Melanoma is an aggressive cancer type with a high tendency to spread to distant body sites, including bones. Despite the availability of effective therapies, many patients still do not fully benefit from treatment. The aim of our study was to evaluate the therapeutic potential of inhibiting the activation of the vascular endothelial growth factor receptor (VEGFR-1) by placenta growth factor (PlGF) using an investigational anti-VEGFR-1 monoclonal antibody (D16F7 mAb). The VEGFR-1 receptor is expressed by endothelial cells of blood vessels that nourish the tumor, protumoral macrophages and melanoma cells. Results indicate that PlGF stimulates the ability of melanoma to infiltrate the surrounding tissues and that treatment with D16F7 mAb counteracts melanoma properties, which contribute to tumor spread, reducing the invasiveness of the tumor and its tropism toward bone tissue. Therefore, blockade of VEGFR-1 stimulation by PlGF represents a suitable strategy to restrain the metastatic potential of melanoma.Data contained in the deposited file are the raw data utilized to produce the graphics included in the Cancers article: "The Anti-Vascular Endothelial Growth Factor Receptor 1 (VEGFR-1) D16F7 Monoclonal Antibody Inhibits Melanoma Adhesion to Soluble VEGFR-1 and Tissue Invasion in Response to Placenta Growth Factor" by Atzori et al.

Melanoma is an aggressive cancer type with a high tendency to spread to distant body sites, including bones. Despite the availability of effective therapies, many patients still do not fully benefit from treatment. The aim of our study was to evaluate the therapeutic potential of inhibiting the activation of the vascular endothelial growth factor receptor (VEGFR-1) by placenta growth factor (PlGF) using an investigational anti-VEGFR-1 monoclonal antibody (D16F7 mAb). The VEGFR-1 receptor is expressed by endothelial cells of blood vessels that nourish the tumor, protumoral macrophages and melanoma cells. Results indicate that PlGF stimulates the ability of melanoma to infiltrate the surrounding tissues and that treatment with D16F7 mAb counteracts melanoma properties, which contribute to tumor spread, reducing the invasiveness of the tumor and its tropism toward bone tissue. Therefore, blockade of VEGFR-1 stimulation by PlGF represents a suitable strategy to restrain the metastatic potential of melanoma.Data contained in the deposited file are the raw data utilized to produce the graphics included in the Cancers article: "The Anti-Vascular Endothelial Growth Factor Receptor 1 (VEGFR-1) D16F7 Monoclonal Antibody Inhibits Melanoma Adhesion to Soluble VEGFR-1 and Tissue Invasion in Response to Placenta Growth Factor" by Atzori et al.