Dividing and conquering the variation among variants in EML4-ALK lung cancer

Trever G. Bivona


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.