2011
DOI: 10.1200/jco.2010.34.0570
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Abstract: The combination of the MET inhibitor tivantinib and erlotinib is well-tolerated. Although the study did not meet its primary end point, evidence of activity was demonstrated, especially among patients with KRAS mutations. Additional study of tivantinib and erlotinib in patients with NSCLC is planned.

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Cited by 344 publications
(266 citation statements)
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References 26 publications
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“…MET amplification causes resistance to gefitinib by driving ERBB3-dependent activation of PI3K (8). Therefore, several MET inhibitors have been administered to EGFR-TKI-na€ ve or resistant NSCLC patients in clinical trials (13,28). PFS was longer in the group treated with the MET inhibitor tivantinib combined with erlotinib than in the group treated with erlotinib alone in a phase II study (13).…”
Section: Discussionmentioning
confidence: 99%
See 2 more Smart Citations
“…MET amplification causes resistance to gefitinib by driving ERBB3-dependent activation of PI3K (8). Therefore, several MET inhibitors have been administered to EGFR-TKI-na€ ve or resistant NSCLC patients in clinical trials (13,28). PFS was longer in the group treated with the MET inhibitor tivantinib combined with erlotinib than in the group treated with erlotinib alone in a phase II study (13).…”
Section: Discussionmentioning
confidence: 99%
“…Our recent study demonstrated that MET amplification and gene copy number gains showed a short response to gefitinib treatments in lung adenocarcinoma with EGFR mutation (12). Recently, MET inhibitors have been administered to NSCLC patients who are na€ ve or resistant to EGFR TKIs in a clinical trial (13). This phase II study showed that PFS was longer in the group treated with erlotinib plus the MET inhibitor tivantinib than in the group treated with erlotinib alone, especially among patients with KRAS mutations (13).…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…In the meantime, based on eight studies (Felip et al, 2008;Schneider et al, 2008;Marchetti et al, 2009;O'Byrne et al, 2011;Sequist et al, 2011;Cadranel et al, 2012;Metro et al, 2012;Milella et al, 2012), the pooled HR for PFS was 1.33 (95%CI: 1.05-1.69, P=0.019 heterogeneity test P=0.10, I 2 =61.9%), shown in Figure 3B. The result suggested that patients with K-ras mutation had a shorter PFS than did wild-type K-ras patients.…”
Section: Predictive and Prognostic Value Of K-ras Mutationmentioning
confidence: 85%
“…Furthermore, EGFR-TKIs were more sensitive than anti-EGFR MoAbs to K-ras gene status. Eleven studies (Endoh et al, 2006;Ichihara et al, 2007;Felip et al, 2008;Schneider et al, 2008;Marchetti et al, 2009;O'Byrne et al, 2011;Sequist et al, 2011;Cadranel et al, 2012;Ludovini et al, 2012;Milella et al, 2012;Johnson et al, 2013) showed the correlation between OS and the K-ras status. Available HRs from the 11 studies were combined to get the pooled HR, shown in Figure 3A.…”
Section: Predictive and Prognostic Value Of K-ras Mutationmentioning
confidence: 99%