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Prostate Cancer Foundation Adds Two New Investigators

Funding Raises the Total of PCF Young Investigators to 50

November 9, 2010 -- The Prostate Cancer Foundation (PCF) announced the addition of two new Young Investigators (YIs) to its Class of 2010. These two new awards raise the number of PCF-supported YI projects to 50. The foundation’s Young Investigator awards are designed to encourage the most innovative minds in cancer research to focus their careers on prostate cancer. The grants provide three years of funding to test transformational research questions for prostate cancer treatments and patients. With the addition of these two grants, the PCF’s 2010 Class of Young Investigators now numbers 27 and represents a $6.1 million investment in the global cancer research community.

Each Young Investigator award provides $225,000 over three years and is matched dollar for dollar by recipients’ research institutions to protect time or bridge salary support prior to a first government grant, making the total award worth $450,000. Since 2008, PCF has invested more than $11.5 million in YI grants.

“The addition of these two Young Investigators realizes our goal of supporting 50 Young Investigators by the close of 2010,” said Jonathan W. Simons, MD, president and CEO of PCF. “Generous donor support for these programs ensures that fresh ideas and innovation continue flowing into prostate cancer research. We are grateful to the donors who made our newest Young Investigators possible—David H. Koch and The Republic of Tea.”

The two new 2010 PCF Young Investigator Award recipients are:

The David H. Koch – PCF Young Investigator (49th PCF YI)

Brett S. Carver, MD - Memorial Sloan-Kettering Cancer Center, New York, NY

Despite advances in the early detection and management of prostate cancer, hormone-refractory disease remains the second most common cause of male cancer deaths in the United States. Inhibition of the androgen receptor (AR), a key signaling pathway responsible for promoting prostate cancer cell growth, invasion and survival, remains a major target for prostate cancer treatment. Another critical signaling pathway, the PI3K pathway, is frequently activated in primary and metastatic prostate cancer. Activation of the PI3K pathway and molecular alterations promoting AR signaling are associated with the development of hormone refractory disease. A number of novel inhibitors of the PI3K and AR pathways are in early clinical development and are promising therapeutic agents for men with prostate cancer.

Dr. Carver’s research will further define the role of the PI3K pathway in promoting hormone-refractory disease, identify which compounds targeting the PI3K and AR pathways provide maximum therapeutic potential, and identify molecular alterations that predict therapeutic response. Collectively this work will identify which combination of therapeutic agents will provide the greatest survival benefit and for which patients.


The Republic of Tea– PCF Young Investigator (50th PCF YI)

Felix Feng, MD - University of Michigan, Ann Arbor, MI

Radiation therapy represents one of the primary treatments for localized prostate cancer. However, there is a clear need to better identify which localized prostate cancers are radiation-resistant and to intensify therapy for these malignancies while minimizing side effects. Dr. Feng's research focuses on two common genetic changes found in prostate cancer, ETS gene fusions and PTEN deletion, and the effects of these alterations on radiation resistance. Dr. Feng and others have found that the presence of either ETS fusions or PTEN deletions affect the ability of prostate cancer cells to repair DNA damage, which is a critical component of radiation response. Dr. Feng now seeks to better understand the mechanisms by which these genetic alterations influence DNA repair, to determine if ETS fusions and/or PTEN deletion can be used as predictors of radiation resistance in prostate cancer biopsies prior to initiation of therapy. He will also investigate whether inhibition of specific DNA repair pathways can be combined with radiation therapy to preferentially kill prostate cancers harboring ETS fusions or PTEN deletion. The long-term goal of this research is to use these genetic alterations to help guide the selection of therapies to improve outcomes for patients with locally advanced prostate cancer.

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