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    The transcription factor HOXD13 promotes melanoma growth by enhancing blood vessel formation and suppressing anti-tumor T-cells. Inhibiting its targets, VEGF and adenosine receptors, reversed this effect in models.

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    Area of Science:

    • Molecular Biology
    • Cancer Research
    • Immunology

    Background:

    • Ultraviolet radiation-induced DNA mutations drive melanoma initiation and neoantigen formation, triggering anti-tumor immunity.
    • Melanoma cells evade immune detection by modulating epigenetics and tumor microenvironment interactions, including angiogenesis.
    • Tumors enhance blood flow while preventing immune cell infiltration, a complex process involving immune evasion strategies.

    Purpose of the Study:

    • To investigate the role of transcription factors (TFs) in melanoma development and immune evasion.
    • To identify specific TFs correlated with angiogenesis and immune cell exclusion in melanoma.
    • To elucidate the molecular mechanisms by which HOXD13 influences tumor growth, angiogenesis, and immune suppression.

    Main Methods:

    • Comparative analysis of TF expression in early-stage melanoma, naevi, and other cancers.
    • Transcriptomics, 3D chromatin profiling, and in vivo melanoma models.
    • Assessment of HOXD13's effect on angiogenesis, T-cell infiltration, and gene regulation.

    Main Results:

    • HOXD13 upregulation drives a melanoblast-like program in melanoma, correlating with increased angiogenesis and suppressed T-cell infiltration.
    • HOXD13 activates VEGFA, SEMA3A, and CD73 by orchestrating 3D chromatin contacts, promoting tumor growth.
    • VEGFA and SEMA3A remodel vasculature; CD73 elevates adenosine, a vasodilator and immune suppressor.

    Conclusions:

    • HOXD13 establishes a dual pro-angiogenic and immunosuppressive axis (HOXD13-CD73/VEGF) in melanoma.
    • HOXD13-induced tumor growth is reversed by combined VEGFR and adenosine receptor (AdR) inhibition in vivo.
    • Identifies a patient subset potentially benefiting from combined AdR and VEGFR inhibitor therapies.