{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ischenko I"],"funding":["Carol M. Baldwin Breast Cancer Research Fund","NIAID NIH HHS","NCI NIH HHS","Catacosinos Cancer Research Award to OP"],"pagination":["1482"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7935870"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(1)"],"pubmed_abstract":["Immune evasion is a hallmark of KRAS-driven cancers, but the underlying causes remain unresolved. Here, we use a mouse model of pancreatic ductal adenocarcinoma to inactivate KRAS by CRISPR-mediated genome editing. We demonstrate that at an advanced tumor stage, dependence on KRAS for tumor growth is reduced and is manifested in the suppression of antitumor immunity. KRAS-deficient cells retain the ability to form tumors in immunodeficient mice. However, they fail to evade the host immune system in syngeneic wild-type mice, triggering strong antitumor response. We uncover changes both in tumor cells and host immune cells attributable to oncogenic KRAS expression. We identify BRAF and MYC as key mediators of KRAS-driven tumor immune suppression and show that loss of BRAF effectively blocks "],"journal":["Nature communications"],"pubmed_title":["KRAS drives immune evasion in a genetic model of pancreatic cancer."],"pmcid":["PMC7935870"],"funding_grant_id":["R01 AI105114","R01 CA236389"],"pubmed_authors":["Ischenko I","Li J","Petrenko O","Powers S","Rao M","D'Amico S","Hayman MJ","Reich NC"],"additional_accession":[]},"is_claimable":false,"name":"KRAS drives immune evasion in a genetic model of pancreatic cancer.","description":"Immune evasion is a hallmark of KRAS-driven cancers, but the underlying causes remain unresolved. Here, we use a mouse model of pancreatic ductal adenocarcinoma to inactivate KRAS by CRISPR-mediated genome editing. We demonstrate that at an advanced tumor stage, dependence on KRAS for tumor growth is reduced and is manifested in the suppression of antitumor immunity. KRAS-deficient cells retain the ability to form tumors in immunodeficient mice. However, they fail to evade the host immune system in syngeneic wild-type mice, triggering strong antitumor response. We uncover changes both in tumor cells and host immune cells attributable to oncogenic KRAS expression. We identify BRAF and MYC as key mediators of KRAS-driven tumor immune suppression and show that loss of BRAF effectively blocks ","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Mar","modification":"2025-04-22T02:09:17.632Z","creation":"2025-04-05T20:12:24.145Z"},"accession":"S-EPMC7935870","cross_references":{"pubmed":["33674596"],"doi":["10.1038/s41467-021-21736-w"]}}