SRD5A2 (Steroid 5 Alpha-Reductase 2)

Pharmacovigilance and clinical reports show that a subset of patients treated with finasteride or dutasteride may experience persistent psychiatric and sexual adverse effects, known as post-finasteride syndrome. The current findings underscore the need for careful patient counseling, systematic monitoring, and further translational studies integrating genetics, neuroendocrine markers, and standardized psychiatric outcomes to identify individuals at risk and advance personalized medicine in this field.

Thus, SRD5A2 has clinical relevance in BPH, prostate cancer and other androgen-mediated conditions. However, limitations of SRD5A2-targeted therapies need to be overcome for future strategies to enhance the efficacy of 5ARI-based treatments.

The genes F2, SRD5A2, NEK2, and HGFAC play critical roles in PPCPs induced PCa progression, with SRD5A2 being particularly significant. These findings suggest that PPCPs may disrupt TIME homeostasis by downregulating SRD5A2 expression, thereby promoting immune evasion of PCa cells and accelerating tumor progression.

Further analyses of the TME, genetic mutations, and drug sensitivity revealed that this signature was closely associated with tumor immunity and treatment response. Collectively, this model highlights the pivotal role of CAFs in shaping the TME and provides novel insights for prognostic prediction and therapeutic strategies in PCa.

Furthermore, the expression of AR, Bcl-2, tumor necrosis factor (TNF)-α, interleukin (IL)-8, IL-6, IL-1β, and cyclooxygenase-2 (COX-2) in prostate tissues was lowered by EJE administration. In conclusion, EJE effectively alleviated benign prostatic hyperplasia, both in cells and in animal models, by regulating inflammation, suggesting it is a potential candidate as a functional ingredient for alleviating BPH.

Our findings provide evidence that the elevated androgens in the brain of GBM patients came from tumor autocrine. Overexpression of Sirt1 reduces FOXO1 acetylation, lowers androgen synthesis enzyme levels, and effectively decreases brain androgen levels, thereby delaying tumor progression.

Additionally, genistein inhibits the activation and nuclear translocation of the AR. Collectively, these findings support the potential of genistein as a therapeutic agent for CRPC, highlighting its role in both inhibiting androgen synthesis and disrupting AR signaling.

SRD5A2 polymorphisms could be a good indicator for prognostic malignancy and a potential tool for personalized medicine of BPH. The findings strongly support the recommendation for further study about SRD5AR2 to enhance its use for screening and prevention and to optimize the medical treatment of BPH.

Men with biochemically recurrent prostate cancer (BCR) who received 8 months of LHRH analog (LHRHa) +/- abiraterone acetate (AAP) were eligible if they had: 1) CT imaging of L3 prior to and after treatment, and 2) nucleated cells collected...An inherited polymorphism in SRD5A2 and T2DM were associated with differential skeletal muscle toxicity. These findings suggest that inherited polymorphisms may contribute to the body composition toxicity observed with HT.

The intra-tumoral metabolism of 11-oxyandrogen precursors is characteristic for low-grade EC of non-TP53-alt molecular subtypes. Our findings support further exploration of circulating 11-oxyandrogens as prognostic biomarkers in EC.

Inherited polymorphisms in androgen synthesis correlated with differences in body composition after exposure to ADT and warrant further investigation as candidate markers for body composition toxicity. Elevated subcutaneous and visceral adiposity were associated with improved response to ASI.

DNA Samples were amplified using PCR technique and they will be analyzed using Single-strand conformation polymorphism (SSCP). As SNPs have decreased stability, damaging and benign character, they can be used as candidate hallmarks in study of Complete Androgen Insensitivity Syndrome.