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Download the ESMO 2012 Abstract Book - Oxford Journals

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Annals of Oncology<br />

d or 5-FU (1,000 mg/m 2 /d1-5 infusion)/cisplatin (100 mg/m 2 d 1) q 28 d. OS<br />

analyses for non-inferiority, by pre-specified stratifications, were performed.<br />

Results: OS for NI from CS (8.6 months) compared to CF (7.9 months) had a HR =<br />

0.92 (two-sided 95% CI, 0.80-1.05). HR = 1.05 being lower than HR = 1.10 non<br />

inferiority margin, derived from a literature meta-analysis, CS remains statistically<br />

significantly non-inferior (p = 0.0068) to CF. The 74% preserved control effect by CS<br />

is well above <strong>the</strong> suggested 50% by Rothmann et al. (Statist-Med2003; 22:239-264),<br />

based on which <strong>the</strong> 1.10 non-inferiority margin was derived. Moreover, statistically<br />

significant safety advantages for <strong>the</strong> CS arm were observed for <strong>the</strong> rates of G3/4<br />

neutropenia (18.6%, CS; 40.0%, CF), G3/4 febrile neutropenia (1.7%, CS; 6.9%, CF),<br />

G3/4 stomatitis (1.3%, CS; 13.6%, CF), renal adverse events (all grades: 18.8%, CS;<br />

33.5%, CF), and severe hypokalemia (3.6%, CS; 10.8%, CF). On <strong>the</strong> o<strong>the</strong>r safety<br />

items, no significant differences were noted between CS and CF, especially regarding<br />

Head and Foot Syndrome which was anecdotal and limited to grade 1/2.<br />

Treatment-related deaths were significantly reduced with CS compared to CF<br />

(respectively 2.5% and 4.9%).<br />

Conclusion: CS is non-inferior to CF while providing safety advantages for <strong>the</strong><br />

patients and is a treatment alternative in advanced gastric carcinoma.<br />

Disclosure: All authors have declared no conflicts of interest.<br />

669PD MET AS PROGNOSTIC FACTOR AND THERAPEUTIC TARGET<br />

IN PRETREATED HEPATOCELLULAR CARCINOMA (HCC):<br />

FINAL RESULTS OF A RANDOMIZED CONTROLLED PHASE<br />

2 TRIAL (RCT) WITH TIVANTINIB (ARQ 197)<br />

B. Daniele 1 , L. Rimassa 2 , C. Porta 3 , I. Borbath 4 , S. Salvagni 5 , J. van Lae<strong>the</strong>m 6 ,<br />

H. van Vlierberghe 7 , R. von Roemeling 8 , G. Abbadessa 9 , A. Santoro 10<br />

1 Clinical Oncology, G. Rummo Hospital, Benevento, ITALY, 2 Oncology<br />

Hematology, Humanitas Cancer Center, Istituto Clinico Humanitas IRCCS,<br />

Rozzano, ITALY, 3 Oncologia Medica, Ospedale San Matteo, Pavia, ITALY,<br />

4 Gastro-Enterology, Cliniques Universitaires St. Luc, Brussels, BELGIUM,<br />

5 Oncology, Azienda Ospedaliera Parma, Parma, ITALY, 6 Gastroenterology,<br />

Erasme University Hospital, Brussels, BELGIUM, 7 Gastroenterology, Ghent<br />

University Hospital, Ghent, BELGIUM, 8 Clinical Development Oncology, Daiichi<br />

Sankyo Pharma Development, Edison, NJ, UNITED STATES OF AMERICA,<br />

9 Clinical Development, ArQule, Inc, Woburn, MA, UNITED STATES OF<br />

AMERICA, 10 Oncology Hematology, Humanitas Cancer Center, Istituto Clinico<br />

Humanitas, Rozzano, ITALY<br />

Background: Tivantinib (T), a selective, oral inhibitor of MET, <strong>the</strong> hepatocyte<br />

growth factor (HGF) receptor, was tolerated in HCC as mono<strong>the</strong>rapy and with<br />

sorafenib.<br />

Methods: Multi center RCT; key selection criteria: unresectable HCC, 1 prior<br />

systemic <strong>the</strong>rapy, PS

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