{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kundu S"],"funding":["Vetenskapsrådet","Uppsala University","Cancerfonden"],"pagination":["225"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8265010"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["40(1)"],"pubmed_abstract":["<h4>Background</h4>Genes in the Ras pathway have somatic mutations in at least 60 % of colorectal cancers. Despite activating the same pathway, the BRAF V600E mutation and the prevalent mutations in codon 12 and 13 of KRAS have all been linked to different clinical outcomes, but the molecular mechanisms behind these differences largely remain to be clarified.<h4>Methods</h4>To characterize the similarities and differences between common activating KRAS mutations and between KRAS and BRAF mutations, we used genome editing to engineer KRAS G12C/D/V and G13D mutations in colorectal cancer cells that had their mutant BRAF V600E allele removed and subjected them to transcriptome sequencing, global proteomics and metabolomics analyses.<h4>Results</h4>By intersecting differentially expressed gene"],"journal":["Journal of experimental & clinical cancer research : CR"],"pubmed_title":["Common and mutation specific phenotypes of KRAS and BRAF mutations in colorectal cancer cells revealed by integrative -omics analysis."],"pmcid":["PMC8265010"],"funding_grant_id":["CAN 2018/772","2016-04423"],"pubmed_authors":["Artursson P","Sjoblom T","Rendo V","Globisch D","Handin N","Ali MA","He L","Kundu S","Conway LP"],"additional_accession":[]},"is_claimable":false,"name":"Common and mutation specific phenotypes of KRAS and BRAF mutations in colorectal cancer cells revealed by integrative -omics analysis.","description":"<h4>Background</h4>Genes in the Ras pathway have somatic mutations in at least 60 % of colorectal cancers. Despite activating the same pathway, the BRAF V600E mutation and the prevalent mutations in codon 12 and 13 of KRAS have all been linked to different clinical outcomes, but the molecular mechanisms behind these differences largely remain to be clarified.<h4>Methods</h4>To characterize the similarities and differences between common activating KRAS mutations and between KRAS and BRAF mutations, we used genome editing to engineer KRAS G12C/D/V and G13D mutations in colorectal cancer cells that had their mutant BRAF V600E allele removed and subjected them to transcriptome sequencing, global proteomics and metabolomics analyses.<h4>Results</h4>By intersecting differentially expressed gene","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jul","modification":"2025-04-03T21:34:21.712Z","creation":"2022-02-10T18:47:39.114Z"},"accession":"S-EPMC8265010","cross_references":{"pubmed":["34233735"],"doi":["10.1186/s13046-021-02025-2"]}}