[PDF][PDF] ALK inhibition for non-small cell lung cancer: from discovery to therapy in record time
DE Gerber, JD Minna - Cancer cell, 2010 - cell.com
DE Gerber, JD Minna
Cancer cell, 2010•cell.comIt was only 3 years ago that an acquired translocation of EML4 with ALK leading to the
expression of an EML4-ALK oncoprotein in non-small cell lung cancer (NSCLC) was
reported. Tumor cells expressing EML4-ALK are" addicted" to its continued function. Now,
crizotinib, an oral ALK inhibitor, is demonstrated to provide dramatic clinical benefit with little
toxicity in patients having such advanced NSCLC, and a mechanism of clinical resistance to
crizotinib is identified. Such therapy" targeted" at oncogenic proteins provides" personalized" …
expression of an EML4-ALK oncoprotein in non-small cell lung cancer (NSCLC) was
reported. Tumor cells expressing EML4-ALK are" addicted" to its continued function. Now,
crizotinib, an oral ALK inhibitor, is demonstrated to provide dramatic clinical benefit with little
toxicity in patients having such advanced NSCLC, and a mechanism of clinical resistance to
crizotinib is identified. Such therapy" targeted" at oncogenic proteins provides" personalized" …
It was only 3 years ago that an acquired translocation of EML4 with ALK leading to the expression of an EML4-ALK oncoprotein in non-small cell lung cancer (NSCLC) was reported. Tumor cells expressing EML4-ALK are "addicted" to its continued function. Now, crizotinib, an oral ALK inhibitor, is demonstrated to provide dramatic clinical benefit with little toxicity in patients having such advanced NSCLC, and a mechanism of clinical resistance to crizotinib is identified. Such therapy "targeted" at oncogenic proteins provides "personalized" medicine and prompts genome-wide mutation analysis of human tumors to find other therapeutic targets.
cell.com
