{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE264nnn/GSE264595/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE264595"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"The XPO7-NPAT axis represents key vulnerabilities in TP53-mutated acute myeloid leukemia (RNA-Seq)","description":"Mutation of TP53, a tumor suppressor in cancer, is common and leads to extremely poor prognosis. To identify vulnerabilities in TP53-mutated tumors, we performed genome-wide CRISPR/Cas9 screens using isogenic Trp53 wild-type and knockout mouse acute myeloid leukemia (AML) lines. Here, we show that histone gene regulation governed by the XPO7-NPAT pathway is essential for survival of TP53-mutated AML cells. In TP53 wild-type cells, XPO7 enhances p53 nuclear localization and functions as a tumor suppressor, but in TP53-mutated cells, XPO7 promotes cell proliferation by retaining NPAT, a histone gene activator, in the nucleus. NPAT depletion led to genome-wide histone loss, enhancing vulnerability to genotoxic stress. Human AML cases show predominant expression of XPO7 and NPAT when TP53 is mutated, suggesting a potential therapeutic vulnerability.","dates":{"publication":"2026/04/22"},"accession":"GSE264595","cross_references":{"GSM":["GSM8223530","GSM8223531","GSM8223520","GSM8223532","GSM8223521","GSM8223533","GSM8223522","GSM8223534","GSM8223523","GSM8223524","GSM8223535","GSM8223536","GSM8223525","GSM8223537","GSM8223526","GSM8223527","GSM8223528","GSM8223529"],"GPL":["21626"],"GSE":["264595"],"taxon":["Mus musculus"]}}