<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chen Y</submitter><funding>Science Foundation of the Postdoctoral Department of Heilongjiang Province</funding><funding>Program of Science and Technology of Sichuan Province</funding><funding>Haiyan Research Funding of the Harbin Medical University Cancer Hospital</funding><pagination>11</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9875443</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(1)</volume><pubmed_abstract>BRAF mutations are the oncogenic drivers in colorectal cancer and V600 mutations (Class1), which lead to RAS-independent active monomers, are the most common mutation types. BRAF non-V600 mutants can be further classified as RAS-independent active dimers (Class2) and RAS-dependent impaired kinase (Class3). We retrospectively reviewed the mutational profiles of 328 treatment-naïve colorectal tumors with BRAF mutations detected using capture-based hybrid next-generation sequencing targeting 400 + cancer-related genes. The clinical and genetic distinctions of patients harboring Class1/2/3 BRAF mutations were investigated, which revealed that tumors with Class1 BRAF mutations showed more unique genomic profiles than those with Class2/3 mutations. Also, by using an external dataset from cBioPor</pubmed_abstract><journal>Biomarker research</journal><pubmed_title>The clinical and genomic distinctions of Class1/2/3 BRAF-mutant colorectal cancer and differential prognoses.</pubmed_title><pmcid>PMC9875443</pmcid><funding_grant_id>JJZD2021-03</funding_grant_id><funding_grant_id>2021YFQ0037</funding_grant_id><funding_grant_id>LBH-Q21118</funding_grant_id><pubmed_authors>Wu M</pubmed_authors><pubmed_authors>Lin T</pubmed_authors><pubmed_authors>Huang H</pubmed_authors><pubmed_authors>Zhang H</pubmed_authors><pubmed_authors>Wu C</pubmed_authors><pubmed_authors>Ma Y</pubmed_authors><pubmed_authors>Gu A</pubmed_authors><pubmed_authors>Liang C</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Ou Q</pubmed_authors><pubmed_authors>E M</pubmed_authors><pubmed_authors>Shao Y</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Ye S</pubmed_authors><pubmed_authors>Guo H</pubmed_authors><pubmed_authors>Weng H</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Pu X</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Sun H</pubmed_authors><pubmed_authors>Deng Y</pubmed_authors><pubmed_authors>Wu X</pubmed_authors></additional><is_claimable>false</is_claimable><name>The clinical and genomic distinctions of Class1/2/3 BRAF-mutant colorectal cancer and differential prognoses.</name><description>BRAF mutations are the oncogenic drivers in colorectal cancer and V600 mutations (Class1), which lead to RAS-independent active monomers, are the most common mutation types. BRAF non-V600 mutants can be further classified as RAS-independent active dimers (Class2) and RAS-dependent impaired kinase (Class3). We retrospectively reviewed the mutational profiles of 328 treatment-naïve colorectal tumors with BRAF mutations detected using capture-based hybrid next-generation sequencing targeting 400 + cancer-related genes. The clinical and genetic distinctions of patients harboring Class1/2/3 BRAF mutations were investigated, which revealed that tumors with Class1 BRAF mutations showed more unique genomic profiles than those with Class2/3 mutations. Also, by using an external dataset from cBioPor</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2026-05-29T05:32:59.256Z</modification><creation>2025-02-18T23:45:00.211Z</creation></dates><accession>S-EPMC9875443</accession><cross_references><pubmed>36694231</pubmed><doi>10.1186/s40364-022-00443-8</doi></cross_references></HashMap>