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Harvard Medical Researchers Discover Angiogenesis-Modulating Proteins to Reduce Tumor Size

Posted by BCI Staff on Tue, Oct 11, 2011

      Blood vessels are often looked upon as a constructive part of a functioning organism; a healthy vascular system indicates strong circulation. An unhealthy vascular system leads to weak circulation, low blood pressure, and a low supply of blood to the extremities of the body.

    However, everything in moderation. There are circumstances where too much of a good thing, in this case vascular growth, can lead to increased medical complications. For instance, cancerous tumors benefit from increased circulation and vessel growth. All living tissue, cancerous or not, requires appropriate levels of oxygen and nutrients to growth and survive.

 Angiogenesis-modulation  In the early stages of tumor development, a network of blood vessels begin to form, a process called angiogenesis, to stimulate tumor growth as it circulates much needed nutrients and oxygen through the tissues. Inevitably, these blood vessels only increase the volume and reproduction rate of the cancerous cells, inflating both malignant and benign tumors alike to often fatal sizes.

 (image courtesy of Biovita)


       Assistant Professor of Neurobiology Chenghua Gu at Harvard Medical School and colleagues have tackled the problem of angiogenesis in cancer patients. They've discovered how two particular proteins, Semaphoren 3E and Plexin-D1, interact with VEGF, the protein with an established role in angiogenesis, to help to modulate the formation of new blood vessel networks.

   To test these interactions, they tracked the development of new blood vessel development in the retinas of newborn mice, and without any interference, angiogenesis was complete in fifteen days.

Angiogenesis modulation   However, once Semaphorin3E was introduced to the mice's systems, the growth of blood vessels within the retina became sporadic and haltering, severely restricting the even flow of blood, and impeding growth.

(image courtesy of PNAS)

       Semaphorin 3E binds with Plexin-D1, and the combination of the proteins is regulated by VEGF. The three proteins collaborate to tell vessels when to grow, how much to grow, and when to change course.  As Plexin-D1 is the main contributor, Professor Chenghua Gu comments that "it might be possible to disrupt Plexin-D1 without interfering with mature blood vessels elsewhere in the body". If achieved, this feat could potentially make it possible to improve upon existing therapies that block angiogenesis.

(video courtesy of Harvard Medical School)

   Currently the drug Avastin is used in cancer patients to prevent the formation of new blood vessel networks that nourish tumors. Avastin focuses exclusively on VEGF, but optimistically can be manipulated to target Semaphorin 3E or Plexin-D1 as well as VEGF to increase efficacy.

The potential that the studies on these proteins offer is groundbreaking, and is an example of the scientific advances that are progressing in centers of research across the globe.

This article is posted by Biotechnology Calendar, Inc., a veteran in the marketing and tradeshow industry. Visit or and register for our the next BioResearch Product Faire™ tradeshow in the northeast to connect with the top researchers and to exhibit new lab products at Cornell University on October 13, 2011.  To learn about the latest lab equipment in their fields, researchers are encouraged to attend. Click the button below for more information.

Cornell Vendor show

Tags: Northeast, Massachusetts, Angiogenesis Modulation, Harvard Medical School

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