Biomolecular markers and involution of hemangiomas.

Background/purpose: Vascular anomalies are a diverse set of lesions with distinct clinical behaviors, whose biomolecular characteristics are largely undefined. Common hemangiomas proliferate during the first year of life, then involute at a variable pace over several years. Other vascular tumors may involute much more quickly (rapidly involuting congenital hemangiomas [RICH]), not at all (lymphatic malformation), or display malignant behavior (angiosarcoma).

Regression of established tumors and metastases by potent vascular endothelial growth factor blockade.

Vascular endothelial growth factor (VEGF) is a critical promoter of blood vessel growth during embryonic development and tumorigenesis. To date, studies of VEGF antagonists have primarily focused on halting progression in models of minimal residual cancer. Consistent with this focus, recent clinical trials suggest that blockade of VEGF may impede cancer progression, presumably by preventing neoangiogenesis.

Anti-VEGF antibody in experimental hepatoblastoma: suppression of tumor growth and altered angiogenesis.

Background: Hepatoblastoma is the most common primary hepatic malignancy of childhood, frequently presenting as advanced disease. Vascular endothelial growth factor (VEGF) is an endothelial mitogen and survival factor critical to growth and angiogenesis in many human cancers. Inhibition of VEGF effectively suppresses tumorigenesis in multiple experimental models.