Project description:Label-free quantitation dataset from 44 representative Acute Myeloid Leukemia (AML) patients from the LAML TCGA dataset, and 6 healthy bone marrow derived controls including 3 lineage-depleted and 3 CD34+ selected bone marrows.

2022-03-09 | MSV000089029 | MassIVE

Proteomic and Phosphoproteomic Landscapes of Acute Myeloid Leukemia

Project description:A deep-scale proteome and phosphoproteome database from 44 representative Acute Myeloid Leukemia (AML) patients from the LAML TCGA dataset, and 6 healthy bone marrow derived controls including 3 lineage-depleted and 3 CD34+ selected bone marrows.

2022-03-07 | MSV000089012 | MassIVE

mRNA-sequencing in drug-resistant acute myeloid leukemia

Project description:mRNA sequencing for AML cells(HL-60) and drug-resistant AML Cells(HL60/MX2).

2022-04-23 | GSE201095 | GEO

Stabilizing the Proteomes of Acute Myeloid Leukemia Cells: Implications for Cancer Proteomics

Project description:Data dependent analysis of acute myeloid leukemia samples in the presence and absence of the serine protease inhibitor DFP

2023-07-26 | MSV000092526 | MassIVE

caArray_golub-00392: Gefitinib (Iressa) induces myeloid differentiation of acute myeloid leukemia

Project description:Cure rates for patients with acute myeloid leukemia (AML) remain low despite ever-increasing dose intensity of cytotoxic therapy. In an effort to identify novel approaches to AML therapy, we recently reported a new method of chemical screening based on the modulation of a gene expression signature of interest. We applied this approach to the discovery of AML-differentiation-promoting compounds. Among the compounds inducing neutrophilic differentiation was DAPH1 (4,5-dianilinophthalimide), previously reported to inhibit epidermal growth factor receptor (EGFR) kinase activity. Here we report that the Food and Drug Administration (FDA)-approved EGFR inhibitor gefitinib similarly promotes the differentiation of AML cell lines and primary patient-derived AML blasts in vitro. Gefitinib induced differentiation based on morphologic assessment, nitro-blue tetrazolium reduction, cell-surface markers, genome-wide patterns of gene expression, and inhibition of proliferation at clinically achievable doses. Importantly, EGFR expression was not detected in AML cells, indicating that gefitinib functions through a previously unrecognized EGFR-independent mechanism. These studies indicate that clinical trials testing the efficacy of gefitinib in patients with AML are warranted. golub-00392 Assay Type: Gene Expression Provider: Affymetrix Array Designs: HG-U133A, HG-U133A_2 Organism: Homo sapiens (ncbitax) Material Types: cell, total_RNA, synthetic_RNA, organism_part, whole_organism*Cell Types: Disease States: Acute Myeloid Leukemia, Normal, Acute Myeloid Leukemia

2015-05-16 | E-GEOD-68954 | biostudies-arrayexpress

AML_profiling - Integrated analysis of proteome, phosphotyrosine-proteome, tyrosine-kinome and tyrosine-phosphatome in acute myeloid leukemia

Project description:LC-MS/MS was used to profile total phosphotyrosine phosphatase in acute myeloid leukemia (AML) in order to find potential biomarkers, drug targets, signatures for AML classification, and its relationship with total phosphotyrosine amount in the samples.

2017-02-16 | PXD001170 | Pride

lncRNA dependencies in acute myeloid leukemia

Project description:lncRNA dependencies in acute myeloid leukemia

| PRJNA354371 | ENA