By Deblina Dam
Angiogenesis, the formation of new capillaries, is an essential process in many physiological and pathological events. New vasculature, in cancers, promotes tumor growth and metastasis. Vascular permeability factor / vascular endothelial growth factor (VPF/VEGF) has been implicated in the new vessel development found in most tumors (GI related tumors, renal cell carcinoma, brain cancer and hematological malignancies).
Several research groups have been investigating, for decades, the regulatory role of VPG/VEGF to elucidate the mechanisms by which this important “pro-angiogenesis” cytokine functions in a variety of tumor models. Based on the results of these studies, several anti-angiogenesis drugs are now available in clinics worldwide, useful in treating cancer and other vascular diseases. However, recent discoveries suggest that therapeutic treatments with anti-angiogenesis drugs do not necessarily extend survival rate of cancer patients for more than a few months, because tumors elicit elusive resistance. Additionally, some reports also propose that VEGF inhibitors which reduce primary tumor growth are capable of promoting tumor invasiveness and metastasis.
Debabrata (Dev) Mukhopadhyay, PhD: Professor of Biochemistry and Molecular Biology, Mayo Clinic School of Medicine and Science, Jachsonville, Florida, has a joint appointment with the Department of Physiology and Biomedical Engineering and Associate Director of Mayo Clinic Comprehensive Cancer centre for Global Collaboration. He and his team as long been working on Angiogenesis, the “Hallmark” of cancer, and have been trying to identify the mechanism of this “SWITCH” in the tumor microenvironment (TME). They say that there is a certain balance between the angiogenic switch and tumor dormancy. There are several pre-clinical and clinical studies to found, based on the concept of “anti-angiogenic therapy.”
The challenges include the side effects associated with this therapy, such as, hypertension, minimal outcome and most importantly, VEGF resistance. Macrophages facilitate resistance to anti-VEGF therapy. The exact mechanism of how anti-angiogenic therapy induces macrophages is yet to be solved. To avoid cancer cellstemness, it is required that VEGF expression inside the tumor cells is blocked. Furthermore, studies on renal cancer have showed better results than when it is applied on patients suffering from colorectal cancer. Does this indicate that Anti-VEGF therapy needs to be personalized?
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