Our innovative research will further address whether in the absence of prostatic SRD5A2, androgenic pathways are blocked leading to an “androgenic to estrogenic switch”, thus creating alternate pathways which maintain prostatic homeostasis. Androgenic vs. estrogenic prostatic drivers during adulthood could potentially explain the differential growth pattern of prostate, and more importantly, different targeted strategies to be used for management of BPH.
We plan to investigate the role of estrogenic pathways when SRD5A2 is absent; determine the prostatic compartment and promoter region responsible for silencing SRD5A2 and evaluate the growth pattern of prostate gland as it relates to methylation and expression of SRD5A2 using non-invasive MRI techniques. Recognition of mechanisms that regulate prostatic androgenic vs. estrogenic pathways is an important step to offering personalized care for the management of prostatic disease.
Epigenetic changes such as methylation of DNA causes silencing of the 5AR 2 which can complicate BPH treatment rendering 5ARI's ineffective