Background: Molecular targeted therapies in NSCLC often results in profound initial patient responses, these responses are short-term due to the development of acquired resistance. In an EML4-ALK NSCLC background, acquired resistance can be developed in two ways ALK dependent (ALK secondary mutations) and ALK independent (alternative oncogenic pathways). In our study, we have shown that increased expression of Aurora kinase A (AURKA) leads to acquired resistance upon treatment with ALK TKI crizotinib. Conclusion: Our results indicate a new mechanism to acquire resistance upon treatment with ALK TKI crizotinib. Inhibition of both ALK and AURKA activity might be beneficial for ALK TKI resistant tumors with increased AURKA gene expression/activity. READ ARTICLE
Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1803
Authors: G. Umapathy, R. Palmer, B. Hallberg
