822P - Correlation of tumour c-Met expression and outcome in patients with renal cell carcinoma (RCC) treated with sunitinib

Date 27 September 2014
Event ESMO 2014
Session Poster Display session
Topics Anti-Cancer Agents & Biologic Therapy
Renal Cell Cancer
Translational Research
Presenter Katriina Peltola
Citation Annals of Oncology (2014) 25 (suppl_4): iv280-iv304. 10.1093/annonc/mdu337
Authors K.J. Peltola1, J. Rautiola1, H. Joensuu2, E. Hänninen3, A. Ristimäki3, P. Bono1
  • 1Helsinki University, Helsinki Cancer Center, 00290 - Helsinki/FI
  • 2Oncology, Helsinki Univerity Central Hospital (HUCH), FI-00290 - Helsinki/FI
  • 3Pathology, Helsinki Univerity Central Hospital (HUCH), HUSLAB, FI-00290 - Helsinki/FI



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.


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.


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 < 0.0001), and tended to have also shorter overall survival (median, 20.1 vs. 33.7 months; p = 0.087). There was no association between tumour c-Met expression and the mean vessel density analysed by IHC for CD31 expression. High c-Met expression was an independent predictor for unfavourable PFS together with the Heng criteria in a Cox proportional hazards model (HR 1.73, 95% CI 1.18 to 2.56; p = 0.005).


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.


P. Bono: Pfizer, Novartis and GSK advisory board honoraria. All other authors have declared no conflicts of interest.