Taken together the data presented in this review, and work by many
other investigators, support the notion that DNA excision repair is
important in a tumor cell's resistance to platinum compounds.
Inhibition of this repair system by combination chemotherapy with
the excision repair inhibitors HU and Ara-C produces synergistic
cell kills and increased levels and persistance of DNA interstrand
crosslinks. The studies with cis-DDP and -DDP in combination with
UV induced thymine dimers suggest that there may be competition for
DNA repair enzymes between the dimer and the platinum lesion.
Whether the competing lesion is an intrastrand crosslink,
interstrand crosslink, or platinum monoadduct (or all of these
lesions) cannot be determined. The similarity between an
intrastrand crosslink and a cyclobutane dimer suggests that these
lesions may compete for repair. However, the increased peak levels
of interstrand crosslinks, and increased persistence of these
lesions at later time points suggest that this lesion may also be a
substrate for the repair system. These observations may be of
clinical relevance. Recently Dr. Kathy Albain of our institution
has completed a Phase III I study using a 12 hour pretreatment with
HU and Ara-C in patients prior to their cis-DDP therapy. She
observed a significant number of responders in this trial (54). She
is currently completing a second Phase IIII study substituting IV
HU for the oral formulation. We anticipate initiating other
clinical trials based upon these observations."
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