Stephen G. Chaney

TL;DR: Its single agent and combination therapy data in ovarian cancer confirm its non-cross resistance with cisplatin/carboplatin and topoisomerase I inhibitors, and the absence of hematologic dose-limiting toxicity have made oxaliplatin an attractive compound for combinations.

TL;DR: A decreased likelihood of resistance development makes oxaliplatin a good candidate for first-line therapy and studies also demonstrate additive and/or synergistic activity with a number of other compounds, however, suggesting the possible use of oxali Platin in combination therapies.

TL;DR: The differences between oxaliplatin and cisplatin in terms of their spectrum of activity and adduct formation are described and molecular and cellular experimental data that potentially explain them are discussed, with particular emphasis on the differential role of DNA repair mechanisms.

TL;DR: The solution structure of the oxaliplatin-GG adduct is solved and it is shown that it is significantly different from the previously published solution structures of the cisPlatin- GG adducts, providing a logical explanation for the differential recognition of cisplatin and oxali platin adducting proteins by mismatch repair and damage-recognition proteins.

TL;DR: The hypothesis that mismatch repair defects in hMutL alpha and hMutS alpha, but not in h MutS beta, contribute to increased net replicative bypass of cisplatin adducts and therefore to drug resistance by preventing futile cycles of translesion synthesis and mismatch correction is supported.