<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Taya M</submitter><funding>Cancer Prevention Research Institute of Texas Recruitment of Established Investigators Award</funding><funding>Mayo Clinic SPORE in Ovarian Cancer Developmental Research Program, Pilot Study Award</funding><funding>National Cancer Institute</funding><funding>NCI NIH HHS</funding><funding>The University of Chicago Women's Board</funding><funding>The University of Chicago Comprehensive Cancer Center</funding><funding>The University of Chicago Women’s Board</funding><funding>2017 Conquer Cancer Foundation/ASCO Young Investigator Award</funding><pagination>e4</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11790989</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>36(1)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>In ovarian cancer (OvCa), tumor cell high glucocorticoid receptor (GR) has been associated with poor patient prognosis. In vitro, GR activation inhibits chemotherapy-induced OvCa cell death in association with transcriptional upregulation of genes encoding anti-apoptotic proteins. A recent randomized phase II study demonstrated improvement in progression-free survival (PFS) for heavily pre-treated OvCa patients randomized to receive therapy with a selective GR modulator (SGRM) plus chemotherapy compared to chemotherapy alone. We hypothesized that SGRM therapy would improve carboplatin response in OvCa patient-derived xenograft (PDX).&lt;h4>Methods&lt;/h4>Six high-grade serous (HGS) OvCa PDX models expressing GR mRNA (&lt;i>NR3C1&lt;/i>) and protein were treated with chemotherapy +/- </pubmed_abstract><journal>Journal of gynecologic oncology</journal><pubmed_title>Investigation of selective glucocorticoid receptor modulation in high-grade serous ovarian cancer PDX models.</pubmed_title><pmcid>PMC11790989</pmcid><funding_grant_id>P30 CA 14599</funding_grant_id><funding_grant_id>NIH1R21CA223426</funding_grant_id><funding_grant_id>P50 CA136393</funding_grant_id><funding_grant_id>RR1900371</funding_grant_id><funding_grant_id>5P50CA136393-09</funding_grant_id><funding_grant_id>P30 CA142543</funding_grant_id><funding_grant_id>P30 CA014599</funding_grant_id><funding_grant_id>R21 CA223426</funding_grant_id><pubmed_authors>Taya M</pubmed_authors><pubmed_authors>Oberg AL</pubmed_authors><pubmed_authors>Heinzen EP</pubmed_authors><pubmed_authors>Chen H</pubmed_authors><pubmed_authors>Hou X</pubmed_authors><pubmed_authors>Fleming GF</pubmed_authors><pubmed_authors>Veneris JT</pubmed_authors><pubmed_authors>Maurer MJ</pubmed_authors><pubmed_authors>Larson MC</pubmed_authors><pubmed_authors>Kazi N</pubmed_authors><pubmed_authors>Conzen SD</pubmed_authors><pubmed_authors>Lastra R</pubmed_authors><pubmed_authors>Weroha SJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Investigation of selective glucocorticoid receptor modulation in high-grade serous ovarian cancer PDX models.</name><description>&lt;h4>Objective&lt;/h4>In ovarian cancer (OvCa), tumor cell high glucocorticoid receptor (GR) has been associated with poor patient prognosis. In vitro, GR activation inhibits chemotherapy-induced OvCa cell death in association with transcriptional upregulation of genes encoding anti-apoptotic proteins. A recent randomized phase II study demonstrated improvement in progression-free survival (PFS) for heavily pre-treated OvCa patients randomized to receive therapy with a selective GR modulator (SGRM) plus chemotherapy compared to chemotherapy alone. We hypothesized that SGRM therapy would improve carboplatin response in OvCa patient-derived xenograft (PDX).&lt;h4>Methods&lt;/h4>Six high-grade serous (HGS) OvCa PDX models expressing GR mRNA (&lt;i>NR3C1&lt;/i>) and protein were treated with chemotherapy +/- </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Jan</publication><modification>2026-04-14T03:26:49.684Z</modification><creation>2025-04-19T16:22:33.915Z</creation></dates><accession>S-EPMC11790989</accession><cross_references><pubmed>38909640</pubmed><doi>10.3802/jgo.2025.36.e4</doi></cross_references></HashMap>