| Literature DB >> 25302160 |
Abstract
The identification of driver mutations and drugs that inhibit their activity has been a major therapeutic advance for patients with advanced lung adenocarcinoma. Unfortunately, the success of these drugs is limited by the universal development of resistance. Treatment failure can result from inadequate drug exposure or selection of resistant malignant clones. Clinically distinct mechanisms of disease progression have been identified and can inform treatment decisions. Investigations into the biochemical mechanisms of tyrosine kinase inhibitor resistance may provide additional therapeutic targets by which the efficacy of targeted therapy can be improved.Entities:
Keywords: Adenocarcinoma; Epidermal growth factor receptor mutation; Lung cancer; Resistance; Targeted therapy; Tyrosine kinase inhibitor
Year: 2014 PMID: 25302160 PMCID: PMC4129521 DOI: 10.5306/wjco.v5.i4.560
Source DB: PubMed Journal: World J Clin Oncol ISSN: 2218-4333