<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE293nnn/GSE293976/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE293976</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Histon lactylation drives HAS2 expression in gastric cancer tumorigensis after H.pylori infection</name><description>Histone lactylation, an epigenetic modification, promotes tumor growth and immune evasion in various cancers. Our study found increased pan-lysine lactylation and H3K18la in gastric tissues, linked to poor prognosis. Inhibiting glycolysis and silencing lactate dehydrogenase reduced H3K18la, boosting CD8+ T-cell activity against gastric cancer. H3K18la activated HAS2 transcription, enhancing MYC nuclear transport and PD-L1 expression..Our data provide a molecular framework for Histone lactylation in the process of gastric cancer.</description><dates><publication>2026/04/09</publication></dates><accession>GSE293976</accession><cross_references><GSM>GSM8895680</GSM><GSM>GSM8895682</GSM><GSM>GSM8895671</GSM><GSM>GSM8895681</GSM><GSM>GSM8895673</GSM><GSM>GSM8895672</GSM><GSM>GSM8895675</GSM><GSM>GSM8895674</GSM><GSM>GSM8895677</GSM><GSM>GSM8895676</GSM><GSM>GSM8895679</GSM><GSM>GSM8895678</GSM><GPL>16791</GPL><GSE>293976</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>