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Multi-omics analysis of myelodysplastic syndromes resistance to epigenetics threrary reveals PI3K/Akt activation mediated by epigenetic silencing of PTEN and epi-transcriptional silencing of MDM2 [epitranscriptome]
PubMed Full text in PMC Similar studies SRA Run Selector
Multi-omics analysis of myelodysplastic syndromes resistance to epigenetics threrary reveals PI3K/Akt activation mediated by epigenetic silencing of PTEN and epi-transcriptional silencing of MDM2
PubMed Full text in PMC Similar studies Analyze with GEO2R
Multi-omics analysis of myelodysplastic syndromes resistance to epigenetics threrary reveals PI3K/Akt activation mediated by epigenetic silencing of PTEN and epi-transcriptional silencing of MDM2 [transcriptome]
PubMed Full text in PMC Similar studies Analyze with GEO2RSRA Run Selector
Multi-omics analysis of myelodysplastic syndromes resistance to epigenetics threrary reveals PI3K/Akt activation mediated by epigenetic silencing of PTEN and epi-transcriptional silencing of MDM2 [methylome]
A methylation signature at diagnosis in patients with high-risk Myelodysplastic Syndromes and secondary Acute Myeloid Leukemia predicts azacitidine response but not relapse
PubMed Full text in PMC Similar studies
Transcriptome profiling by RNA-sequencing of the AML cell lines UCSD-AML1 and ELF-153.
PubMed Similar studies Analyze with GEO2RSRA Run Selector
Gene expression data of serially sorted primary AML patient blasts prior and after treatment with the DNMT inhibitor decitabine (DAC)
PubMed Similar studies Analyze with GEO2R
Copy-number profiling by SNP array of 4 acute myeloid leukemia (AML) cell lines
PubMed Similar studies
miRNA expression profiling in a murine model of KrasG12D induced CMML-like MPD
Mitotic perturbation is a key mechanism of action of decitabine in myeloid tumor treatment II
Mitotic perturbation is a key mechanism of action of decitabine in myeloid tumor treatment
Non-canonical immune response to inhibition of DNA methylation via stabilization of dsRNAs from endogenous retroviruses
Analysis of genome-wide methylation and gene expression induced by decitabine treatment in HL60 leukemia cell line
Preclinical efficacy of azacitidine and venetoclax for infant KMT2A-rearranged ALL reveals a new therapeutic strategy
Transcriptomic profiling of KMT2A-rearranged infant acute lymphoblastic leukemia (ALL) cells after treatment witith azacitidine and decitabine.
Genome-wide methylation profiling of KMT2A-rearranged infant Acute Lymphoblastic Leukemia (ALL) cells after treatment with azacitidine, decitabine and zebularine
Immunologic predictors for clinical responses during immune checkpoint blockade in patients with myelodysplastic syndromes
Investigating microenvironment in MDS
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