Background: Anaplastic lymphoma kinase (ALK) have been recognized as the most important predictor of response to crizotinib. However, 20-30% of patients harboring ALK fusion non-small-cell lung cancer patients show a poor response requiring investigation for underlying mechanisms... Conclusions: BCL2L11 loss, PI3K-AKT-mTOR signaling pathway (PTEN, PIK3CA mutations), SMARCA4 mutations or EML4-ALK fusion (non A20) might contribute to molecular mechanisms of primary resistance to crizotinib in ALK+NSCLC.Further investigations are warranted to overcome these primary resistance. READ ARTICLE
Annals of Oncology DOI:10.1016/j.annonc.2020.10.404
Authors: W-X. Wang, C. Xu, Q-X. Zhang, W. Zhuang, Z-B. Song, Y-C. Zhu, G. Chen, M-Y. Fang, T-F. Lv, Y. Song
Background: Anaplastic lymphoma kinase (ALK) rearrangement is a validated therapeutic driver gene in non-small cell lung cancer (NSCLC). More than 30 different fusion partner genes of ALK in NSCLC have been reportedand most of these ALK fusions respond well to ALK inhibitors crizotinib. With the development of next-generation sequencing (NGS), more novel partners for ALK rearrangement have been identified. Here, we aimed to report the landscape of ALK rearrangement in Chinese patients with solid tumors... Conclusions: Novel ALK fusions are detected in patients with not only NSCLC but also other solid tumors. NGS fusion assay is an optional method for screening novel fusions. READ ARTICLE
Journal of Clinical Oncology DOI:10.1200/JCO.2020.38.15_suppl.3555
Authors: Sheng Yang, Fuyu Gong, Guoqiang Wang, Xiaohui He