Research led by investigators at Beth Israel Deaconess Medical Center (BIDMC) helps explain how a group of angiogenesis inhibitor molecules serve as an important defense mechanism against the development and spread of cancer, offering key insights into why cancerous tumors grow at different rates among different individuals.
The findings, which could help lead to the development of new drug treatments to help keep existing tumors at bay, are reported in the early edition of the Proceedings of the National Academy of Sciences (PNAS) and in the Feb. 22 edition of the publication.
Angiogenesis, the process by which new blood vessels are derived from preexisting capillaries, is considered essential for tumor growth. The "angiogenic switch" is turned on when levels of angiogenesis stimulator molecules (VEGF, bFGF) exceed those of angiogenesis inhibitor molecules. These proteins – which include tumstatin, endostatin and thrombospondin-1 – are naturally present in body fluids or tissues, providing a counterbalance to the stimulator molecules.
Earlier studies by the papers senior author Raghu Kalluri, PhD, published in Science and Cancer Cell in 2002 and 2003, respectively, helped to explain the mechanisms by which tumstatin and endostatin prevent the growth of new blood vessels.
Bonnie Prescott | EurekAlert!
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