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UCLA researchers discover a potential target for therapy for patients with a deadly prostate cancer
Date:11/8/2010

regulation is required to maintain castration resistant prostate cancers, meaning that the turning on of the pathway may be a cause of the hormone therapy resistance, making it an even more attractive target for therapy.

Armed with a hypothetical target at which to aim molecular therapies, Reiter and his team set out to develop novel therapeutics to block N-cadherin. They developed two monoclonal antibodies to test on their cell lines and animal models and found that the antibodies slowed the growth in their prostate cancer cell lines and mouse models and blocked the spread of castration resistant prostate cancer in mouse models. Reiter said this finding may mean the antibodies could potentially be used to block the spread of prostate cancer in men diagnosed with this aggressive form of the castration resistant disease, making it easier to treat and potentially improving outcomes in this patient population. It could also be effective in preventing men treated for early stage disease from progressing to castration resistance since the antibodies prevented that progression in the cell lines and mouse models, Reiter said.

"We believe these findings show that the up regulation of N-cadherin is one of the mechanisms that leads to castration resistance and it could be targeted perhaps in conjunction with other pathways already being studied that lead to resistance," Reiter said. "These findings may provide us with yet another way to treat these cancers."

Although many men have indolent or slow growing prostate cancers that often are only observed over time, a significant percent of patients present with castration resistant disease or later develop castration resistance, which is very difficult to treat effectively. It would be very useful to have another tool in the arsenal to fight this type of prostate cancer, Reiter said.

The next step for Reiter and his team is to improve the antibodies and understand the mechanism by which N
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Contact: Kim Irwin
kirwin@mednet.ucla.edu
310-206-2805
University of California - Los Angeles
Source:Eurekalert

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