During recent years, many gene mutations have been reported in lung adenocarcinoma, and target agents against driver mutations have been explored. MNNG HOS transforming gene (MET) exon 14 mutation and ALK receptor tyrosine kinase (ALK) translocation were usually mutually exclusive. However, here, we describe a case that had intratumor heterogeneity on both genetic and pathologic characteristics. Patients whose tumors harbored MET exon 14 splice site mutations or ALK rearrangement derived meaningful clinical benefit from crizotinib.4, 5 Our findings may have profound clinical implications for potential therapeutic targeting during disease progression. READ ARTICLE
Journal of Thoracic Oncology DOI:10.1016/j.jtho.2018.10.149
Authors: Tian Qiu, Fanshuang Zhang, Weihua Li, Lei Guo, Jianming Ying