Dividing and conquering the variation among variants in EML4-ALK lung cancer
Year: 2017
Type: article
Abstract: Activating gene rearrangements in the anaplastic lymphoma kinase are present in approximately 2–7% of lung adenocarcinomas (ALK + cancers) (1,2). Patients with ALK + lung adenocarcinoma often benefit from treatment with an ALK tyrosine kinase inhibitor (TKI), such as crizotinib, ceritinib, and alectinib (2). However, acquired ALK TKI resistance remains an obstacle to long-term patient survival in patients who do respond to initial therapy and a distinct subset of ALK + patients fails to experience an initial tumor regression, exhibiting intrinsic resistance (2). Identifying the basis of both innate and acquired resistance is essential to improve clinical outcomes.
Source: Translational Cancer Research
Author: Trever G. Bivona
Language: English
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Funder: National Cancer Institute
Award: G1213983933
OpenAlex ID: W2604252933
