Therefore we searched for gain-of-function mutations in the human SRD5A2 gene which might explain hyperandrogenic disorders such as the polycystic ovary syndrome, premature adrenarche and prostate cancer.
In this study, the identification of a therapeutic inhibitor of 3-oxo-5-alpha-steroid 4-dehydrogenase 2 using in <i>silico</i> approach has been done to treat prostate cancer.
After subgroup analyses by ethnicity and source of control, we also observed a similar trend in Latinos, other-ethnicity, population-based, and hospital-based groups under corresponding genetic models.Our findings indicate that SRD5A2rs9282858 polymorphism may be a susceptible factor to PCa.
Men castrated before puberty (eunuchs) or men with inherited deficiency of type II 5α-reductase (with failure to convert testosterone to the more potent dihydrotestosterone) (DHT) do not develop PCa.
There were significant associations of genetic polymorphisms in steroid 5α-reductase 1 (SRD5A1) (reference SNPs: rs3736316, rs3822430, rs1560149, rs248797, and rs472402) and SRD5A2 (rs2300700) with the risk of high-grade prostate cancer in the placebo arm of the Prostate Cancer Prevention Trial; 2 SNPs were significantly associated with an increased risk (SRD5A1 rs472402 [odds ratio, 1.70; 95% confidence interval, 1.05-2.75; Ptrend = .03] and SRD5A2rs2300700 [odds ratio, 1.94; 95% confidence interval, 1.19-3.18; Ptrend = .01]).
CYP19 1531 C>T, SRD5A2 gene V89L, CYP17 gene -34 T/C, PSA-158 (G/A) regions were evaluated for the association between polymorphisms and benign prostatic hyperplasia and prostate cancer in study population.
Furthermore, SRD5A2rs523349 polymorphism may be a promising biomarker for metastatic prostate cancer patients treated with primary ADT and a molecular target for advanced prostate cancer.
To investigate the role of germline variations in cytochrome P450 17A1 (CYP17A1) and steroid-5α-reductase, α-polypeptides 1 and 2 (SRD5A1 and SRD5A2) genes in PCa.
Polymorphisms in the genes SRD5A1 and SRD5A2 encoding androgen biosynthetic 5α-reductase enzymes have been associated with an altered risk of biochemical recurrence after radical prostatectomy in localized prostate cancer.
However, no clear consensus has been reached on the association between the SRD5A2V89L, A49T and TA repeat polymorphisms and prostate cancer (PCa) risk.
The biological role of steroid 5alpha-reductase isozymes (encoded by the SRD5A1 and SRD5A2 genes) and angiogenic factors that play important roles in the pathogenesis and vascularization of prostate cancer (PC) is poorly understood.
Meanwhile, SRD5A2V89L polymorphism was significantly associated with an increased PCa risk in men aged < or =65 under the co-dominant (OR, 1.70; 95% CI, 1.09-2.66 for LL vs. VV; P = 0.02; P(heterogeneity) = 0.31) and recessive (OR, 1.75; 95% CI, 1.14-2.68 for LL vs. (VV + VL); P = 0.01; P(heterogeneity) = 0.12) models.
Two polymorphisms in the SRD5a2 gene, V89L (rs523349) and A49T (rs9282858), have been studied for associations with prostate cancer risk, with conflicting results.
To estimate the prostate cancer risk conferred by individual single nucleotide polymorphisms (SNPs), SNP-SNP interactions, and/or cumulative SNP effects, we evaluated the association between prostate cancer risk and the genetic variants of 12 key genes within the steroid hormone pathway (CYP17, HSD17B3, ESR1, SRD5A2, HSD3B1, HSD3B2, CYP19, CYP1A1, CYP1B1, CYP3A4, CYP27B1, and CYP24A1).
Association among polymorphisms in the steroid 5alpha-reductase type II (SRD5A2) gene, prostate cancer risk, and pathologic characteristics of prostate tumors in an Ecuadorian population.
We investigated the relationship between polymorphisms in four genes, androgen receptor (AR), prostate-specific antigen (PSA), 5alpha-reductase type II (SRD5A2) and cytochrome P450c17alpha (CYP17) and PC and benign prostatic hyperplasia (BPH).
Polymorphisms related to high androgen metabolism and/or response in the 5alpha-reductase type 2 (SRD5A2) and the androgen receptor (AR) genes, respectively, have been linked to prostate cancer.
To explore the possible joint effects of these pathways in prostate cancer severity, we studied 1,090 Caucasian prostate cancer cases to evaluate whether tumor severity is influenced by a history of benign prostatic hyperplasia (BPH) interacting with genotypes involved in inflammation or androgen metabolism including MSR1, RNASEL, AR, CYP3A4, CYP3A43, CYP3A5 and SRD5A2.
Large studies on variants in some androgen-metabolizing genes [SRD5A2, CYP17A1, and hydroxysteroid dehydrogenase (HSD)17B1] do not show a convincing links to prostate cancer, though there are insufficient data to draw conclusions on other genes related to androgen metabolism, including UDP-glycosyltransferases (UGT), sulfotransferases (SULT), CYP3A, and estrogen-related genes.