Angiogenesis, vasculogenesis, and vasculogenic mimicry in ovarian cancer.

Neovascularization is essential for tumor growth and metastasis. An adequate vasculature feeds tumor growth and enhances the potential of metastasis. For many years, tumor vessels were thought to be lined exclusively by endothelial cells (ECs). However, therapeutic benefits from the promising antiangiogenic strategy targeting genetically stable ECs are frequently limited by the development of resistance, implying an oversimplified view of tumor vasculature. In fact, latest studies have revealed that in addition to ECs, other cells including bone marrow-derived and plastic tumor cells do contribute to tumor vascularization, which is also indicated in ovarian cancer, the most lethal gynecologic malignancy characterized by widespread metastases within the peritoneal cavity upon diagnosis. Given the principle that tumor progression and metastasis are dependent on a persistent blood supply, it is logical that the capability of generating neovessels through diverse mechanisms of ovarian cancer is associated with its malignant potential. This review will discuss the diverse origins of ovarian cancer vascular cells and emphasize their clinical relevance (in the hope of providing insight into the prognostic assessment of women at risk for aggressive disease behavior) and alternative targets for therapeutic intervention.