作者: Jérôme Viguier , Valérie Boige , Catherine Miquel , Marc Pocard , Bruno Giraudeau
DOI: 10.1158/1078-0432.CCR-04-2216
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摘要: Purpose: The aim of our study was to assess whether the polymorphism nucleotide excision repair enzyme, cross-complementing rodent deficiency, complementation group 1 (ERCC1), had an effect on tumor response in patients treated with standard chemotherapy regimens for a metastatic colorectal cancer. We have studied synonymous that causes single change C T at codon 118 converting common usage (AAC) less used (AAT), both coding asparagine. This results decreased ERCC1 gene expression, which impairs activity. Experimental Design: Ninety-one median age 55.1 years cancer were included retrospective study. analyzed normal tissue all patients. Results: Twenty (22%) homozygous AAC ( C/C genotype), 30 (33%) AAT T/T and 41 (45%) heterozygous C/T genotype). objective rate oxaliplatin combination 5-fluorouracil (5-FU) significantly higher genotype compared groups (61.9%, 42.3%, 21.4%, respectively; P = 0.018). By contrast, no significant difference observed when either 5-FU alone (45%, 29.2%, 33.3%, 0.407) or irinotecan (46.1%, 25.0%, 27.3%, 0.305). Conclusions: Our observations allowed us define first useful predictive criterion oxaliplatin/5-FU