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Vol. 60, Issue 6, 1153-1160, December 2001
Department of Medicine and the Cancer Center, University of
California, San Diego, La Jolla, California
Cisplatin (cDDP) is effective against some human tumors, but many are
intrinsically resistant and, even among initially sensitive tumors,
acquired resistance develops commonly during treatment. It has not been
possible to prove which biochemical mechanisms control sensitivity to
cDDP. Gene knockout studies in yeast, Dictyostelium discoideum, and mammalian cells have begun to unambiguously
identify genes whose products function to modulate the cytotoxicity of cDDP. This review summarizes information currently available about the
function of these genes. This comprehensive compilation points to the
involvement of regulatory pathways known to mediate apoptosis, cell
cycle checkpoint activation, and transcriptional rescue as regulators
of cDDP sensitivity. Elucidation of the molecular mechanisms that
mediate cDDP resistance holds promise for the design of pharmacological strategies for preventing, overcoming, or reversing this form of drug resistance.
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