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Cetuximab is a standard-of-care treatment for  RAS  wild-type metastatic colorectal cancer (mCRC) but not for those harbor a  KRAS  mutation since MAPK pathway is constitutively activated. Nevertheless, cetuximab also exerts its effect by its immunomodulatory activity despite the presence of RAS mutation. The aim of this study was to determine the impact of polymorphism  FcγRIIIa  V158F and killer immunoglobulin-like receptor (KIR) genes on the outcome of mCRC patients with  KRAS  mutations treated with cetuximab. This multicenter Phase II clinical trial included 70 mCRC patients with  KRAS  mutated. We found  KIR2DS4  gene was significantly associated with OS (HR 2.27; 95% CI, 1.08–4.77; P = 0.03). In non-functional receptor homozygotes the median OS was 2.6 months longer than in carriers of one copy of full receptor. Multivariate analysis confirmed  KIR2DS4  as a favorable prognostic marker for OS (HR 6.71) in mCRC patients with  KRAS  mutation treated with cetuximab. These data support the potential therapeutic of cetuximab in  KRAS  mutated mCRC carrying non-functional receptor  KIR2DS4  since these patients significantly prolong their OS even after heavily treatment.  KIR2DS4  typing could be used as predictive marker for identifying RAS mutated patients that could benefit from combination approaches of anti-EGFR monoclonal antibodies and other immunotherapies to overcome the resistance mediated by mutation in RAS.

Combination of KIR2DS4 and FcγRIIa polymorphisms predicts the response to cetuximab in KRAS mutant metastatic colorectal cancer