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Prostate cancer

Androgen receptor; protein kinase DNA-activated catalytic polypeptide (PRKDC; DNAPK)

Cell culture and mouse studies suggest inhibiting components of the DNA damage response could help treat prostate cancer. In cell culture and mouse xenograft models of prostate cancer, anti-androgen receptor therapies increased sensitivity to DNA damage, and DNA-damaging therapies such as radiation increased androgen receptor-dependent expression of genes encoding DNA repair proteins. In these models, radiation plus anti-androgen receptor therapy decreased cell growth compared with either treatment alone. In cultured prostate cancer cells, dihydrotestosterone (DHT) partially reversed the growth inhibitory effect of a DNAPK inhibitor plus radiation. Next steps include screening DNAPK inhibitors in disease models.

SciBX 6(41); doi:10.1038/scibx.2013.1160
Published online Oct. 24, 2013

Work from first study unpatented; licensing status not applicable

Patent and licensing status unavailable for second study

Goodwin, J.F. et al. Cancer Discov.; published online Sept. 11, 2013;
Contact: Karen E. Knudsen, Thomas Jefferson University, Philadelphia, Pa.

Polkinghorn, W.R. et al. Cancer Discov.; published online Sept. 11, 2013;
Contact: Charles L. Sawyers, Memorial Sloan-Kettering Cancer Center, New York, N.Y.