<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/GSE282nnn/GSE282370/</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=GSE282370</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Chromosome 5q deletion drives evolution to aneuploidy in an iPSC model of complex karyotype leukemia</name><description>Aneuploidy is a hallmark of a unique group of high-risk myeloid malignancies including acute myeloid leukemias (AML), known as AML with complex karyotype (AML-CK). AML-CK is nearly universally associated with TP53 mutations and deletions on the long arm of chromosome 5 (del(5q)), however, the drivers and trajectories of AML-CK evolution have not been established. We performed single cell transcriptomics on iPSC based hematopoietic progenitor cell model of TP53 mutant/TP53 mutant + del5q driven to CK. Comparisons were performed between 2 AML-CK primary patient samples (R332, RO20518) and 2 isolated del5q MDS parient samples (AGC, TWN).</description><dates><publication>2026/05/21</publication></dates><accession>GSE282370</accession><cross_references><GSM>GSM8642095</GSM><GSM>GSM8642106</GSM><GSM>GSM8642105</GSM><GSM>GSM8642104</GSM><GSM>GSM8642103</GSM><GSM>GSM8642102</GSM><GSM>GSM8642101</GSM><GSM>GSM8642100</GSM><GSM>GSM8642099</GSM><GSM>GSM8642098</GSM><GSM>GSM8642097</GSM><GSM>GSM8642096</GSM><GPL>21697</GPL><GPL>24676</GPL><GSE>282370</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>