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    3years
    Clinicopathological features and resistance mechanism in HIP1-ALK-rearranged lung cancer: A multicenter study. (PubMed, Genes Chromosomes Cancer)
    One patient who received first-line lorlatinib treatment achieved partial response for >26.5 months...Brigatinib treatment appeared to be effective for a patient who failed crizotinib treatment because of the L1152V/Q1146K mutations, which might be related to increased binding affinity to these mutants...Although HIP1-ALK-rearranged NSCLC appears to initially respond well to ALK-TKIs, crizotinib resistance may be correlated with the AKAP9-BRAF fusion, ALK compound mutations (L1152V/Q1146K), and the ALK L1196M mutation. Larger studies are needed to evaluate the significance of HIP1-ALK-rearranged NSCLC.
    Clinical • Journal
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    BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • EML4 (EMAP Like 4) • HIP1 (Huntingtin Interacting Protein 1)
    |
    BRAF mutation • ALK rearrangement • ALK fusion • ALK mutation • BRAF fusion • EML4-ALK L1196M • ALK L1196M • ALK L1152V
    |
    Xalkori (crizotinib) • Lorbrena (lorlatinib) • Alunbrig (brigatinib)