Broadly, our group studies fundamental metabolic processes that govern prostate cancer progression. Our discoveries have revealed that cancer engages what are usually normal physiologic processes or their variants and redirects them for the purposes of tumor progression and treatment resistance. Overall, we have found that the biotransformation of steroids in peripheral tissues (e.g., prostate cancer) from inactive to active steroids (e.g., DHT), and vice versa, regulate not only broad transcriptional programs, but also and more importantly multiple clear clinical phenotypes in humans.

The first line of therapy for metastatic prostate cancer is androgen deprivation therapy, which suppresses testicular androgens that fuel cancer cells to grow and spread, including gonadal testosterone and intratumoral concentrations of the most potent androgen, dihydrotestosterone (DHT). While ADT is successful early on, cancer cells eventually become resistant and learn to make their own DHT (termed castration-resistant prostate cancer; CRPC). Our lab investigates how CRPC cells make their own androgens, and how blocking these pathways may help treat the disease.

For more information on the Sharifi Lab please visit: www.nimasharifilab.com