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- W4310472605 abstract "Abstract Incidence and mortality of lung adenocarcinoma are high, and the epigenetic mechanism of DNA methylation has a critical effect on LUAD at all stages. Our work used GEO and TCGA databases to identify differentially methylated genes (DMGs) in LUAD to explore how DNA methylation works in immunotherapy resistance. Candidate pathogenic genes were highly correlated to hub-methylated differentially expressed genes (SLC2A1, HLF, FAM83A, SCARF1, C2orf40). Core genes were correlated with the pathways regulating cancer development. Using the TISIDB database to estimate immune cell infiltration and immune factor levels, a relation of tumor gene levels with immune infiltration suggested the possible effect of core genes on regulating tumor microenvironment (TME). The functional pathways and key genes were analyzed via GESA and GEVA (GO, KEGG) to identify functionally enriched pathways and key genes. According to CMap, there was a significantly negative correlation between drug expression profiles (BX-912, JAK3-inhibitor-VI, panobinostat, purvalanol-A, and scriptaid) and differentially expressed genes. Therefore, we hypothesized that these drugs could enhance LUAD anti-tumor therapy." @default.
- W4310472605 created "2022-12-10" @default.
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- W4310472605 date "2022-11-30" @default.
- W4310472605 modified "2023-10-16" @default.
- W4310472605 title "Identification of hub-methylated differentially expressed genes in lung adenocarcinoma and immunotherapy resistance" @default.
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- W4310472605 doi "https://doi.org/10.21203/rs.3.rs-2317392/v1" @default.
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