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822PCORRELATION OF TUMOUR C-MET EXPRESSION AND OUTCOME IN PATIENTS WITH RENAL CELL CARCINOMA (RCC) TREATED WITH SUNITINIB.

ABSTRACT Aim: Treatment of patients with RCC has improved substantially since the introduction of targeted therapies, but no biomarkers are available for predicting efficacy of such therapies. The proto-oncogene c-Met is involved in tumour angiogenesis, development and metastasis. In RCC c-Met expression is associated with poor prognosis suggesting a therapeutic role for c-Met inhibitors. The main objective of this study was to evaluate c-Met expression in metastatic RCC (mRCC). To our knowledge, c-Met expression has not previously been evaluated as a biomarker in patients with mRCC treated with VEGFR targeted agents. Methods: Clinical data and tumour tissue were available from 137 patients with mRCC treated with sunitinib at the Helsinki University Hospital between Oct 18, 2006 and May 31, 2012. Tumour c-Met expression was analysed from formalin-fixed paraffin-embedded samples using an anti-c-Met rabbit monoclonal ready-to-use antibody (Roche) and a BenchMark XT immunostainer (Ventana Medical Systems). c-Met expression was scored independently by 2 evaluators, and the discrepant cases were re-assessed jointly. Results: 78 (57%) of the 137 RCCs had no (-) or weak (+) c-Met expression (low expression group) and 59 (43%) had moderate (++ ) or strong (+++) expression (high expression group). Patients with high expression had shorter progression-free survival (PFS) than those with low expression (median, 6.5 vs. 14.2 months, p Conclusions: c-Met expression is associated with poor survival in a RCC patient population treated with sunitinib. Tumour c-Met expression warrants further investigation as a potential biomarker particularly in patients treated with dual c-Met/VEGFR inhibitors. Disclosure: P. Bono: Pfizer, Novartis and GSK advisory board honoraria. All other authors have declared no conflicts of interest.