<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/GSE317nnn/GSE317759/</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=GSE317759</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>FB23-2 exerts therapeutic effects against T-ALL through the FTO/m6A/MYC axis.</name><description>T-cell acute lymphoblastic leukemia (T-ALL) is a pediatric hematological malignancy that presents significant challenges. RNA N6-methyladenosine (m6A) methylation is crucial in tumorigenesis, and the m6A demethylase FTO has emerging importance in cancers; however, its specific role in T-ALL pathogenesis remains incompletely understood. In vitro studies employed T-ALL cell lines treated with the FTO inhibitor FB23-2. Our findings indicate that FB23-2 may exert therapeutic effects against T-ALL primarily through the FTO/m6A/MYC axis.</description><dates><publication>2026/05/19</publication></dates><accession>GSE317759</accession><cross_references><GSM>GSM9477752</GSM><GSM>GSM9477753</GSM><GSM>GSM9477750</GSM><GSM>GSM9477751</GSM><GPL>24676</GPL><GSE>317759</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>