<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Rebecca VW</submitter><funding>NCI NIH HHS</funding><funding>NIH HHS</funding><pubmed_abstract>Resistance to combination BRAF/MEK inhibitor (BRAFi/MEKi) therapy arises in nearly every patient with &lt;i>BRAF&lt;/i>&lt;sup>V600E/K&lt;/sup> melanoma, despite promising initial responses. Achieving cures in this expanding BRAFi/MEKi-resistant cohort represents one of the greatest challenges to the field; few experience additional durable benefit from immunotherapy and no alternative therapies exist. To better personalize therapy in cancer patients to address therapy relapse, umbrella trials have been initiated whereby genomic sequencing of a panel of potentially actionable targets guide therapy selection for patients; however, the superior efficacy of such approaches remains to be seen. We here test the robustness of the umbrella trial rationale by analyzing relationships between genomic status of </pubmed_abstract><journal>bioRxiv : the preprint server for biology</journal><pagination>2023.01.20.524923</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9882271</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Dasatinib Resensitizes MAPK Inhibitor Efficacy in Standard-of-Care Relapsed Melanomas.</pubmed_title><pmcid>PMC9882271</pmcid><funding_grant_id>R50 CA211199</funding_grant_id><funding_grant_id>S10 OD023586</funding_grant_id><funding_grant_id>U54 CA224070</funding_grant_id><funding_grant_id>P30 CA010815</funding_grant_id><funding_grant_id>P01 CA114046</funding_grant_id><funding_grant_id>K01 CA245124</funding_grant_id><funding_grant_id>P01 CA025874</funding_grant_id><funding_grant_id>R01 CA047159</funding_grant_id><funding_grant_id>R01 CA182890</funding_grant_id><pubmed_authors>Fingerman D</pubmed_authors><pubmed_authors>Ji H</pubmed_authors><pubmed_authors>Herlyn M</pubmed_authors><pubmed_authors>Bravo J</pubmed_authors><pubmed_authors>Villanueva J</pubmed_authors><pubmed_authors>Rebecca VW</pubmed_authors><pubmed_authors>Liu Q</pubmed_authors><pubmed_authors>Brown GS</pubmed_authors><pubmed_authors>Gopal YNV</pubmed_authors><pubmed_authors>Fane ME</pubmed_authors><pubmed_authors>Nathanson K</pubmed_authors><pubmed_authors>Wei M</pubmed_authors><pubmed_authors>Xiao M</pubmed_authors><pubmed_authors>Godok T</pubmed_authors><pubmed_authors>Kossenkov A</pubmed_authors><pubmed_authors>Davies MA</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Alicea GM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Dasatinib Resensitizes MAPK Inhibitor Efficacy in Standard-of-Care Relapsed Melanomas.</name><description>Resistance to combination BRAF/MEK inhibitor (BRAFi/MEKi) therapy arises in nearly every patient with &lt;i>BRAF&lt;/i>&lt;sup>V600E/K&lt;/sup> melanoma, despite promising initial responses. Achieving cures in this expanding BRAFi/MEKi-resistant cohort represents one of the greatest challenges to the field; few experience additional durable benefit from immunotherapy and no alternative therapies exist. To better personalize therapy in cancer patients to address therapy relapse, umbrella trials have been initiated whereby genomic sequencing of a panel of potentially actionable targets guide therapy selection for patients; however, the superior efficacy of such approaches remains to be seen. We here test the robustness of the umbrella trial rationale by analyzing relationships between genomic status of </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-05T11:27:53.446Z</modification><creation>2025-04-05T11:27:53.446Z</creation></dates><accession>S-EPMC9882271</accession><cross_references><pubmed>36711814</pubmed><doi>10.1101/2023.01.20.524923</doi></cross_references></HashMap>