April 23, 2014
 
prostate cancer discovery  
   THE BRADY UROLOGICAL INSTITUTE • JOHNS HOPKINS MEDICINE

   A PUBLICATION OF THE PATRICK C . WALSH PROSTATE CANCER RESEARCH FUND
   Volume VI, Winter 2011
 
   
 

Hevin, the Missing Gene that Might Help Stop Cancer

What does fetal development have to do with cancer? More than you might think. Although one process is healthy and good, and the other is harmful, both involve intense periods of growth. The big difference is that in cancer, certain switches that should be able to stop cells from dividing either aren’t there, or are not working as they should. And, in cancer — when it starts, and also as it progresses — some pathways that were designed to do their main work before birth are reactivated.

One of these is a switch called Hevin. It’s a gene that is “dynamically regulated during prostate development, but it’s disrupted in prostate cancer,” says Paula Hurley, Ph.D. She is interested in learning more about Hevin because it can help keep tumors from forming, “and in many forms of cancer, it is significantly reduced or lost.” Hurley is working to trace the molecular pathways that Hevin uses to stop cancers from forming, and to find out whether the shutdown of this gene makes a man more susceptible to prostate cancer forming and advancing. “Understanding the molecular underpinnings contributing to prostate cancer will help us develop targeted therapies,” she says, drugs specially designed to work with these pathways to stop prostate cancer in its tracks.

   


 

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