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    BIOMARKER:

    KRAS mutation + SMARCA4 mutation

    i
    Other names: SMARCA4, SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily A, Member 4, Mitotic Growth And Transcription Activator, ATP-Dependent Helicase SMARCA4, Global Transcription Activator Homologous Sequence, Transcription Activator BRG1, Sucrose Nonfermenting-Like 4, BRG1-Associated Factor 190A, Protein Brahma Homolog 1, BRM/SWI2-Related Gene 1, Homeotic Gene Regulator, Brahma Protein-Like 1, Nuclear Protein GRB1, Protein BRG-1, SNF2-Like 4, SNF2-Beta, BAF190A, SNF2L4
    Entrez ID:
    3845; 6597
    Related biomarkers:
    Expression
    Mutation
    CNA
    Others
    over1year
    Association of TTF-1 Expression with Outcomes to Immunotherapy and KRAS G12C Inhibition in Lung Adenocarcinoma (IASLC-WCLC 2023)
    Lack of TTF-1 expression was associated with impaired outcomes to IO, chemo-IO, and G12Ci in KRAS mutated advanced LUAD.
    Tumor mutational burden • PD(L)-1 Biomarker • IO biomarker
    |
    EGFR (Epidermal growth factor receptor) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • STK11 (Serine/threonine kinase 11) • KEAP1 (Kelch Like ECH Associated Protein 1) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • TTF1 (Transcription Termination Factor 1) • NKX2-1 (NK2 Homeobox 1)
    |
    TP53 mutation • KRAS mutation • EGFR mutation • STK11 mutation • KRAS wild-type • KEAP1 mutation • RAS wild-type • SMARCA4 mutation • KRAS mutation + SMARCA4 mutation • NKX2-1 expression
    2years
    Molecular characterization of primary and secondary resistance to RET inhibitors in patients with advanced NSCLC and RET fusions (AACR-NCI-EORTC 2022)
    55 patients received pralsetinib, 36 selpercatinib, 4 other RETi. Conclusions SMARCA4 and KRAS baseline co-mutations may have a role in primary resistance to RETi. Secondary RET mutations and MET/MYC amplifications were identified after treatment with RETi.
    Clinical
    |
    KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • MET (MET proto-oncogene, receptor tyrosine kinase) • RET (Ret Proto-Oncogene) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4)
    |
    TP53 mutation • KRAS mutation • MET amplification • RET fusion • KRAS G12V • MYC amplification • RET mutation • MET mutation • KRAS G12 • SMARCA4 mutation • KRAS mutation + SMARCA4 mutation
    |
    Retevmo (selpercatinib) • Gavreto (pralsetinib)
    over2years
    Mechanisms of primary and secondary resistance to RET inhibitors in patients with RET-positive advanced NSCLC (ESMO 2022)
    55 patients received pralsetinib, 36 selpercatinib, 4 other RETi. Secondary RET mutations, novel RET rearrangements and MET/MYC amplifications were identified after treatment with RETi. More than half of pts had insufficient ctDNA at PD, making tissue biopsy essential to identify resistance mechanisms.
    Clinical
    |
    KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • MET (MET proto-oncogene, receptor tyrosine kinase) • RET (Ret Proto-Oncogene) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4)
    |
    TP53 mutation • KRAS mutation • MET amplification • RET fusion • KRAS G12V • MYC amplification • RET mutation • MET mutation • RET rearrangement • KRAS G12 • SMARCA4 mutation • KRAS mutation + SMARCA4 mutation • RET positive
    |
    Retevmo (selpercatinib) • Gavreto (pralsetinib)