ALK Inhibition for Non-Small Cell Lung Cancer: From Discovery to Therapy in Record Time

David E. Gerber; John D. Minna

doi:10.1016/j.ccr.2010.11.033

ALK Inhibition for Non-Small Cell Lung Cancer: From Discovery to Therapy in Record Time

David E. Gerber, John D. Minna

Research output: Contribution to journal › Review article › peer-review

194 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	548-551
Number of pages	4
Journal	Cancer Cell
Volume	18
Issue number	6
DOIs	https://doi.org/10.1016/j.ccr.2010.11.033
State	Published - Dec 14 2010

ASJC Scopus subject areas

Oncology
Cell Biology
Cancer Research

Access to Document

10.1016/j.ccr.2010.11.033

Cite this

@article{48ed80c9e7a54e5c8a66d551c60bcfc6,

title = "ALK Inhibition for Non-Small Cell Lung Cancer: From Discovery to Therapy in Record Time",

abstract = "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.",

author = "Gerber, {David E.} and Minna, {John D.}",

note = "Funding Information: Supported by Lung Cancer SPORE NCI P50CA70907.",

year = "2010",

month = dec,

day = "14",

doi = "10.1016/j.ccr.2010.11.033",

language = "English (US)",

volume = "18",

pages = "548--551",

journal = "Cancer Cell",

issn = "1535-6108",

publisher = "Cell Press",

number = "6",

}

TY - JOUR

T1 - ALK Inhibition for Non-Small Cell Lung Cancer

T2 - From Discovery to Therapy in Record Time

AU - Gerber, David E.

AU - Minna, John D.

N1 - Funding Information: Supported by Lung Cancer SPORE NCI P50CA70907.

PY - 2010/12/14

Y1 - 2010/12/14

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=78650026375&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78650026375&partnerID=8YFLogxK

U2 - 10.1016/j.ccr.2010.11.033

DO - 10.1016/j.ccr.2010.11.033

M3 - Review article

C2 - 21156280

AN - SCOPUS:78650026375

SN - 1535-6108

VL - 18

SP - 548

EP - 551

JO - Cancer Cell

JF - Cancer Cell

IS - 6

ER -

ALK Inhibition for Non-Small Cell Lung Cancer: From Discovery to Therapy in Record Time

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this