STS (Steroid Sulfatase) is a Protein Coding gene. Diseases associated with STS include Ichthyosis, X-Linked and Ichthyosis . Among its related pathways are Gamma carboxylation, hypusine formation and arylsulfatase activation and Metabolism . GO annotations related to this gene include sulfuric ester hydrolase activity and steryl-sulfatase activity . An important paralog of this gene is ARSE .
Ovarian cancer is the most lethal malignancy afflicting women in the . One of the main barriers to improving the survival of patients with ovarian cancer is indentifying novel agents that will improve existing therapy. This barrier is the result of the heterogeneity of epithelial ovarian cancers (EOC) and the lack of models that accurately predict the sensitivity of ovarian cancers so systemic therapies. Currently, the researchers are developing a living tumor bank of intraperitoneal models of EOC, allowing them to generate tumor models in severely immunocompromised (SCID) mice from individual EOC patients having their primary debulking surgery performed at the Mayo Clinic. The researchers hope to expand the models to generate sufficient tumor mass from each founder line. This expansion will establish sufficient materials to compare the expression profiles of established models to the source patient and re-establish tumor materials for mice for testing novel and existing therapies in vivo. The researchers will attempt to validate their tumor models by comparing the benefits of chemotherapy with and without insulin-like growth factor (IGF) pathway targeting in SCID mouse models and the source patients who are receiving IGF-targeted therapy as part of their front-line phase II clinical trial, TRIO 014. The clinical efficacy of treatment on TRIO 014 will ultimately be compared to the efficacy of IGF targeting in models from the source patient. Specifically their aims are: (1) expand in vivo founder models of ovarian cancer/primary peritoneal carcinoma derived from patient tissue; (2) compare the expression profile of tumor from expanded models to source patient tumor; and (3) explore the efficacy of insulin-like growth factor targeting between matched patient and in vivo models.
In humans, the CYP17A1 gene is largely associated with endocrine effects and steroid hormone metabolism.    Furthermore, mutations in the CYP17A1 gene are associated with rare forms of congenital adrenal hyperplasia, in particular 17α-hydroxylase deficiency/17,20-lyase deficiency and isolated 17,20-lyase deficiency. Overall, CYP17A1 is an important target for inhibition in the treatment of prostate cancer because it produces androgen that is required for tumor cell growth.   Currently, the FDA has approved only one CYP17A1 inhibitor, abiraterone, which contains a steroidal scaffold that is similar to the endogenous CYP17A1 substrates. Abiraterone is structurally similar to the substrates of other cytochrome P450 enzymes involved in steroidogenesis, and interference can pose a liability in terms of side effects. Using nonsteroidal scaffolds is expected to enable the design of compounds that interact more selectively with CYP17A1.  Potent inhibitors of the CYP17A1 enzyme provide a last line defense against ectopic androgenesis in advanced prostate cancer.