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    BIOMARKER:

    DDR2 overexpression

    i
    Other names: CD167b Antigen, MIG20a, NTRKR3, TYRO10, CD167 Antigen-Like Family Member B, Discoidin Domain Receptor Tyrosine Kinase 2, Discoidin Domain-Containing Receptor Tyrosine Kinase 2
    Entrez ID:
    4921
    Related biomarkers:
    Mutation
    1year
    Abrogating Regulatory T Cells Overcomes Tumor-Specific T cell Exhaustion and Prevents Metastatic Pancreatic Cancer (P977) (IMMUNOLOGY 2023)
    Our data supports the novel hypothesis that Ddr2 overexpression drives intratumoral Treg accumulation and promotes metastasis. In summary, Tregs are key drivers of T cell exhaustion and immunosuppression in pancreatic cancer and may prove a valuable clinical target for tumors that evade immune checkpoint blockade.
    PD(L)-1 Biomarker • IO biomarker • Metastases
    |
    CD8 (cluster of differentiation 8) • PD-1 (Programmed cell death 1) • IFNG (Interferon, gamma) • LAG3 (Lymphocyte Activating 3) • GZMB (Granzyme B) • DDR2 (Discoidin domain receptor 2) • FOXP3 (Forkhead Box P3)
    |
    DDR2 overexpression
    2years
    DDR2 regulates angiogenesis via HSP-90 modulation in ovarian cancer (AACR 2022)
    We also identified that DDR2’s role in angiogenesis is mediated by the Hsp70/90 chaperone machinery. In summary, we have identified that DDR2 regulates angiogenesis in ovarian cancer.
    BRCA Biomarker
    |
    TP53 (Tumor protein P53) • BRCA2 (Breast cancer 2, early onset) • CD31 (Platelet and endothelial cell adhesion molecule 1) • DDR2 (Discoidin domain receptor 2) • HSP90AA1 (Heat Shock Protein 90 Alpha Family Class A Member 1Heat Shock Protein 90 Alpha Family Class A Member 1) • HSPA4 (Heat Shock Protein Family A (Hsp70) Member 4)
    |
    DDR2 overexpression
    almost3years
    Amplification of DDR2 mediates Sorafenib resistance through NF-κB/c-Rel signaling in hepatocellular carcinoma. (PubMed, Cell Biol Int)
    Blocking NF-κB signaling using the NF-κB signaling inhibitor, Bardoxolone Methyl, increased the response of HCC cells to Sorafenib. Further analysis showed that DNA amplification of DDR2 is an important mechanism leading to DDR2 overexpression in HCC. Our results demonstrated that DDR2 is a potential therapeutic target in patients with HCC, and targeting DDR2 represents a promising approach to increase Sorafenib sensitivity in patients with HCC.
    Journal
    |
    DDR2 (Discoidin domain receptor 2)
    |
    DDR2 overexpression
    |
    sorafenib