{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE303nnn/GSE303272/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE303272"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Targeting S100A9 to inhibit the malignant progression of acute myeloid leukemia","description":"This study aims to identify potential small molecule inhibitors targeting S100A9 using CADD (Computer-Aided Drug Design) virtual screening, and to investigate their effects on Acute Myeloid Leukemia (AML) cell lines. S100A9 is a key regulator in the pathogenesis and progression of AML, and targeting it may provide a promising therapeutic approach to mitigate the malignant advancement of AML. Through virtual screening, we selected B2, a small molecule compound, as a promising candidate for further experimental validation. The study focuses on the interaction between B2 and S100A9 and evaluates the compound’s ability to inhibit AML cell proliferation and survival. The effects of B2 on gene expression and cellular processes in AML cell lines were analyzed to better understand its potential as a therapeutic agent. This research provides new insights into the molecular targeting of S100A9 in AML treatment, with the aim of developing more effective and targeted therapeutic strategies.","dates":{"publication":"2026/08/12"},"accession":"GSE303272","cross_references":{"GSM":["GSM9122208","GSM9122207","GSM9122209","GSM9122204","GSM9122206","GSM9122205"],"GPL":["24676"],"GSE":["303272"],"taxon":["Homo sapiens"],"PMID":["[42135826]"]}}