Title: Overcoming resistance to antiangiogenic therapies
Authors: Tejpar, Sabine ×
Prenen, Hans
Mazzone, Max #
Issue Date: 2012
Publisher: AlphaMed Press
Series Title: The Oncologist vol:17 issue:8 pages:1039-50
Article number: 10.1634/theoncologist.2012-0068
Abstract: The concept of targeting new blood vessel formation, or angiogenesis, in tumors is an important advancement in cancer therapy, resulting, in part, from the development of such biologic agents as bevacizumab, a monoclonal antibody directed against vascular endothelial growth factor (VEGF)-A. The rationale for antiangiogenic therapy is based on the hypothesis that if tumors are limited in their capacity to obtain a new blood supply, so too is their capacity for growth and metastasis. Additional evidence suggests that pruning and/or "normalization" of irregular tumor vasculature and reduction of hypoxia may facilitate greater access of cytotoxic chemotherapy (CT) to the tumor. Indeed, for metastatic colorectal cancer, bevacizumab in combination with established CT regimens has efficacy superior to that of CT alone. Despite ~2-month longer progression-free and overall survival times than with CT alone, patients still progress, possibly because of alternative angiogenic "escape" pathways that emerge independent of VEGF-A, or are driven by hypoxic stress on the tumor. Other VEGF family members may contribute to resistance, and many factors that contribute to the regulation of tumor angiogenesis function as part of a complex network, existing in different concentrations and spatiotemporal gradients and producing a wide range of biologic responses. Integrating these concepts into the design and evaluation of new antiangiogenic therapies may help overcome resistance mechanisms and allow for greater efficacy over longer treatment periods.
ISSN: 1083-7159
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Molecular Digestive Oncology (+)
Clinical Digestive Oncology (+)
Laboratory of Tumor Inflammation and Angiogenesis (Vesalius Research Center) (+)
× corresponding author
# (joint) last author

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