ALK alterations and inhibition in lung cancer

Research output: Contribution to journalReview article

14 Scopus citations

Abstract

The advent of precision medicine in non-small cell lung cancer has remarkably altered the direction of research and improved clinical outcomes. The identification of molecular subsets with differential response to targeted therapies began with the identification of epidermal growth factor receptor mutated tumors in subsets of non-small cell lung cancer (NSCLC). Emboldened by unprecedented response rates to kinase inhibitors seen in that subset, the oncologic community searched for other molecular subsets featuring oncogene addiction. An early result of this search was the discovery of NSCLC driven by activating rearrangements of the anaplastic lymphoma kinase (ALK) gene. In an astoundingly brief period following the recognition of ALK-positive NSCLC, details of the biology, clinicopathologic features, development of targeted inhibitors, mechanisms of therapeutic resistance, and new generations of treatment were elucidated. This review summarizes the current understanding of the pathologic features, diagnostic approach, treatment options, resistance mechanisms, and future research areas for ALK-positive NSCLC.

Original languageEnglish (US)
Pages (from-to)81-88
Number of pages8
JournalSeminars in Cancer Biology
Volume42
DOIs
StatePublished - Feb 1 2017

Keywords

  • Adenocarcinoma
  • Crizotinib
  • Oncogene addiction
  • Personalized medicine
  • Precision medicine
  • Targeted therapy

ASJC Scopus subject areas

  • Cancer Research

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