<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Corry SM</submitter><funding>Cancer Research UK</funding><funding>Medical Research Council</funding><funding>Public Health Agency</funding><funding>Wellcome Trust</funding><funding>Biotechnology and Biological Sciences Research Council</funding><pagination>2502-2517</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9664095</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>71(12)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>Stroma-rich tumours represent a poor prognostic subtype in stage II/III colon cancer (CC), with high relapse rates and limited response to standard adjuvant chemotherapy.&lt;h4>Design&lt;/h4>To address the lack of efficacious therapeutic options for patients with stroma-rich CC, we stratified our human tumour cohorts according to stromal content, enabling identification of the biology underpinning relapse and potential therapeutic vulnerabilities specifically within stroma-rich tumours that could be exploited clinically. Following human tumour-based discovery and independent clinical validation, we use a series of &lt;i>in vitro&lt;/i> and stroma-rich &lt;i>in vivo&lt;/i> models to test and validate the therapeutic potential of elevating the biology associated with reduced relapse in human</pubmed_abstract><journal>Gut</journal><pubmed_title>Activation of innate-adaptive immune machinery by poly(I:C) exposes a therapeutic vulnerability to prevent relapse in stroma-rich colon cancer.</pubmed_title><pmcid>PMC9664095</pmcid><funding_grant_id>MC_PC_17117</funding_grant_id><funding_grant_id>A31287</funding_grant_id><funding_grant_id>15333</funding_grant_id><funding_grant_id>A28223</funding_grant_id><funding_grant_id>24387</funding_grant_id><funding_grant_id>29834</funding_grant_id><funding_grant_id>EAT/4905/13</funding_grant_id><funding_grant_id>A17196</funding_grant_id><funding_grant_id>MR/M016587/1</funding_grant_id><funding_grant_id>A26825</funding_grant_id><funding_grant_id>MR/S021205/1</funding_grant_id><funding_grant_id>26045</funding_grant_id><funding_grant_id>206314/Z/17/Z</funding_grant_id><funding_grant_id>A21139</funding_grant_id><funding_grant_id>A29834</funding_grant_id><funding_grant_id>S_4137</funding_grant_id><funding_grant_id>BB/T002824/1</funding_grant_id><funding_grant_id>STL/5175/15</funding_grant_id><funding_grant_id>110371/Z/15/Z</funding_grant_id><funding_grant_id>G0400302</funding_grant_id><pubmed_authors>Maguire S</pubmed_authors><pubmed_authors>Malla SB</pubmed_authors><pubmed_authors>White M</pubmed_authors><pubmed_authors>Amirkhah R</pubmed_authors><pubmed_authors>Lawler M</pubmed_authors><pubmed_authors>Coleman HG</pubmed_authors><pubmed_authors>McCooey AJ</pubmed_authors><pubmed_authors>Kerr EM</pubmed_authors><pubmed_authors>Maughan T</pubmed_authors><pubmed_authors>Tejpar S</pubmed_authors><pubmed_authors>Leonard NA</pubmed_authors><pubmed_authors>Leedham SJ</pubmed_authors><pubmed_authors>Tsantoulis P</pubmed_authors><pubmed_authors>Small DM</pubmed_authors><pubmed_authors>Sakhnevych S</pubmed_authors><pubmed_authors>S:CORT and ACRCelerate consortia</pubmed_authors><pubmed_authors>Cortes-Lavaud X</pubmed_authors><pubmed_authors>Loughrey MB</pubmed_authors><pubmed_authors>Jackstadt RF</pubmed_authors><pubmed_authors>Lannagan TR</pubmed_authors><pubmed_authors>Gillespie MA</pubmed_authors><pubmed_authors>McCorry AM</pubmed_authors><pubmed_authors>Corry SM</pubmed_authors><pubmed_authors>Fisher NC</pubmed_authors><pubmed_authors>Campbell AD</pubmed_authors><pubmed_authors>McDade SS</pubmed_authors><pubmed_authors>Byrne RM</pubmed_authors><pubmed_authors>Richman SD</pubmed_authors><pubmed_authors>Redmond KL</pubmed_authors><pubmed_authors>Sansom OJ</pubmed_authors><pubmed_authors>Ryan AE</pubmed_authors><pubmed_authors>Longley DB</pubmed_authors><pubmed_authors>Dunne PD</pubmed_authors><pubmed_authors>Rogan E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Activation of innate-adaptive immune machinery by poly(I:C) exposes a therapeutic vulnerability to prevent relapse in stroma-rich colon cancer.</name><description>&lt;h4>Objective&lt;/h4>Stroma-rich tumours represent a poor prognostic subtype in stage II/III colon cancer (CC), with high relapse rates and limited response to standard adjuvant chemotherapy.&lt;h4>Design&lt;/h4>To address the lack of efficacious therapeutic options for patients with stroma-rich CC, we stratified our human tumour cohorts according to stromal content, enabling identification of the biology underpinning relapse and potential therapeutic vulnerabilities specifically within stroma-rich tumours that could be exploited clinically. Following human tumour-based discovery and independent clinical validation, we use a series of &lt;i>in vitro&lt;/i> and stroma-rich &lt;i>in vivo&lt;/i> models to test and validate the therapeutic potential of elevating the biology associated with reduced relapse in human</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2026-06-15T05:54:05.985Z</modification><creation>2024-11-12T17:37:03.615Z</creation></dates><accession>S-EPMC9664095</accession><cross_references><pubmed>35477539</pubmed><doi>10.1136/gutjnl-2021-326183</doi></cross_references></HashMap>