<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/GSE325nnn/GSE325279/</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 array</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE325279</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>ALDH1 inhibitor, DIMATE, Preserves Immune Function While Inducing Immunogenic Remodelling in AML</name><description>DIMATE Preserves Immune Cells in AML Our study provides a comprehensive characterization of the immuno‑pharmacological effects of DIMATE, a selective ALDH1 inhibitor currently evaluated in the First‑in‑Human ODYSSEY trial. We show that DIMATE preserves the core functions of circulating immune populations—including PBMCs, T cells, NK cells, and phagocytes—while inducing a coordinated pro‑inflammatory and ER‑stress response in AML cells that culminates in the exposure of ecto‑calreticulin, a canonical hallmark of immunogenic cell death (ICD).</description><dates><publication>2026/07/01</publication></dates><accession>GSE325279</accession><cross_references><GSM>GSM9599483</GSM><GSM>GSM9599484</GSM><GSM>GSM9599481</GSM><GSM>GSM9599482</GSM><GSM>GSM9599487</GSM><GSM>GSM9599488</GSM><GSM>GSM9599485</GSM><GSM>GSM9599486</GSM><GPL>16699</GPL><GSE>325279</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>