Human EML4-ALK Fusion Gene Mutation

This kit is used to qualitatively detect 12 mutation types of EML4-ALK fusion gene in samples of human non-small cell lung cancer patients in vitro. The test results are for clinical reference only and should not be used as the sole basis for individualized treatment of patients. Clinicians should make comprehensive judgments on the test results based on factors such as the patient's condition, drug indications, treatment response, and other laboratory test indicators. Lung cancer is the most common malignant tumor worldwide, and 80%~85% of the cases are non-small cell lung cancer (NSCLC). Gene fusion of echinoderm microtubule-associated protein-like 4 (EML4) and anaplastic lymphoma kinase (ALK) is a novel target in NSCLC, EML4 and ALK are respectively located in human the P21 and P23 bands on chromosome 2 and are separated by approximately 12.7 million base pairs. At least 20 fusion variants have been found, among which the 12 fusion mutants in Table 1 are common, where mutant 1 (E13; A20) is the most common one, followed by mutants 3a and 3b (E6; A20), accounting for about 33% and 29% of patients with EML4-ALK fusion gene NSCLC, respectively. ALK inhibitors represented by Crizotinib are small-molecule targeted drugs developed for ALK gene fusion mutations. By inhibiting the activity of the ALK tyrosine kinase region, blocking its downstream abnormal signaling pathways, thereby inhibiting the growth of tumor cells , to achieve targeted therapy for tumors. Clinical studies have shown that Crizotinib has an effective rate of more than 61% in patients with EML4-ALK fusion mutations, while it has almost no effect on wild-type patients. Therefore, the detection of EML4-ALK fusion mutation is the premise and basis for guiding the use of Crizotinib drugs.