<HashMap><database>biostudies-literature</database><scores/><additional><submitter>LoRusso PM</submitter><funding>Stand Up To Cancer</funding><funding>NCATS NIH HHS</funding><funding>Gateway for Cancer Research</funding><funding>NCI NIH HHS</funding><pagination>e0248097</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8026051</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(4)</volume><pubmed_abstract>Although combination BRAF and MEK inhibitors are highly effective for the 40-50% of cutaneous metastatic melanomas harboring BRAFV600 mutations, targeted agents have been ineffective for BRAFV600wild-type (wt) metastatic melanomas. The SU2C Genomics-Enabled Medicine for Melanoma Trial utilized a Simon two-stage optimal design to assess whether comprehensive genomic profiling improves selection of molecular-based therapies for BRAFV600wt metastatic melanoma patients who had progressed on standard-of-care therapy, which may include immunotherapy. Of the response-evaluable patients, binimetinib was selected for 20 patients randomized to the genomics-enabled arm, and nine were treated on the alternate treatment arm. Response rates for 27 patients treated with targeted recommendations included </pubmed_abstract><journal>PloS one</journal><pubmed_title>Identifying treatment options for BRAFV600 wild-type metastatic melanoma: A SU2C/MRA genomics-enabled clinical trial.</pubmed_title><pmcid>PMC8026051</pmcid><funding_grant_id>G-12-500</funding_grant_id><funding_grant_id>P30 CA008748</funding_grant_id><funding_grant_id>UL1 TR001863</funding_grant_id><funding_grant_id>SU2C-AACR-DT0612</funding_grant_id><pubmed_authors>Sekulic A</pubmed_authors><pubmed_authors>Halperin R</pubmed_authors><pubmed_authors>Lao C</pubmed_authors><pubmed_authors>Byron SA</pubmed_authors><pubmed_authors>DeVeaux M</pubmed_authors><pubmed_authors>Kiefer JA</pubmed_authors><pubmed_authors>Calvert VS</pubmed_authors><pubmed_authors>Izatt T</pubmed_authors><pubmed_authors>Nasser S</pubmed_authors><pubmed_authors>Keats J</pubmed_authors><pubmed_authors>Schork N</pubmed_authors><pubmed_authors>Eder JP</pubmed_authors><pubmed_authors>Schmidt J</pubmed_authors><pubmed_authors>Sekar S</pubmed_authors><pubmed_authors>Manica B</pubmed_authors><pubmed_authors>Craig DW</pubmed_authors><pubmed_authors>Hendricks WPD</pubmed_authors><pubmed_authors>Bryce AH</pubmed_authors><pubmed_authors>Cowey CL</pubmed_authors><pubmed_authors>Markovic SN</pubmed_authors><pubmed_authors>Fecher LA</pubmed_authors><pubmed_authors>Fox L</pubmed_authors><pubmed_authors>Vogelzang NJ</pubmed_authors><pubmed_authors>Joseph RW</pubmed_authors><pubmed_authors>Durecki D</pubmed_authors><pubmed_authors>Petricoin EF</pubmed_authors><pubmed_authors>Perlmutter J</pubmed_authors><pubmed_authors>Gorman M</pubmed_authors><pubmed_authors>Legendre C</pubmed_authors><pubmed_authors>Enriquez D</pubmed_authors><pubmed_authors>LoRusso PM</pubmed_authors><pubmed_authors>Zelterman D</pubmed_authors><pubmed_authors>Zismann V</pubmed_authors><pubmed_authors>Aldrich J</pubmed_authors><pubmed_authors>Trent JM</pubmed_authors><pubmed_authors>Liang WS</pubmed_authors><pubmed_authors>Pilat MJ</pubmed_authors><pubmed_authors>Naveed F</pubmed_authors><pubmed_authors>Sivaprakasam K</pubmed_authors><pubmed_authors>Basu GD</pubmed_authors><pubmed_authors>Carpten J</pubmed_authors><pubmed_authors>Weise A</pubmed_authors><pubmed_authors>Sosman JA</pubmed_authors><pubmed_authors>Boerner SA</pubmed_authors><pubmed_authors>Adkins J</pubmed_authors><pubmed_authors>Solit DB</pubmed_authors><pubmed_authors>Tassone E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Identifying treatment options for BRAFV600 wild-type metastatic melanoma: A SU2C/MRA genomics-enabled clinical trial.</name><description>Although combination BRAF and MEK inhibitors are highly effective for the 40-50% of cutaneous metastatic melanomas harboring BRAFV600 mutations, targeted agents have been ineffective for BRAFV600wild-type (wt) metastatic melanomas. The SU2C Genomics-Enabled Medicine for Melanoma Trial utilized a Simon two-stage optimal design to assess whether comprehensive genomic profiling improves selection of molecular-based therapies for BRAFV600wt metastatic melanoma patients who had progressed on standard-of-care therapy, which may include immunotherapy. Of the response-evaluable patients, binimetinib was selected for 20 patients randomized to the genomics-enabled arm, and nine were treated on the alternate treatment arm. Response rates for 27 patients treated with targeted recommendations included </description><dates><release>2021-01-01T00:00:00Z</release><publication>2021</publication><modification>2026-04-29T00:20:27.921Z</modification><creation>2022-02-09T15:59:30.727Z</creation></dates><accession>S-EPMC8026051</accession><cross_references><pubmed>33826614</pubmed><doi>10.1371/journal.pone.0248097</doi></cross_references></HashMap>