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Interrogation and modulation of novel race-related alternatively spliced androgen receptor target genes in prostate cancer

The age-adjusted incidence and mortality rates for prostate cancer (PCa) among African American (AA) men are 1.6- and 2.4-fold greater, respectively, than among white men. Although much of this disparity remains after controlling for factors related to social determinants of health, very few studies have utilized this population-based difference to identify the molecular mechanisms underlying race-related tumor aggressiveness. The studies proposed here address the urgent need to interrogate and modulate, for therapeutic application, the molecular mechanisms underlying the more aggressive PCa biology in AA men and to elucidate the importance of these mechanisms for response to current therapeutic strategies.

At the Duke Cancer Institute (DCI), a number of novel alternatively spliced genes in AA versus white PCa were identified, and it has now been demonstrated that AA variants track with more aggressive cancer invasion characteristics of PCa in AA men. In addition, novel single nucleotide polymorphisms (SNPs) located in splicing regulatory regions of such genes that associate with PCa risk, aggressiveness and survival have been identified. Subsets of these genes are androgen receptor (AR) targets, which are relevant given the role that AR signaling plays in the progression of PCa, the use of anti-androgen therapy and the association of AR signaling with PCa health disparities. In parallel, at North Carolina Central University (NCCU), AMP-activated protein kinase (AMPK) signaling, which operates in a regulatory loop with AR, has been interrogated, with AMPK inhibiting AR and with AR inhibition activating AMPK, thus having significance for race-related aggressive prostate cancer. At the Biomanufacturing Research Institute and Technology Enterprise (BRITE) at NCCU, eight novel small molecules that activate AMPK activity have been identified.

 

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