Journal
MODERN PATHOLOGY
Volume 25, Issue 3, Pages 347-369Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/modpathol.2011.215
Keywords
lung adenocarcinoma; EML4-ALK rearrangement; epidermal growth factor receptor (EGFR); KRAS mutation; molecular classification; personalized medicine; targeted therapy
Categories
Ask authors/readers for more resources
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. Modern Pathology (2012) 25, 347-369; doi:10.1038/modpathol.2011.215; published online 27 January 2012
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available