<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wang Q</submitter><funding>This study was supported by The Medical Engineering Cross research fund of Shanghai Jiaotong University "Star of Jiaotong University" program</funding><pagination>1759</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12480298</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Metabolic reprogramming is a hallmark of cancer development, including in lung adenocarcinoma (LUAD). This study aimed to explore the relationships between metabolic gene methylation, expression, and protein levels with LUAD risk using Mendelian randomization, leveraging multi-omic data to identify potential molecular targets for early detection and treatment.&lt;h4>Methods&lt;/h4>The study utilized summary-level data from methylation, expression, and protein quantitative trait loci (QTL) studies. Genetic associations with LUAD risk were sourced from the TRICL Consortium for discovery analysis and validated using data from the FinnGen cohort. Mendelian randomization was conducted to evaluate associations between metabolic gene-related molecular features and LUAD risk, while co</pubmed_abstract><journal>Discover oncology</journal><pubmed_title>Multiomic Mendelian randomization analysis of metabolic gene methylation expression and protein levels in lung adenocarcinoma.</pubmed_title><pmcid>PMC12480298</pmcid><funding_grant_id>24X010301595</funding_grant_id><pubmed_authors>Wang Q</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Zou Q</pubmed_authors><pubmed_authors>Geng J</pubmed_authors><pubmed_authors>Liu G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Multiomic Mendelian randomization analysis of metabolic gene methylation expression and protein levels in lung adenocarcinoma.</name><description>&lt;h4>Background&lt;/h4>Metabolic reprogramming is a hallmark of cancer development, including in lung adenocarcinoma (LUAD). This study aimed to explore the relationships between metabolic gene methylation, expression, and protein levels with LUAD risk using Mendelian randomization, leveraging multi-omic data to identify potential molecular targets for early detection and treatment.&lt;h4>Methods&lt;/h4>The study utilized summary-level data from methylation, expression, and protein quantitative trait loci (QTL) studies. Genetic associations with LUAD risk were sourced from the TRICL Consortium for discovery analysis and validated using data from the FinnGen cohort. Mendelian randomization was conducted to evaluate associations between metabolic gene-related molecular features and LUAD risk, while co</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-06-03T23:56:52.12Z</modification><creation>2026-05-03T03:12:03.404Z</creation></dates><accession>S-EPMC12480298</accession><cross_references><pubmed>41021077</pubmed><doi>10.1007/s12672-025-03600-1</doi></cross_references></HashMap>