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TranscriptomicsGene expression profiling in primary AML cells treated with decitabine and cytarabine
Acute myeloid leukemia (AML), and other myeloid malignancies, are frequently treated with hypomethylating agents like decitabine. Alterations in the epigenome, induced by decitabine, are likely to result in gene expression changes. The effects of decitabine have not been systemically studied using p...
ORGANISM(S): Homo sapiens 
2012-12-18 | E-GEOD-40442 | biostudies-arrayexpress
ProteomicsPosttranslational splicing modifications as a key mechanism in cytarabine resistance in AML
Despite the approval of several drugs for AML, cytarabine is still widely used as a therapeutic approach. However, most patients show resistance and only 10% of them overcome the disease. Using high-throughput screening analysis, we show that phosphorylation levels of SR proteins were elevated durin...
ORGANISM(S): Homo sapiens (Human) 
2023-07-04 | PXD034010 | Pride
Aml Cytarabine Phosphorylation 
GenomicsLow pass whole methylome enzymatic sequencing of four AML cell lines untreated and after treatment with different concentrations of 5-azacytidine (AZA), 5-aza-2′-deoxycytidine (DEC), Cytarabine (ARAC) and GSK3685032 (GSK5032) for 3 and 7 days
We conducted low-coverage whole-genome enzymatic methylation sequencing (EM-seq) on four commercially available AML cell lines to assess their global DNA methylation profiles following treatment with varying concentrations (0–3000 nM) of three different hypomethylating agents—5-azacytidine (AZA), 5-...
ORGANISM(S): Homo sapiens 
2025-04-10 | E-MTAB-14969 | biostudies-arrayexpress
GenomicsMechanism of cytarabine-induced neurotoxicity [HTGTS]
Mechanism of cytarabine-induced neurotoxicity [HTGTS]
PRJNA1243425 | ENA
ProteomicsImmunopeptidomics of Acute Myeloid Leukemia (AML) Blast cells after Therapy-Induced Senescence (TIS) with Cytarabine.
Resistance or relapse upon chemotherapy are major determinants of treatment failure in acute myeloid leukemia (AML). Therapy-induced senescence (TIS) is a potential outcome of chemotherapy, but its immunological consequences in AML remain unclear. We show that ex-vivo chemotherapy induces senescence...
ORGANISM(S): Homo sapiens (Human) 
2026-08-13 | PXD068731 | Pride
Immunopeptidomics Therapy-induced senescence Tis Hla Ligandome Mhc Cytarabine Ligandomics Immunopeptidome Timstof scp Acute myeloid leukemia Aml 
GenomicsMechanism of cytarabine-induced neurotoxicity [CRISPR Screen]
Mechanism of cytarabine-induced neurotoxicity [CRISPR Screen]
PRJNA1243422 | ENA
GenomicsMechanism of cytarabine-induced neurotoxicity [amplicon-Seq]
Mechanism of cytarabine-induced neurotoxicity [amplicon-Seq]
PRJNA1243430 | ENA
GenomicsMechanism of cytarabine-induced neurotoxicity [PS-Seq]
Mechanism of cytarabine-induced neurotoxicity [PS-Seq]
PRJNA1243423 | ENA
GenomicsMechanism of cytarabine-induced neurotoxicity [ATAC-Seq]
Mechanism of cytarabine-induced neurotoxicity [ATAC-Seq]
PRJNA1243413 | ENA
GenomicsMechanism of cytarabine-induced neurotoxicity [END-Seq]
Mechanism of cytarabine-induced neurotoxicity [END-Seq]
PRJNA1243415 | ENA
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