Background: In this study, we evaluated the possibility that KRAS mutational status might be predictive of oxaliplatin (OXA)
efficacy. We also explored the role of excision repair cross complementing group-1 (ERCC-1).
Methods: Ninety anti-epidermal growth factor receptor-naive advanced colorectal cancer patients were retrospectively analysed.
In all patients KRAS mutational status was assessed. In 60 patients mRNA ERCC-1 expression was also investigated. Response rate
(RR) and progression-free survival (PFS) after FOLFOX-6±bevacizumab were evaluated according to KRAS status and mRNA
Results: Among 90 patients 47% wild-type (wt) and 53% mutated (mt) KRAS tumours were found. Response rate was 26% in the wt
KRAS group, whereas it was 56% in the mt KRAS group; the difference is statistically significant in the total sample (P¼0.008) and
when only patients receiving FOLFOX-6±bevacizumab as first-line are considered (P¼0.01). Progression-free survival was longer
in mt than in wt KRAS patients over all patients (10 vs 8 months, respectively, P¼0.001) and in those treated as first-line (10 vs 8
months, respectively, P¼0.0069). Mt KRAS patients experienced a longer survival (24 vs 18 months; P¼0.01). ERCC-1 mRNA
expression was not found to correlate with FOLFOX activity in our analysis.
Conclusion: Our results suggest that activating mutation of KRAS oncogene may predict response to OXA. Basal expression of
ERCC-1 mRNA does not explain the high efficacy of FOLFOX-6 in mt KRAS patients.
- Colorectal cancer