Molecular pathology of lung cancer: Key to personalized medicine

Liang Cheng, Riley E. Alexander, Gregory T. MacLennan, Oscar W. Cummings, Rodolfo Montironi, Antonio Lopez-Beltran, Harvey M. Cramer, Darrell D. Davidson, Shaobo Zhang

Research output: Contribution to journalArticle

146 Scopus citations


The majority of lung adenocarcinoma patients with epidermal growth factor receptor-(EGFR) mutated or EML4-ALK rearrangement-positive tumors are sensitive to tyrosine kinase inhibitors. Both primary and acquired resistance in a significant number of those patients to these therapies remains a major clinical problem. The specific molecular mechanisms associated with tyrosine kinase inhibitor resistance are not fully understood. Clinicopathological observations suggest that molecular alterations involving so-called 'driver mutations' could be used as markers that aid in the selection of patients most likely to benefit from targeted therapies. In this review, we summarize recent developments involving the specific molecular mechanisms and markers that have been associated with primary and acquired resistance to EGFR-targeted therapy in lung adenocarcinomas. Understanding these mechanisms may provide new treatment avenues and improve current treatment algorithms.

Original languageEnglish (US)
Pages (from-to)347-369
Number of pages23
JournalModern Pathology
Issue number3
StatePublished - Mar 1 2012


  • EML4-ALK rearrangement
  • epidermal growth factor receptor (EGFR)
  • KRAS mutation
  • lung adenocarcinoma
  • molecular classification
  • personalized medicine
  • targeted therapy

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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