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    BIOMARKER:

    EML4-ALK variant 3a

    i
    Other names: EML4, EMAP Like 4, Restrictedly Overexpressed Proliferation-Associated Protein, Echinoderm Microtubule-Associated Protein-Like 4, Echinoderm Microtubule Associated Protein Like 4, Ropp 120, C2orf2, EMAP-4, EMAPL4, ROPP120, ELP120, NBLST3, CD246, Anaplastic Lymphoma Kinase, Anaplastic Lymphoma Kinase (Ki-1), CD246 Antigen, Mutant Anaplastic Lymphoma Kinase, ALK, ALK Receptor Tyrosine Kinase, Anaplastic Lymphoma Receptor Tyrosine Kinase, ALK Tyrosine Kinase Receptor
    Entrez ID:
    238; 27436
    Related biomarkers:
    Expression
    Mutation
    CNA
    Fusion
    Others
    2years
    Potential Therapeutic Strategy for EGFR-Mutant Lung Cancer With Concomitant EML4-ALK Rearrangement-Combination of EGFR Tyrosine Kinase Inhibitors and ALK Inhibitors. (PubMed, JTO Clin Res Rep)
    PC-9_v3a-gef and PC-9_v3b-gef cells were resistant to gefitinib and ALK inhibitors alone, but ALK inhibitors enhanced gefitinib-induced cytotoxicity. Furthermore, combination treatment with osimertinib and ceritinib caused a decrease in liver tumor size of the patient with liver metastases. Our data suggest that combination treatment with EGFR and ALK inhibitors can be a therapeutic strategy for treating NSCLC with concomitant EGFR mutation and EML4-ALK rearrangement.
    Journal
    |
    EGFR (Epidermal growth factor receptor) • EML4 (EMAP Like 4)
    |
    EGFR mutation • EGFR exon 19 deletion • EGFR expression • ALK rearrangement • ALK fusion • EML4-ALK variant 3 • EML4-ALK rearrangement • ALK V3a • ALK V3b • EML4-ALK variant 3a
    |
    Tagrisso (osimertinib) • gefitinib • Zykadia (ceritinib)
    over3years
    [VIRTUAL] Patient-derived lung cancer organoids for the selection of therapeutic options in an ALK-rearranged tumor. (ASCO 2021)
    One patient was deemed as sensitive to carboplatin but tumor showed to be resistant...The patient started alectinib but showed progression after 12 months...Treatment was switched to brigatinib with no response...The In vitro results demonstrated no activity of lorlatinib but a strong response to crizotinib... We present clinical evidence that PDOs are an alternative tool in oncogenic addicted tumors helping to guide treatment decisions and increasing a more personalized sequential treatment approach.
    Clinical • IO biomarker
    |
    ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • EML4 (EMAP Like 4)
    |
    TP53 mutation • ALK rearrangement • EML4-ALK fusion • ALK fusion • ALK C1156Y • ALK I1171T • ALK I1171 • ALK V3a • EML4-ALK C1156Y • EML4-ALK I1171T • EML4-ALK variant 3a
    |
    Xalkori (crizotinib) • carboplatin • Alecensa (alectinib) • Lorbrena (lorlatinib) • Zykadia (ceritinib) • Alunbrig (brigatinib)