Genetic landscape of patients with ALK-rearranged non –small-cell lung cancer (NSCLC) and response to ceritinib in ASCEND-1 study
Anaplastic lymphoma kinase (ALK) fusion oncogene is present in 3 –7% of patients with non–small-cell lung cancer (NSCLC) with the most common partner being echinoderm microtubule-associated protein-like 4 (EML4).1,2 Crizotinib was the first ALK inhibitor (ALKi) approved for patients with ALK-rearranged (ALK+) NSCLC, although the duration of disease control is generally short lived. Common acquired resistance mechanisms to crizotinib include ALK resistance mutations (∼30%),3 ALK amplification/copy number gain (∼10%), and activation of alternative oncogenic drivers (∼45%), with the remaining (∼15%) being unknown.
Source: Lung Cancer - Category: Cancer & Oncology Authors: D.S-W. Tan, M. Thomas, D-W. Kim, S. Szpakowski, P. Urban, R. Mehra, L.Q.M. Chow, S. Sharma, B.J. Solomon, E. Felip, D.R. Camidge, J. Vansteenkiste, L. Petruzzelli, S. Pantano, A.T. Shaw Source Type: research
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