Exploring the therapeutic rationale for angiogenesis blockade in cervical cancer

This review highlights the molecular and pathologic evidence that cervical cancer is driven by angiogenesis and presents a summary of the recent clinical research in antiangiogenesis therapy for advanced cervical cancer with a focus on the use of bevacizumab.

The articles chosen for this review reveal the rationale for antiangiogenesis agents in cervical cancer from 3 perspectives: pathologic, molecular, and clinical data.

Several translational investigations have revealed that proangiogenic signaling cascades are active in cervical carcinogenesis and can be used to improve patient outcomes in advanced disease. For example, in a recently published study of patients with recurrent and metastatic cervical cancer, bevacizumab was the first targeted agent to improve overall survival in a gynecologic cancer when successfully combined with 2 different chemotherapy regimens.

Because of recent advances in screening, aggressive management of cervical intraepithelial neoplasia, and human papillomavirus vaccination, cervical cancer is preventable and curable with radical surgery plus lymphadenectomy surgery or chemoradiation plus brachytherapy if detected early. Unfortunately, for patients with metastatic or recurrent disease, effective therapeutic options are limited for this aggressive life-threatening condition. However, molecularly targeted agents have provided a critical opportunity to improve patient outcomes beyond optimizing cytotoxic chemotherapy regimens so that they may benefit from other agents or emergent therapies in the future.