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    BIOMARKER:

    ERRFI1 deletion

    i
    Other names: ERRFI1 , ERBB Receptor Feedback Inhibitor 1, MIG-6, Mitogen-Inducible Gene 6 Protein, GENE-33, MIG6, RALT, Receptor-Associated Late Transducer
    Entrez ID:
    54206
    Related biomarkers:
    Mutation
    2ms
    MIG6 loss increased RET inhibitor tolerant persister cells in RET-rearranged non-small cell lung cancer. (PubMed, Cancer Lett)
    EGFR inhibition with afatinib or cetuximab in combination with RET TKIs was effective in addressing drug persistence. Consistently, knocking out EGFR or RET led to high sensitivity to RET or EGFR inhibitor respectively. Here, we have provided a comprehensive analysis of adaptive and acquired resistance against RET-rearranged NSCLC.
    Journal
    |
    RET (Ret Proto-Oncogene) • KIF5B (Kinesin Family Member 5B) • ERRFI1 (ERBB Receptor Feedback Inhibitor 1)
    |
    RET fusion • RET mutation • ERRFI1 deletion • RET positive
    |
    Erbitux (cetuximab) • Gilotrif (afatinib)
    1year
    MIG6 loss confers resistance to ALK/ROS1 inhibitors in NSCLC through EGFR activation by low-dose EGF. (PubMed, JCI Insight)
    In addition, this confirmed that MIG6 loss induces resistance to ROS1-TKIs in ROS1-positive cell lines. This study found a novel factor that plays a role in ALK and ROS1-TKI resistance by activating the EGFR pathway with low-dose ligands.
    Journal
    |
    EGFR (Epidermal growth factor receptor) • ALK (Anaplastic lymphoma kinase) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • ERRFI1 (ERBB Receptor Feedback Inhibitor 1)
    |
    ALK positive • ROS1 positive • ERRFI1 deletion
    1year
    MIG6 mediates adaptive and acquired resistance to ALK/ROS1 fusion kinase inhibition through EGFR bypass signaling. (PubMed, Mol Cancer Ther)
    A MIG6 deletion was also found in a patient after progressing to ROS1 inhibition. Collectively, this study identifies MIG6 as a novel regulator for EGFR-mediated adaptive and acquired resistance to ALK/ROS1 inhibitors and suggests EGFR to MIG6 ratios and MIG6 damaging alterations as biomarkers to predict responsiveness to ALK/ROS1 and EGFR inhibitors.
    Preclinical • Journal
    |
    ALK (Anaplastic lymphoma kinase) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • ERRFI1 (ERBB Receptor Feedback Inhibitor 1)
    |
    EGFR mutation • ALK mutation • ROS1 fusion • GSPT1 deletion • ALK-ROS1 fusion • ERRFI1 deletion
    2years
    Serial profiling of circulating tumor DNA identifies dynamic evolution of clinically actionable genomic alterations in high-risk neuroblastoma. (PubMed, Cancer Discov)
    Finally, ctDNA-defined ERRFI1 loss-of-function variants were validated in neuroblastoma cellular models, with the mutant proteins exhibiting loss of wild-type ERRFI1's tumor suppressive functions. Taken together, ctDNA is prevalent in children with high-risk neuroblastoma and should be followed throughout neuroblastoma treatment.
    Journal • Circulating tumor DNA
    |
    ERRFI1 (ERBB Receptor Feedback Inhibitor 1)
    |
    ERRFI1 deletion