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    BIOMARKER:

    YES1 overexpression

    i
    Other names: YES1, YES Proto-Oncogene 1, Src Family Tyrosine Kinase, V-Yes-1 Yamaguchi Sarcoma Viral Oncogene Homolog 1, Tyrosine-Protein Kinase Yes, Proto-Oncogene C-Yes, YES1 Proto-Oncogene, Src Family Tyrosine Kinase, Proto-Oncogene Tyrosine-Protein Kinase YES, Yamaguchi Sarcoma Oncogene, Cellular Yes-1 Protein, P61-YES, P61-Yes, HsT441, C-Yes
    Entrez ID:
    7525
    Related biomarkers:
    Expression
    CNA
    Others
    Associations

    News

    Trials
    1year
    Tyrosine-protein kinase Yes controls endothelial junctional plasticity and barrier integrity by regulating VE-cadherin phosphorylation and endocytosis. (PubMed, Nat Cardiovasc Res)
    In contrast, in EC-specific Src-deficiency, VE-cadherin internalization is maintained, and leakage is suppressed. In conclusion, Yes-mediated phosphorylation regulates constitutive VE-cadherin turnover, thereby maintaining endothelial junction plasticity and vascular integrity.
    Journal
    |
    YES1 (YES Proto-Oncogene 1, Src Family Tyrosine Kinase) • CDH5 (Cadherin 5)
    |
    YES1 overexpression
    2years
    SRC Family Kinase Inhibition Targets YES1 and YAP1 as Primary Drivers of Lung Cancer and as Mediators of Acquired Resistance to ALK and Epidermal Growth Factor Receptor Inhibitors. (PubMed, JCO Precis Oncol)
    Our results demonstrate the therapeutic potential of SFK inhibition in primary tumorigenesis and AR driven by YES1/YAP1 signaling.
    Preclinical • Journal
    |
    EGFR (Epidermal growth factor receptor) • YAP1 (Yes associated protein 1) • YES1 (YES Proto-Oncogene 1, Src Family Tyrosine Kinase)
    |
    EGFR mutation • ALK positive • ALK fusion • ALK mutation • YES1 amplification • YAP1 overexpression • YES1 overexpression
    |
    MSK-IMPACT
    over2years
    YES1 and MYC Amplifications as Synergistic Resistance Mechanisms to Different Generation ALK Tyrosine Kinase Inhibitors in Advanced NSCLC: Brief Report of Clinical and Preclinical Proofs. (PubMed, JTO Clin Res Rep)
    In conclusion, YES1 and MYC amplifications are candidates to justify a rapid acquired resistance to crizotinib entailing primary brigatinib and lorlatinib resistance. In this context, a combination strategy of ALK TKI with dasatinib could be effective to overcome a rapid resistance.
    Preclinical • Journal
    |
    ALK (Anaplastic lymphoma kinase) • MYC (V-myc avian myelocytomatosis viral oncogene homolog)
    |
    ALK positive • MYC amplification • YES1 overexpression
    |
    Xalkori (crizotinib) • dasatinib • Lorbrena (lorlatinib) • Alunbrig (brigatinib)
    almost3years
    miR-133a targets YES1 to reduce cisplatin resistance in ovarian cancer by regulating cell autophagy. (PubMed, Cancer Cell Int)
    Our results suggest that the miR-133a/YES1 axis plays a critical role in cisplatin resistance in human ovarian cancer by regulating cell autophagy, which might serve as a promising therapeutic target for ovarian cancer chemotherapy treatment in the future.
    Journal
    |
    YES1 (YES Proto-Oncogene 1, Src Family Tyrosine Kinase)
    |
    YES1 overexpression
    |
    cisplatin
    over3years
    EphA2-YES1-ANXA2 pathway promotes gastric cancer progression and metastasis. (PubMed, Oncogene)
    In addition, the activation of EphA2-YES1-ANXA2 pathway is correlated with poor prognosis. Thus, our results establish EphA2-YES1-ANXA2 axis as a novel pathway that drives GC invasion and metastasis, targeting this pathway would be an efficient way for the treatment of GC.
    Journal
    |
    YES1 (YES Proto-Oncogene 1, Src Family Tyrosine Kinase)
    |
    YES1 overexpression