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    BIOMARKER:

    KRAS G12C + KRAS G12V

    i
    Other names: KRAS, KRAS proto-oncogene GTPase, KRAS1, KRAS2, NS, NS3, OES, CFC2, RALD, K-Ras, RASK2, KI-RAS, C-K-RAS, K-RAS2A, K-RAS2B, K-RAS4A, K-RAS4B, K-Ras 2, C-K-RAS, c-Ki-ras, c-Ki-ras2, Kirsten rat sarcoma viral oncogene homolog
    Entrez ID:
    3845
    Related biomarkers:
    Expression
    Mutation
    CNA
    Others
    12ms
    Clinical impact of KRAS mutations in metastatic pancreatic ductal adenocarcinoma (PDAC). (ASCO-GI 2024)
    A Cox Proportional Hazard analysis of OS across all patients found that Gemcitabine and Gemcitabine with Nabpaclitaxel had significantly higher HR than FOLFIRINOX... Our data suggest that FOLFIRINOX has a longer TTNT than other first-line regimens for KRAS G12C, G12V, G12D, and G12R. KRAS G12C was associated with the shortest OS among common KRAS mutations. >
    Clinical • Metastases
    |
    KRAS (KRAS proto-oncogene GTPase)
    |
    KRAS mutation • KRAS G12C • KRAS G12D • KRAS G12V • KRAS wild-type • RAS wild-type • KRAS G12 • KRAS G13 • KRAS G12C + KRAS G12V
    |
    gemcitabine • 5-fluorouracil • albumin-bound paclitaxel • irinotecan • leucovorin calcium
    over1year
    RAS-mutations in population-based and real-life metastatic colorectal cancer cohorts (ESMO-GI 2023)
    In this cohort with population-based and real-world patients, no differences in patient characteristics or treatment modalities were seen between different RAS mt, except a higher frequency of right-colon primaries among KRAS mt compared with NRAS mt. KRAS -G12S conferred a worse OS compared with some other KRAS mt, whereas no other differences in OS were seen. It therefore seems as if different RAS mt behave quite similar.
    Clinical • Metastases
    |
    KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • NRAS (Neuroblastoma RAS viral oncogene homolog) • RAS (Rat Sarcoma Virus)
    |
    BRAF V600E • KRAS mutation • KRAS G12C • NRAS mutation • BRAF V600 • KRAS G12D • KRAS G12V • RAS mutation • NRAS Q61K • KRAS G12A • KRAS G12 • NRAS Q61 • KRAS G12S • NRAS Q61R • KRAS G13 • KRAS Q61H • NRAS G12D • NRAS G12 • NRAS G13 • KRAS A146T • NRAS A146T • NRAS A146 • KRAS G12C + KRAS G12V • KRAS Q61K • NRAS G12S
    over1year
    Preclinical and clinical evaluation of the RAF/MEK clamp avutometinib (VS-6766) in combination with the mTOR inhibitor everolimus for the treatment of KRAS mutated non-small cell lung cancer (AACR 2023)
    The combination of avutometinib and everolimus overcomes the activation of the PI3K/AKT/mTOR pathway which is an adaptive resistance mechanism to MAPK pathway inhibition. We have shown that avutometinib and everolimus induce synergistic anti-tumor effects preclinically, and preliminary data suggest clinically meaningful ORR and PFS in patients with KRAS mt NSCLC including non-G12C variants.
    Preclinical • Combination therapy
    |
    KRAS (KRAS proto-oncogene GTPase) • RPS6 (Ribosomal Protein S6) • AKT1S1 (AKT1 Substrate 1)
    |
    KRAS mutation • KRAS G12C • KRAS G12D • KRAS G12V • KRAS G12A • KRAS Q61H • KRAS G13A • KRAS G12C + KRAS G12V
    |
    everolimus • avutometinib (VS-6766)