{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Richards J"],"funding":["Cancer Research UK","Medical Research Council","National Institute for Health Research (NIHR)","Chief Scientist Office","Wellcome Trust"],"pagination":["2176-82"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4281708"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["72(9)"],"pubmed_abstract":["Prostate cancer progression can be associated with androgen receptor (AR) mutations acquired following treatment with castration and/or an antiandrogen. Abiraterone, a rationally designed inhibitor of CYP17A1 recently approved for the treatment of docetaxel-treated castration-resistant prostate cancer (CRPC), is often effective, but requires coadministration with glucocorticoids to curtail side effects. Here, we hypothesized that progressive disease on abiraterone may occur secondary to glucocorticoid-induced activation of mutated AR. We found that prednisolone plasma levels in patients with CRPC were sufficiently high to activate mutant AR. Mineralocorticoid receptor antagonists, such as spironolactone and eplerenone that are used to treat side effects related to mineralocorticoid excess,"],"journal":["Cancer research"],"pubmed_title":["Interactions of abiraterone, eplerenone, and prednisolone with wild-type and mutant androgen receptor: a rationale for increasing abiraterone exposure or combining with MDV3100."],"pmcid":["PMC4281708"],"funding_grant_id":["CL-2008-22-001","C51/A7401","G0801473","A15573","13239"],"pubmed_authors":["Attard G","de Bono JS","Nowakowska K","Richards J","Carreira S","Goodall J","Wingate A","Pezaro C","Arlt W","Taylor AE","Lim AC","McEwan IJ","Hay CW"],"additional_accession":[]},"is_claimable":false,"name":"Interactions of abiraterone, eplerenone, and prednisolone with wild-type and mutant androgen receptor: a rationale for increasing abiraterone exposure or combining with MDV3100.","description":"Prostate cancer progression can be associated with androgen receptor (AR) mutations acquired following treatment with castration and/or an antiandrogen. Abiraterone, a rationally designed inhibitor of CYP17A1 recently approved for the treatment of docetaxel-treated castration-resistant prostate cancer (CRPC), is often effective, but requires coadministration with glucocorticoids to curtail side effects. Here, we hypothesized that progressive disease on abiraterone may occur secondary to glucocorticoid-induced activation of mutated AR. We found that prednisolone plasma levels in patients with CRPC were sufficiently high to activate mutant AR. Mineralocorticoid receptor antagonists, such as spironolactone and eplerenone that are used to treat side effects related to mineralocorticoid excess,","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 May","modification":"2025-06-26T03:07:01.236Z","creation":"2025-06-26T03:07:01.236Z"},"accession":"S-EPMC4281708","cross_references":{"pubmed":["22411952"],"doi":["10.1158/0008-5472.CAN-11-3980","10.1158/0008-5472.can-11-3980"]}}