^
    Contact us  to learn more about
    our Premium Content:  News alerts, weekly reports and conference planners
    BIOMARKER:

    PDE4D overexpression

    i
    Other names: PDE4D, Phosphodiesterase 4D, CAMP-Specific 3',5'-Cyclic Phosphodiesterase 4D, DPDE3, PDE43, Phosphodiesterase 4D, CAMP-Specific (Dunce (Drosophila)-Homolog Phosphodiesterase E3), Phosphodiesterase 4D, CAMP-Specific (Phosphodiesterase E3 Dunce Homolog, Drosophila), Phosphodiesterase E3 Dunce Homolog (Drosophila), CAMP-Specific Phosphodiesterase PDE4D6, Phosphodiesterase 4D, CAMP-Specific, Testicular Tissue Protein Li 136, ACRDYS2, HSPDE4D, PDE4DN2, STRK1
    Entrez ID:
    5144
    1year
    PDE4D drives rewiring of the MAPK pathway in BRAF-mutated melanoma resistant to MAPK inhibitors. (PubMed, Cell Commun Signal)
    In summary, our research showed that PDE4D drives rewiring of the MAPK pathway in BRAF-mutated melanoma resistant to MAPK inhibitors and suggests that PDE4 inhibition is a novel therapeutic option for treatment of BRAF-mutated melanoma patients.
    Journal
    |
    BRAF (B-raf proto-oncogene) • PDE4D (Phosphodiesterase 4D)
    |
    BRAF V600E • BRAF mutation • BRAF V600 • PDE4D overexpression
    almost2years
    GNAS mutation inhibits growth and induces phosphodiesterase 4D expression in colorectal cancer cell lines. (PubMed, Int J Cancer)
    In conclusion, our findings demonstrate that GNAS mutation results in the growth suppression of CRC cells. Moreover, the GNAS mutation-induced overexpression of PDE4D provides a potential avenue to impede the proliferation of CRC cells through the use of PDE4 inhibitors.
    Preclinical • Journal
    |
    GNAS (GNAS Complex Locus) • PDE4D (Phosphodiesterase 4D)
    |
    GNAS mutation • PDE4D overexpression
    2years
    Toxic PARP trapping upon cAMP-induced DNA damage reinstates the efficacy of endocrine therapy and CDK4/6 inhibitors in treatment-refractory ER+ breast cancer. (PubMed, Nat Commun)
    However, during SOC resistance, an ER-to-EGFR switch induces PDE4D overexpression via c-Jun. Notably, combining SOC with inhibitors of PDE4D, EGFR or PARP1 overcomes SOC resistance irrespective of the BRCA1/2 status, providing actionable targets for restoring SOC efficacy.
    Journal • BRCA Biomarker • PARP Biomarker
    |
    EGFR (Epidermal growth factor receptor) • ER (Estrogen receptor) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • PARP1 (Poly(ADP-Ribose) Polymerase 1) • PDE4D (Phosphodiesterase 4D) • JUN (Jun proto-oncogene)
    |
    ER positive • PDE4D overexpression