Robert J. Matusik, Ph.D.

Dr. Matusik’s laboratory has been engaged in studies of various aspects of molecular genetics and transgenic mouse models of prostate cancer. His laboratorydiscoveredthat the androgen regulated probasin promoter directs prostate-specific gene expression in the mouse,making it possible to transgenes to the prostate fornew models of prostatic disease. Bystudying the androgen receptor (AR) transcription factor regulation of genes, his laboratorywas the first to identified Forkhead BoxA1 (FOXA1) was an important AR co-regulatorin the prostate. The AR/FOXA1 paradigm is now widely accepted and mutations in FOXA1 define a subset of prostate cancer patients.They were the first to report that loss of FOXA1 in bladder cancer results in a decrease of overall survival.Further, theyreported that FOXA1 is required for mouse prostatic development and that the conditional KO of FOXA1 reprograms AR regulated genes. In addition, they show that FOXA1 bridges AR to the Nuclear Factor I family (NFIA, NFIB, NFIC, NFIX)to regulate prostate development and prostate cancer. Primary neuroendocrineprostate cancer (NEPC, small cell) is very rare but failure to the new drugs for androgen blockade results in 25-30% of the adenocarcinomas transdifferentiating into therapy (t) induce tNEPC.They showed that NEPC signals human adenocarcinoma systemically to result in castrate resistant prostate cancer (CRPC). They have identified the neuropeptides secreted by the NEPC that regulate the NFкBpathway to induce CRPC. New work showsthat the NFкB pathwayplays a major role to regulate AR activity in benign prostatic hyperplasia (BPH) resulting in failure to medical therapy.Current work is focused on how prostaglandins play an important role in BPH growth and failure of medical therapy.

CompleteListofPublishedWorkincanbefoundinMyBibliography(151manuscripts)

h-index58; i10-index 136; Citations 12901.

https://www.ncbi.nlm.nih.gov/myncbi/robert.matusik.1/bibliography/publi…