HSD3B1 (Hydroxy-Delta-5-Steroid Dehydrogenase 3 Beta- And Steroid Delta-Isomerase 1)

Our findings identify GPR133 as a novel tumor suppressor in prostate cancer. Loss of GPR133 expression is a key event in the progression to CRPC that promotes therapeutic resistance by activating the intratumoral androgen synthesis pathway. GPR133 may serve as a valuable prognostic biomarker and a potential therapeutic target for advanced prostate cancer.

This validated mitochondrial risk model delivers a clinically actionable biomarker for BLCA prognosis stratification and guides personalized therapeutic selection, enabling precision treatment intensification.

The HSD3B1 germline variant (1245C) is linked to earlier ADT failure and diminished efficacy of abiraterone but does not affect enzalutamide in the treatment of PCa patients. These findings underscore its potential as a biomarker to guide personalized treatment in PCa.

No significant associations were found between polymorphisms in CYP17A1, HSD3B1 and TT levels. The HSD3B1 CA genotype showed a non-significant trend toward increased PCa risk (OR = 2.39, p = 0.183) that requires validation in larger studies before any clinical relevance can be established.

These findings collectively indicate that chronic low-dose DBP exposure induces transgenerational reproductive impairment through endocrine disruption and oxidative stress mechanisms, progressively compromising ovarian function and fertility across generations via HPO axis dysregulation. The study provides critical evidence for multigenerational reproductive risk associated with environmental phthalate exposure.

Poly (ADP-ribose) polymerase (PARP) inhibitors have shown survival benefits in carriers of BRCA1/2 mutations, while HSD3B1 adrenal-permissive carriers might benefit from early intensified androgen blockade treatment. This review explores the impact of pathogenic germline alterations associated with prostate cancer, with a focus on common, clinically actionable variants.

Postmenopausal cases had higher progesterone receptor IHC positivity (AA 75% vs. CC 83%, p < 0.05) and numerically more frequent ESR1 copy number gains (AA 2.0% vs. CC 4.0%). Results highlight context-specific associations between germline HSD3B1 genotypes and tumor biology in BC and EC.

We show that long-term estrogen deprivation (LTED) or tamoxifen treatment induces HSD3B1 expression and enzymatic activity, sustaining DHEA metabolism and ER signaling in resistant ER+ breast cancer cells...Our findings establish HSD3B1 as a critical mediator of endocrine resistance and identify LRH1 as an upstream regulator. Targeting HSD3B1 or LRH1 may offer a new therapeutic strategy to restore endocrine sensitivity in ER+ breast cancer.

GPX4 - an antioxidant peroxidase and ferroptosis regulator - was downregulated.Bipolar androgen therapy employing supraphysiologic testosterone isunderclinical evaluation for efficacy against treatment-resistant metastatic CRPC, although the high androgen dose raises safety concerns. Vitamin D and androgen administered concurrently at physiologic levels may offer a superior alternativefor arresting CRPC.

P1/2, N=18, Completed, Indiana University | Recruiting --> Completed | N=27 --> 18

These findings highlight NEK2's essential role in regulating testicular descent and spermatogenesis, implicating it as a potential target for cryptorchidism.

The differences in expression by HSD3B1 genotype were especially notable in lung and liver metastases. Our study indicates that in prostate cancers, HSD3B1 germline c.1100 allele status may not directly influence tumor-intrinsic genomics but is associated with novel functions beyond androgen signaling.