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DNA repair: enzymatic mechanisms and relevance to drug response.
The types of DNA adducts formed by the major classes of chemotherapeutic agents, the enzymatic pathways that play a role in the repair of thoseAdducts, the evidence that DNA repair is enhanced in drug-resistant cell lines and tumors, and strategies for utilizing selective inhibition of DNA repair to overcome resistance are examined.
Oxaliplatin: mechanism of action and antineoplastic activity.
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.
Recognition and processing of cisplatin- and oxaliplatin-DNA adducts.
Two‐polymerase mechanisms dictate error‐free and error‐prone translesion DNA synthesis in mammals
Results highlight the central role of polζ in both error‐prone and error‐free TLS in mammalian cells, and show that bypass of a single lesion may involve at least three different DNA polymerases, operating in different two‐polymerase combinations.
Oxaliplatin: a review of preclinical and clinical studies.
- E. Raymond, S. Chaney, A. Taamma, E. Cvitkovic
- Biology, MedicineAnnals of oncology : official journal of the…
- 1 October 1998
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.
Cellular and molecular pharmacology of oxaliplatin.
- E. Raymond, S. Faivre, S. Chaney, J. Woynarowski, E. Cvitkovic
- Biology, ChemistryMolecular cancer therapeutics
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.
The role of hMLH1, hMSH3, and hMSH6 defects in cisplatin and oxaliplatin resistance: correlation with replicative bypass of platinum-DNA adducts.
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.
p53 and p21 regulate error-prone DNA repair to yield a lower mutation load.
Efficient nucleotide excision repair of cisplatin, oxaliplatin, and Bis-aceto-ammine-dichloro-cyclohexylamine-platinum(IV) (JM216) platinum intrastrand DNA diadducts.
It is shown that the types of DNA lesions generated by three platinum drugs, cisplatin, oxaliplatin and (Bis-aceto-ammine-dichloro-cyclohexylamine-platinum(IV) (JM216), are repaired in vitro with similar kinetics by the mammalian nucleotide excision repair pathway.
Comparative neurotoxicity of oxaliplatin, cisplatin, and ormaplatin in a Wistar rat model.
- J. Holmes, J. Stanko, S. Chaney
- Biology, ChemistryToxicological sciences : an official journal of…
- 1 December 1998
The results suggest that ormaplatin is uniquely neurotoxic immediately following treatment in the Wistar rat model, however, following an 8-week recovery period both orma platin and oxaliplatin are more neurotoxic than cisplatin and this neurotoxicity correlates with a greater retention of platinum by the DRG.