2014
DOI: 10.1016/j.lungcan.2014.02.001
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Overcoming the resistance to Crizotinib in patients with Non-Small Cell Lung Cancer harboring EML4/ALK translocation

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Cited by 43 publications
(21 citation statements)
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“…NSCLCs harboring epidermal growth factor receptor (EGFR) mutations or anaplastic lymphoma kinase (ALK) gene rearrangements have been successfully targeted with tyrosine kinase inhibitors (TKIs) [2,3]. However, the rate of EGFR positive mutation is about 20% and ALK rearrangement is only about 5-7% [4], and thus most NSCLC cases do not respond to these TKIs [1,5]. In such cases, conventional chemotherapy using platinum-based compounds are recommended [6,7].…”
Section: Introductionmentioning
confidence: 99%
“…NSCLCs harboring epidermal growth factor receptor (EGFR) mutations or anaplastic lymphoma kinase (ALK) gene rearrangements have been successfully targeted with tyrosine kinase inhibitors (TKIs) [2,3]. However, the rate of EGFR positive mutation is about 20% and ALK rearrangement is only about 5-7% [4], and thus most NSCLC cases do not respond to these TKIs [1,5]. In such cases, conventional chemotherapy using platinum-based compounds are recommended [6,7].…”
Section: Introductionmentioning
confidence: 99%
“…This also holds true for crizotinib, given that mutations in the TK domains of the different targets of crizotinib is currently the best studied and most prevalent form of resistance to this drug, accounting for up to 25% of all cases resistant to ALK therapy (14). …”
Section: Resistance Mechanisms Of Crizotinibmentioning
confidence: 98%
“…The first (and most common) mechanism of resistance identified involves modification of the crizotinib target [67], accounting for approximately 25% of resistance [68]. The most studied of these mutations is the substitution of a leucine by a methionine at the 1196 position (L1196M) in the ALK tyrosine kinase domain, the equivalent of the T790M mutation for EGFR.…”
Section: Secondary Resistancementioning
confidence: 99%