{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Xu Q"],"funding":["Medical Research Council"],"pagination":["e2107599119"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8832965"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["119(6)"],"pubmed_abstract":["Oncogenic imbalance of DNA methylation is well recognized in cancer development. The ten-eleven translocation (TET) family of dioxygenases, which facilitates DNA demethylation, is frequently dysregulated in cancers. How such dysregulation contributes to tumorigenesis remains poorly understood, especially in solid tumors which present infrequent mutational incidence of <i>TET</i> genes. Here, we identify loss-of-function mutations of <i>TET</i> in 7.4% of human lung adenocarcinoma (LUAD), which frequently co-occur with oncogenic <i>KRAS</i> mutations, and this co-occurrence is predictive of poor survival in LUAD patients. Using an autochthonous mouse model of <i>Kras<sup>G12D</sup></i> -driven LUAD, we show that individual or combinational loss of <i>Tet</i> genes markedly promotes tumor de"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Loss of TET reprograms Wnt signaling through impaired demethylation to promote lung cancer development."],"pmcid":["PMC8832965"],"funding_grant_id":["MR/J007773/1"],"pubmed_authors":["Zhou JX","Walsh CP","Ji H","Xu GL","Wang C","Xu Q","Gao J","Xu ZM","Sui P"],"additional_accession":[]},"is_claimable":false,"name":"Loss of TET reprograms Wnt signaling through impaired demethylation to promote lung cancer development.","description":"Oncogenic imbalance of DNA methylation is well recognized in cancer development. The ten-eleven translocation (TET) family of dioxygenases, which facilitates DNA demethylation, is frequently dysregulated in cancers. How such dysregulation contributes to tumorigenesis remains poorly understood, especially in solid tumors which present infrequent mutational incidence of <i>TET</i> genes. Here, we identify loss-of-function mutations of <i>TET</i> in 7.4% of human lung adenocarcinoma (LUAD), which frequently co-occur with oncogenic <i>KRAS</i> mutations, and this co-occurrence is predictive of poor survival in LUAD patients. Using an autochthonous mouse model of <i>Kras<sup>G12D</sup></i> -driven LUAD, we show that individual or combinational loss of <i>Tet</i> genes markedly promotes tumor de","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2026-05-31T07:04:35.083Z","creation":"2025-04-20T00:20:28.143Z"},"accession":"S-EPMC8832965","cross_references":{"pubmed":["35110400"],"doi":["10.1073/pnas.2107599119"]}}