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A study led by researchers at Boston University School of Medicine (BUSM) demonstrates a
new mechanism involving a signaling protein and its receptor that may block the formation of new
blood vessels and cancer growth. The findings are published in the December issue of Science
Angiogenesis creates new blood vessels in a process that can lead to the onset and progression
of several diseases such as cancer and age-related macular degeneration.
Vascular endothelial growth factor (VEGF) is a signaling protein produced by damaged cells, which
binds to one of its receptors VEGFR-2, located on the surface of blood vessel cells. Once VEGF is
bound to its receptor, it is activated and sends a biochemical signal to the inside of the blood vessel
cell to initiate angiogenesis. There are currently multiple Federal Drug Administration-approved
medications that target this process. However these medications are limited by insufficient efficacy
and the development of resistance.
The researchers demonstrated that a biochemical process called methylation, which can regulate
gene expression, also affects VEGFR-2, and this can lead to angiogenesis. Using multiple methods,
the researchers were able to interfere with the methylation process of VEGFR-2 and subsequently block
angiogenesis and tumor growth.
"The study points to the methylation of VEGFR-2 as an exciting, yet unexplored drug target for
cancer and ocular angiogenesis, ushering in a new paradigm in anti-angiogenesis therapy," said
Nader Rahimi, PhD, associate professor of pathology, BUSM, who served as the study's senior investigator.