<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Griffin D</submitter><funding>FP7 Health (FP7-HEALTH)</funding><funding>Cancer Research UK</funding><funding>FP7 Health</funding><pagination>1088-1101</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7616621</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>22(12)</volume><pubmed_abstract>Patients with class I V600EBRAF-mutant (MT) colorectal cancer exhibit a poor prognosis, and their response to combined anti-BRAF/EGFR inhibition remains limited. An unmet need exits for further understanding the biology of V600EBRAFMT colorectal cancer. We used differential gene expression of BRAFWT and MT colorectal cancer cells to identify pathways underpinning BRAFMT colorectal cancer. We tested a panel of molecularly/genetically subtyped colorectal cancer cells for their sensitivity to the unfolded protein response (UPR) activator BOLD-100. To identify novel combination strategies for BOLD-100, we performed RNA sequencing and high-throughput drug screening. Pathway enrichment analysis identified significant enrichment of the UPR and DNA repair pathways in BRAFMT colorectal cancer. We f</pubmed_abstract><journal>Molecular cancer research : MCR</journal><pubmed_title>Ruthenium Drug BOLD-100 Regulates BRAFMT Colorectal Cancer Cell Apoptosis through AhR/ROS/ATR Signaling Axis Modulation.</pubmed_title><pmcid>PMC7616621</pmcid><funding_grant_id>602901</funding_grant_id><funding_grant_id>C13749/A24744</funding_grant_id><funding_grant_id>24744</funding_grant_id><pubmed_authors>Lavin D</pubmed_authors><pubmed_authors>Savage KI</pubmed_authors><pubmed_authors>Van Schaeybroeck S</pubmed_authors><pubmed_authors>Sessler T</pubmed_authors><pubmed_authors>Bazett M</pubmed_authors><pubmed_authors>Griffin D</pubmed_authors><pubmed_authors>Carson R</pubmed_authors><pubmed_authors>Tiwari VK</pubmed_authors><pubmed_authors>Carie A</pubmed_authors><pubmed_authors>Karelia S</pubmed_authors><pubmed_authors>Moss D</pubmed_authors><pubmed_authors>McDade S</pubmed_authors><pubmed_authors>Pankovich J</pubmed_authors><pubmed_authors>Kennedy R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Ruthenium Drug BOLD-100 Regulates BRAFMT Colorectal Cancer Cell Apoptosis through AhR/ROS/ATR Signaling Axis Modulation.</name><description>Patients with class I V600EBRAF-mutant (MT) colorectal cancer exhibit a poor prognosis, and their response to combined anti-BRAF/EGFR inhibition remains limited. An unmet need exits for further understanding the biology of V600EBRAFMT colorectal cancer. We used differential gene expression of BRAFWT and MT colorectal cancer cells to identify pathways underpinning BRAFMT colorectal cancer. We tested a panel of molecularly/genetically subtyped colorectal cancer cells for their sensitivity to the unfolded protein response (UPR) activator BOLD-100. To identify novel combination strategies for BOLD-100, we performed RNA sequencing and high-throughput drug screening. Pathway enrichment analysis identified significant enrichment of the UPR and DNA repair pathways in BRAFMT colorectal cancer. We f</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2026-06-01T06:37:14.327Z</modification><creation>2025-04-04T00:46:42.711Z</creation></dates><accession>S-EPMC7616621</accession><cross_references><pubmed>39083088</pubmed><doi>10.1158/1541-7786.MCR-24-0151</doi></cross_references></HashMap>