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Lack of correlation between repair of DNA interstrand cross‐links and hypersensitivity of hamster cells towards mitomycin C and cisplatin
Author(s) -
Larminat Florence,
Cambois Gilles,
Zdzienicka Małgorzata Z.,
Defais Martine
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01209-5
Subject(s) - mitomycin c , cisplatin , dna repair , mutant , cytotoxic t cell , nucleotide excision repair , dna damage , dna , microbiology and biotechnology , chinese hamster , hamster , biology , chemistry , cancer research , gene , genetics , in vitro , chemotherapy
The ability to repair DNA interstrand cross‐links may be an important factor contributing to mitomycin C (MMC) and cisplatin cytotoxicities. We have assessed the repair of interstrand cross‐links induced by MMC in two MMC‐hypersensitive hamster cell mutants and their resistant parental cell line. Using a gene‐specific repair assay, we found no evidence for repair of MMC cross‐links in either parental or mutant cells, suggesting that persistence of DNA interstrand cross‐links is not responsible for the differential toxicity of MMC towards hypersensitive cells. Repair of cisplatin‐induced interstrand cross‐links was efficient in resistant as well as in mutant cells. Therefore we concluded that a defect in excision repair of interstrand cross‐links was not responsible for the cytotoxic effects of MMC and cisplatin in these hypersensitive mutants.