<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Becker MA</submitter><funding>Cancer Research UK</funding><funding>NIDDK NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>2909-16</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3880137</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(12)</volume><pubmed_abstract>Ovarian cancer mortality ranks highest among all gynecologic cancers with growth factor pathways playing an integral role in tumorigenesis, metastatic dissemination, and therapeutic resistance. The HER and VEGF receptor (VEGFR) are both overexpressed and/or aberrantly activated in subsets of ovarian tumors. While agents targeting either the HER or VEGF pathways alone have been investigated, the impact of these agents have not led to overall survival benefit in ovarian cancer. We tested the hypothesis that cotargeting HER and VEGFR would maximize antitumor efficacy at tolerable doses. To this end, ovarian cancer xenografts grown intraperitoneally in athymic nude mice were tested in response to AC480 (pan-HER inhibitor, "HERi"), cediranib (pan-VEGFR inhibitor "VEGFRi"), or BMS-690514 (combin</pubmed_abstract><journal>Molecular cancer therapeutics</journal><pubmed_title>Dual HER/VEGF receptor targeting inhibits in vivo ovarian cancer tumor growth.</pubmed_title><pmcid>PMC3880137</pmcid><funding_grant_id>C2259/A16569</funding_grant_id><funding_grant_id>T32 DK007352</funding_grant_id><funding_grant_id>P50 CA136393</funding_grant_id><funding_grant_id>UKC9700/A596</funding_grant_id><pubmed_authors>Becker MA</pubmed_authors><pubmed_authors>Krempski JW</pubmed_authors><pubmed_authors>Kalli KR</pubmed_authors><pubmed_authors>Wong TW</pubmed_authors><pubmed_authors>Farzan T</pubmed_authors><pubmed_authors>Haluska P</pubmed_authors><pubmed_authors>Harrington SC</pubmed_authors><pubmed_authors>Hou X</pubmed_authors><pubmed_authors>Weroha SJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Dual HER/VEGF receptor targeting inhibits in vivo ovarian cancer tumor growth.</name><description>Ovarian cancer mortality ranks highest among all gynecologic cancers with growth factor pathways playing an integral role in tumorigenesis, metastatic dissemination, and therapeutic resistance. The HER and VEGF receptor (VEGFR) are both overexpressed and/or aberrantly activated in subsets of ovarian tumors. While agents targeting either the HER or VEGF pathways alone have been investigated, the impact of these agents have not led to overall survival benefit in ovarian cancer. We tested the hypothesis that cotargeting HER and VEGFR would maximize antitumor efficacy at tolerable doses. To this end, ovarian cancer xenografts grown intraperitoneally in athymic nude mice were tested in response to AC480 (pan-HER inhibitor, "HERi"), cediranib (pan-VEGFR inhibitor "VEGFRi"), or BMS-690514 (combin</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Dec</publication><modification>2026-04-08T03:02:09.397Z</modification><creation>2019-03-27T01:19:22Z</creation></dates><accession>S-EPMC3880137</accession><cross_references><pubmed>24130056</pubmed><doi>10.1158/1535-7163.mct-13-0547</doi><doi>10.1158/1535-7163.MCT-13-0547</doi></cross_references></HashMap>