may be a requisite event in the development of many malignant neoplasms. Molecular alterations that occur at high frequency in the pathogenesis of prostate cancer often involve genes implicated in the regulation of cell death. There is now ample reason to speculate that the susceptibility of individual malignant neoplasms to undergo apoptosis in response to a given therapeutic intervention may be a useful parameter in predicting therapeutic response. This realization has profound implications with respect to the design and implementation of treatment strategies for prostate cancer based on the biology of this disease.
