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    BIOMARKER:

    EML4-ALK I1171T

    i
    Other names: 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, 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
    Entrez ID:
    238; 27436
    Related biomarkers:
    Expression
    Mutation
    CNA
    Fusion
    Others
    over2years
    Longitudinal minimally invasive monitoring of resistance mutations in ALK rearranged lung cancer patients (AACR 2022)
    ALK rearrangements are detected in approximately 4% of patients with advanced non-small cell lung cancer (NSCLC), and the tyrosine kinase inhibitors (TKIs) crizotinib, alectinib, brigatinib, ceritinib, and lorlatinib have been approved by the FDA for the treatment of ALK-positive NSCLC. The dPCR method was highly sensitive in detecting gene mutations with low allele frequency. It was also found to be able to monitor variable resistance mutations over time during ALK-TKI treatment. In addition, we found that the appearance of G1202R did not always indicate clinical acquisition of resistance that required drug modification.
    Clinical
    |
    ALK (Anaplastic lymphoma kinase) • EML4 (EMAP Like 4)
    |
    ALK positive • ALK rearrangement • ALK mutation • ALK G1202R • ALK C1156Y • ALK G1269A • ALK I1171T • EML4-ALK L1196M • ALK I1171 • ALK L1196M • ALK L1152R • ALK S1206Y • ALK V1180L • EML4-ALK G1202R • EML4-ALK G1269A • ALK L1196M + ALK C1156Y • EML4-ALK I1171T • EML4-ALK S1206Y
    |
    Xalkori (crizotinib) • Alecensa (alectinib) • Lorbrena (lorlatinib) • Zykadia (ceritinib) • Alunbrig (brigatinib)
    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)
    over3years
    BRAF V600E mutation as a novel mechanism of acquired resistance to ALK inhibition in ALK-rearranged lung adenocarcinoma: A case report. (PubMed, Medicine (Baltimore))
    We present a case of ALK-rearranged lung adenocarcinoma with acquired resistance to ALK inhibition, in which the BRAF V600E mutation is a novel resistance mechanism. This provides evidence that BRAF V600E mutation is one mechanism of ALK-TKI resistance.
    Clinical • Preclinical • Journal
    |
    BRAF (B-raf proto-oncogene) • EML4 (EMAP Like 4)
    |
    BRAF V600E • BRAF V600 • ALK rearrangement • EML4-ALK rearrangement • ALK I1171T • ALK I1171 • EML4-ALK I1171T
    |
    Xalkori (crizotinib) • Alecensa (alectinib) • Lorbrena (lorlatinib)