$10 of every entry fee is donated to cancer research, specifically a lab studying angiogenesis.  Sandy Ryeom, runner and lab researcher, gives us periodic updates so you can see how you money is being spent. Here are her updates:

 

Sandra Ryeom, Ph.D.


Vascular Biology Program

Department of Surgery

Karp Building, 12.129

300 Longwood Avenue

Boston, MA 02115

Tel: 617.919.2345, Fax: 617.730.0231

Email: sandra.ryeom@childrens.harvard.edu

Ryeom Lab

Research Update: May 2008

As we continue our studies trying to understand how blood vessels grow to nourish cancer cells, funding support from Platypus Sports (via Wenatchee Marathon, Alefest Bike Ride, Vela Bella Bike Ride and Leavenworth Oktoberfest Marathon proceeds) will continue to play an important role in moving this work forward.  This process of new blood vessel growth to support tumor growth is called angiogenesis and is a field that was founded by Dr. Judah Folkman, the Director of the Vascular Biology Program here at Children’s Hospital. Sadly, Dr. Folkman passed away very unexpectedly this past January 2008.  He was an incredible mentor to my group, was full of energy and still had so much left to do.  He was constantly and tirelessly working to bring new therapies discovered in the lab to patients for the fight against cancer. His loss has made us even more determined to honor his legacy by pushing forward our studies investigating the ways that we can stop these blood vessels from growing.

One of the projects that my group has made significant progress on this past year is the identification of a specific cell type and a specific protein that may be useful in predicting whether a cancer has recurred, well before this cancer can be detected by currently available radiologic imaging techniques.  Our work suggests that the levels of a specific protein called thrombospondin-1 that is involved in the process of angiogenesis, may indicate the re-growth of a tumor.  This protein is detected in platelets, small cells that circulate in the blood stream known to be important for wound healing, clotting and tumor growth.  We continue to utilize mouse models of tumor growth and cancer to investigate the role of platelets in tumorigenesis and specifically how the protein thrombospondin-1 contributes to this process.

In these economically challenging times, obtaining funding from the federal government and specifically the National Institutes of Health (NIH) continues to be difficult.  Your support of our research enables us to continue our focus on multiple projects in order to comprehensively study cancer growth and prevention from the specific angle of understanding the process of angiogenesis.

With gratitude for your support!

Sandra

 

 

Sandra Ryeom, Ph.D.

Vascular Biology

Children’s Hospital

Harvard Medical School

300 Longwood Ave

Boston, MA 02115

sandra.ryeom@childrens.harvard.edu

 

Research Update: September 2007

              My group has been focused on understanding how to stop angiogenesis, or the formation of new blood vessels to support tumor growth.  We have recently made progress on two major projects in the lab.

              • We have been trying to understand how Down syndrome individuals are protected against cancer.  Specifically we have been investigating which gene (or genes) on chromosome 21 may be involved in preventing cancer in this population.  Recently, our work using mouse models of Down syndrome have identified one of the genes involved in preventing cancer in this population.  This gene is referred to as the Down Syndrome Candidate Region-1 (DSCR1) gene and was initially identified due to its location on chromosome 21.  It is now known to be involved in blocking angiogenesis and our initial studies show that DSCR1 may play a significant role in preventing cancer in the Down syndrome population.  DSCR1 may function to block angiogenesis and ultimately prevent tumor growth. The goal of this work is to determine whether the DSCR1 gene product can be utilized as preventative anti-cancer therapy for the non-Down syndrome population.

              • Another project in the lab has been focused on understanding how mutations in the hereditary breast cancer gene BRCA1, may initiate tumor growth.  Women with a mutation in this gene have a 65% risk of developing breast cancer.  Recent studies in our lab suggests that one of the previously unexplored functions of this gene may be to regulate proteins that block angiogenesis or prevent blood vessel growth to nourish tumor cells.  We are investigating how BRCA1 regulates angiogenesis and this work may allow us to treat women with BRCA1 mutations with non-toxic anti-angiogenic therapies.  These prophylactic therapies may suppress angiogenesis and thus prevent the growth of breast and ovarian tumors.

 

Your support of our work is very much appreciated!

Sandy




















saturday, april 18, 2009