The Freedland Laboratory specializes in prostate cancer prevention, management and outcomes. Stephen Freedland, MD, is a surgeon and research scientist, with a National Institutes of Health-funded basic science laboratory. The Freedland Lab features expertise in epidemiology through Adriana Vidal, PhD, and preclinical models with Michael Freeman, PhD, as well as clinical trials by Freedland. The team works seamlessly to translate important work to the patients as quickly as possible.
Preclinical animal studies within the Freedland Lab, as well as with other investigators, consistently show that obesity enhances prostate cancer growth. This creates an opportunity for us to exploit the link between obesity and prostate cancer growth to identify and target drivers of aggressive disease.
One of the mechanisms through which obesity may increase prostate cancer risk is inflammation. Thus, the Freedland Lab is now performing the first in-depth analysis of tissue inflammatory markers that will allow us to characterize the specific inflammatory cell types present in the prostates of men with and without prostate cancer. Particularly, we will be investigating whether race modifies the associations between inflammatory markers and prostate cancer risk, given that inflammation varies by race, and black men have a 67 percent higher prostate cancer risk than white men, in addition to more than twice the mortality.
An additional goal of the Freedland Laboratory is to increase our knowledge of the interaction between nutritional carbohydrates and prostate cancer. Previous findings by Freedland Lab demonstrated that reducing dietary consumption of carbohydrates delays prostate cancer growth and impairs the glucose/insulin axis. Building on that finding, we are currently testing whether carbohydrate quality, in addition to quantity, affects prostate cancer growth. In this study, we hope to identify biomarkers and mechanisms that can link carbohydrates to tumor growth beyond the glucose/insulin pathway.
The Freedland Lab is also using an in vivo model to look at the effects of cholesterol signaling reduction and restoration on castration-resistant prostate cancer. This study will help address mechanisms of resistance for men with high-risk prostate cancer.