<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wei Y</submitter><funding>Medical Research Council</funding><funding>wellcome trust</funding><funding>Wellcome Trust</funding><funding>Academy of Medical Sciences</funding><pagination>385</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8487486</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(1)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>The objective of this study was to employ ensemble clustering and tree-based risk model approaches to identify interactions between clinicogenomic features for colorectal cancer using the 100,000 Genomes Project.&lt;h4>Results&lt;/h4>Among the 2211 patients with colorectal cancer (mean age of diagnosis: 67.7; 59.7% male), 16.3%, 36.3%, 39.0% and 8.4% had stage 1, 2, 3 and 4 cancers, respectively. Almost every patient had surgery (99.7%), 47.4% had chemotherapy, 7.6% had radiotherapy and 1.4% had immunotherapy. On average, tumour mutational burden (TMB) was 18 mutations/Mb and 34.4%, 31.3% and 25.7% of patients had structural or copy number mutations in KRAS, BRAF and NRAS, respectively. In the fully adjusted Cox model, patients with advanced cancer [stage 3 hazard ratio (HR)  =</pubmed_abstract><journal>BMC research notes</journal><pubmed_title>Application of ensemble clustering and survival tree analysis for identifying prognostic clinicogenomic features in patients with colorectal cancer from the 100,000 Genomes Project.</pubmed_title><pmcid>PMC8487486</pmcid><funding_grant_id>SBF006\1084</funding_grant_id><funding_grant_id>204841/Z/16/Z</funding_grant_id><funding_grant_id>HDR-9004</funding_grant_id><funding_grant_id>MR/S006753/1</funding_grant_id><pubmed_authors>Papachristou N</pubmed_authors><pubmed_authors>Savage K</pubmed_authors><pubmed_authors>Fowler T</pubmed_authors><pubmed_authors>Chan GC</pubmed_authors><pubmed_authors>Williams E</pubmed_authors><pubmed_authors>Pullinger J</pubmed_authors><pubmed_authors>Lopez FJ</pubmed_authors><pubmed_authors>Walsh E</pubmed_authors><pubmed_authors>Maleady-Crowe F</pubmed_authors><pubmed_authors>Genomics England Research Consortium</pubmed_authors><pubmed_authors>Lahnstein L</pubmed_authors><pubmed_authors>Hubbard TJP</pubmed_authors><pubmed_authors>Welland MJ</pubmed_authors><pubmed_authors>Stuckey A</pubmed_authors><pubmed_authors>Chang WH</pubmed_authors><pubmed_authors>Sieghart A</pubmed_authors><pubmed_authors>Caulfield MJ</pubmed_authors><pubmed_authors>Hamblin A</pubmed_authors><pubmed_authors>Mueller M</pubmed_authors><pubmed_authors>O'Donovan P</pubmed_authors><pubmed_authors>Ambrose JC</pubmed_authors><pubmed_authors>Scott RH</pubmed_authors><pubmed_authors>Mueller S</pubmed_authors><pubmed_authors>Tucci A</pubmed_authors><pubmed_authors>Moutsianas L</pubmed_authors><pubmed_authors>Bleda M</pubmed_authors><pubmed_authors>Leigh SEA</pubmed_authors><pubmed_authors>Patch C</pubmed_authors><pubmed_authors>Thomas ERA</pubmed_authors><pubmed_authors>Brittain H</pubmed_authors><pubmed_authors>Jones LJ</pubmed_authors><pubmed_authors>Arumugam P</pubmed_authors><pubmed_authors>Kasperaviciute D</pubmed_authors><pubmed_authors>Henderson S</pubmed_authors><pubmed_authors>Pereira MB</pubmed_authors><pubmed_authors>Rogers T</pubmed_authors><pubmed_authors>Wei Y</pubmed_authors><pubmed_authors>Boardman-Pretty F</pubmed_authors><pubmed_authors>Kayikci M</pubmed_authors><pubmed_authors>Thompson SR</pubmed_authors><pubmed_authors>Murugaesu N</pubmed_authors><pubmed_authors>Leong IUS</pubmed_authors><pubmed_authors>Kousathanas A</pubmed_authors><pubmed_authors>Witkowska K</pubmed_authors><pubmed_authors>Tanguy M</pubmed_authors><pubmed_authors>Lai AG</pubmed_authors><pubmed_authors>Smith SC</pubmed_authors><pubmed_authors>Jackson R</pubmed_authors><pubmed_authors>Giess A</pubmed_authors><pubmed_authors>Rendon A</pubmed_authors><pubmed_authors>Sosinsky A</pubmed_authors><pubmed_authors>Perez-Gil D</pubmed_authors><pubmed_authors>Need AC</pubmed_authors><pubmed_authors>Sawant K</pubmed_authors><pubmed_authors>Boustred CR</pubmed_authors><pubmed_authors>Siddiq A</pubmed_authors><pubmed_authors>Odhams CA</pubmed_authors><pubmed_authors>Rahim T</pubmed_authors><pubmed_authors>Wood SM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Application of ensemble clustering and survival tree analysis for identifying prognostic clinicogenomic features in patients with colorectal cancer from the 100,000 Genomes Project.</name><description>&lt;h4>Objective&lt;/h4>The objective of this study was to employ ensemble clustering and tree-based risk model approaches to identify interactions between clinicogenomic features for colorectal cancer using the 100,000 Genomes Project.&lt;h4>Results&lt;/h4>Among the 2211 patients with colorectal cancer (mean age of diagnosis: 67.7; 59.7% male), 16.3%, 36.3%, 39.0% and 8.4% had stage 1, 2, 3 and 4 cancers, respectively. Almost every patient had surgery (99.7%), 47.4% had chemotherapy, 7.6% had radiotherapy and 1.4% had immunotherapy. On average, tumour mutational burden (TMB) was 18 mutations/Mb and 34.4%, 31.3% and 25.7% of patients had structural or copy number mutations in KRAS, BRAF and NRAS, respectively. In the fully adjusted Cox model, patients with advanced cancer [stage 3 hazard ratio (HR)  =</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Oct</publication><modification>2025-06-01T00:55:28.46Z</modification><creation>2025-06-01T00:55:28.46Z</creation></dates><accession>S-EPMC8487486</accession><cross_references><pubmed>34600575</pubmed><doi>10.1186/s13104-021-05789-0</doi></cross_references></HashMap>