667PD - A randomised multicentre trial of epirubicin, oxaliplatin and capecitabine (EOC) + panitumumab in advanced oesophago-gastric cancer (REAL3): updated...

Date 01 October 2012
Event ESMO Congress 2012
Session Gastrointestinal tumors, non-colorectal
Topics Anticancer agents
Oesophageal Cancer
Gastric Cancer
Biological Therapy
Presenter Tom Waddell
Authors T.S. Waddell1, J. Reis-Filho2, D. Gonzalez-De-Castro3, I. Chau1, A. Wotherspoon4, S. Gupta5, C. Saffery1, G. Middleton6, J. Wadsley7, D. Cunningham8
  • 1Department Of Medicine, Royal Marsden Hospital, SM25PT - Sutton/UK
  • 2Department Of Molecular Pathology, Institute for Cancer Research, London/UK
  • 3Department Of Molecular Diagnostics, Institute for Cancer Research, Sutton/UK
  • 4Department Of Histopathology, Royal Marsden Hospital, SW3 6JJ - London/UK
  • 5Statistics Department, Royal Marsden Hospital, SW3 6JJ - London/UK
  • 6St. Lukes Cancer Centre, Royal Surrey County Hospital, Guildford/UK
  • 7Department Of Oncology, Weston Park Hospital, Sheffield/UK
  • 8Gi And Lymphoma Research Unit, Royal Marsden Hospital, SM25PT - Sutton/UK



EGFR overexpression occurs in 30-90% of oesophago-gastric adenocarcinomas (OGA), and correlates with poor prognosis. The REAL-3 trial evaluated the addition of the anti-EGFR antibody panitumumab (P) to epirubicin, oxaliplatin and capecitabine (EOC) in advanced OGA.


Patients with untreated, metastatic or locally advanced OGA were randomised to EOC (E 50mg/m2, O 130mg/m2, C 1250mg/m2/day) or mEOC + P (E 50mg/m2, O 100mg/m2, C 1000mg/m2/day, P 9mg/kg). Primary endpoint was overall survival (OS); secondary endpoints were progression-free survival (PFS), response rate (RR), toxicity, and biomarker evaluation. Response was evaluated by RECIST after 4 and 8 cycles.


553 patients were recruited (EOC 275, mEOC + P 278). Median OS was 11.3 months with EOC compared to 8.8 months with mEOC + P (HR 1.37: 95% CI 1.07-1.76, p = 0.013). Median PFS was 7.4 and 6.0 months respectively (HR 1.22: 95% CI 0.98-1.52, p = 0.068), with RR being 42% compared to 46% (odds ratio 1.16: 95% CI 0.81-1.57, p = 0.467). In the mEOC + P arm, OS was significantly improved in patients with G1-3 rash (77%, n = 209) on treatment compared to those without (23%, n = 63); median OS 10.2 vs 4.3 months (p < 0.001), with similar significant improvements seen in RR and PFS. Multivariate analysis demonstrated a negatively prognostic role for KRAS mutation (HR 2.1: 95% CI 1.10-4.05, p = 0.025) and PIK3CA mutation (HR 3.2: 95% CI 1.01-10.40, p = 0.048). The above information is being presented at ASCO 2012. Updated translational results will be available for presentation at ESMO Congress. This will include correlation of rash with toxicity endpoints and data relating to EGFR and KRAS amplification in this population.


I. Chau: I have a compensated advisory role with Roche. I have also received honoraria and research funding from Roche.

D. Cunningham: I have received research funding from Amgen, Roche, Merck-Serono. I have undertaken uncompensated advisory roles for Amgen and Roche. I have provided an uncompensated expert testimony for Amgen.

All other authors have declared no conflicts of interest.