ALK Inhibition for Non-Small Cell Lung Cancer

From Discovery to Therapy in Record Time

Research output: Contribution to journalArticle

171 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)548-551
Number of pages4
JournalCancer Cell
Volume18
Issue number6
DOIs
StatePublished - Dec 14 2010

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Non-Small Cell Lung Carcinoma
Precision Medicine
Oncogene Proteins
Neoplasms
Genome
Mutation
Therapeutics
Proteins
crizotinib

ASJC Scopus subject areas

  • Cancer Research
  • Cell Biology
  • Oncology

Cite this

ALK Inhibition for Non-Small Cell Lung Cancer : From Discovery to Therapy in Record Time. / Gerber, David E.; Minna, John D.

In: Cancer Cell, Vol. 18, No. 6, 14.12.2010, p. 548-551.

Research output: Contribution to journalArticle

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