Abstract
EML4-ALK fusion, observed in about 3-7% of human lung adenocarcinoma, is one of the most important oncogenic drivers in initiating lung tumorigenesis. Previous studies report that kinase activities of EML4-ALK are mainly dependent on dimerization or autophosphorylation of the kinase domain. Recently, emerging evidence begins to link cancer-related genes to condensate assembly, indicative of the important role of phase separation in tumorigenesis. However, it still remains largely unknown whether phase separation contributes to the oncogenic activation of EML4-ALK and how EML4-ALK fusion exactly fires downstream signaling and drives lung cancer formation.
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