Going beneath the tip of the iceberg. Identifying and understanding EML4-ALK variants and TP53 mutations to optimize treatment of ALK fusion positive (ALK+) NSCLC.

Abstract excerpt

Since the discovery of echinoderm microtubule-associated protein-like 4 (EML4) and anaplastic lymphoma kinase (ALK) gene fusion in non-small cell lung carcinoma (NSCLC) in 2007, more than 10 EML4-ALK variants based on the exon breakpoints in EML4 have been identified. Unlike other receptor tyrosine kinase fusion positive NSCLC such as ROS1 or RET fusion, EML4-ALK is the dominant fusion variant in ALK+ NSCLC...

Topics

• Anaplastic Lymphoma Kinase
• Carcinoma, Non-Small-Cell Lung
• Humans
• Lung Neoplasms
• Mutation
• Oncogene Proteins, Fusion
• Protein-Tyrosine Kinases
• Proto-Oncogene Proteins
• Receptor Protein-Tyrosine Kinases
• Retrospective Studies
• Tumor Suppressor Protein p53