<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hossen MN</submitter><funding>University of Oklahoma Stephenson Cancer Center</funding><funding>National Cancer Institute Cancer Center</funding><funding>Biostatistics and Research Design Shared Resource</funding><funding>Office of Cancer Research</funding><funding>Institutional Development Award (IDeA)</funding><funding>NCI NIH HHS</funding><funding>Oklahoma Medical Research Foundation (OMRF)</funding><funding>NIGMS NIH HHS</funding><funding>University of Oklahoma Health Sciences Center</funding><pagination>e2200491</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9631030</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>9(31)</volume><pubmed_abstract>By exploiting the self-therapeutic properties of gold nanoparticles (GNPs) a molecular axis that promotes the growth of high-grade serous ovarian cancer (HGSOC), one of the deadliest gynecologic malignancies with poorly understood underlying molecular mechanisms, has been identified. The biodistribution and toxicity of GNPs administered by intravenous or intraperitoneal injection, both as a single dose or by repeated dosing over two weeks are first assessed; no biochemical or histological toxicity to vital organs is found. Using an orthotopic patient-derived xenograft (PDX) model of HGSOC, the authors then show that GNP treatment robustly inhibits tumor growth. Investigating the molecular mechanisms underlying the GNP efficacy reveals that GNPs downregulate insulin growth factor binding pr</pubmed_abstract><journal>Advanced science (Weinheim, Baden-Wurttemberg, Germany)</journal><pubmed_title>Gold Nanoparticles Disrupt the IGFBP2/mTOR/PTEN Axis to Inhibit Ovarian Cancer Growth.</pubmed_title><pmcid>PMC9631030</pmcid><funding_grant_id>P20GM135009</funding_grant_id><funding_grant_id>P30CA225500</funding_grant_id><funding_grant_id>R01 CA136494</funding_grant_id><funding_grant_id>P30 CA225520</funding_grant_id><funding_grant_id>2048130</funding_grant_id><funding_grant_id>P20 GM103639</funding_grant_id><pubmed_authors>Fung KM</pubmed_authors><pubmed_authors>Bieniasz M</pubmed_authors><pubmed_authors>Dwivedi SKD</pubmed_authors><pubmed_authors>Bhattacharya R</pubmed_authors><pubmed_authors>Xu C</pubmed_authors><pubmed_authors>Wang L</pubmed_authors><pubmed_authors>Asfa S</pubmed_authors><pubmed_authors>Elechalwar CK</pubmed_authors><pubmed_authors>Gulla SK</pubmed_authors><pubmed_authors>Wilhelm S</pubmed_authors><pubmed_authors>Dey A</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Rao G</pubmed_authors><pubmed_authors>Sheth V</pubmed_authors><pubmed_authors>Robertson JD</pubmed_authors><pubmed_authors>Mukherjee P</pubmed_authors><pubmed_authors>Hossen MN</pubmed_authors></additional><is_claimable>false</is_claimable><name>Gold Nanoparticles Disrupt the IGFBP2/mTOR/PTEN Axis to Inhibit Ovarian Cancer Growth.</name><description>By exploiting the self-therapeutic properties of gold nanoparticles (GNPs) a molecular axis that promotes the growth of high-grade serous ovarian cancer (HGSOC), one of the deadliest gynecologic malignancies with poorly understood underlying molecular mechanisms, has been identified. The biodistribution and toxicity of GNPs administered by intravenous or intraperitoneal injection, both as a single dose or by repeated dosing over two weeks are first assessed; no biochemical or histological toxicity to vital organs is found. Using an orthotopic patient-derived xenograft (PDX) model of HGSOC, the authors then show that GNP treatment robustly inhibits tumor growth. Investigating the molecular mechanisms underlying the GNP efficacy reveals that GNPs downregulate insulin growth factor binding pr</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2025-04-05T12:34:07.501Z</modification><creation>2025-02-19T00:31:37.459Z</creation></dates><accession>S-EPMC9631030</accession><cross_references><pubmed>36104215</pubmed><doi>10.1002/advs.202200491</doi></cross_references></HashMap>