Dataset Information

Label-free quantitative proteome of AML CD34+ and mobilized PB CD34+ cells

ABSTRACT: The label-free quantitative proteome was generated for 42 primary AML patient samples enriched for CD34+ cells (or mononuclear cells in the case of NPMcyt sameples) and as controls 6 mobilized peripheral blood CD34+ cells were included. Furthermore, 6 AML cell lines were included, and also primary mesenchymal stem cells grown under normaoxia or hypoxia were included.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Cell, Bone Marrow, Blood

DISEASE(S): Acute Leukemia

SUBMITTER: Jan Jacob Schuringa

LAB HEAD: Jan Jacob Schuringa

PROVIDER: PXD030463 | Pride | 2022-03-15

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	Sample_and_Data_Relationship_Format_SDRF_file.txt	Txt
	Schuringa_AML_global_proteomics-proteinGroups_log10_normalized.xlsx	Xlsx
	Schuringa_AML_global_proteomics-proteinGroups_log10_normalized_LFQ_intensities.xlsx	Xlsx

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Publications

Prospective Isolation and Characterization of Genetically and Functionally Distinct AML Subclones.

de Boer Bauke B Prick Janine J Pruis Maurien G MG Keane Peter P Imperato Maria Rosaria MR Jaques Jennifer J Brouwers-Vos Annet Z AZ Hogeling Shanna M SM Woolthuis Carolien M CM Nijk Marije T MT Diepstra Arjan A Wandinger Sebastian S Versele Matthias M Attar Ricardo M RM Cockerill Peter N PN Huls Gerwin G Vellenga Edo E Mulder André B AB Bonifer Constanze C Schuringa Jan Jacob JJ

Cancer cell 20180920 4

Intra-tumor heterogeneity caused by clonal evolution is a major problem in cancer treatment. To address this problem, we performed label-free quantitative proteomics on primary acute myeloid leukemia (AML) samples. We identified 50 leukemia-enriched plasma membrane proteins enabling the prospective isolation of genetically distinct subclones from individual AML patients. Subclones differed in their regulatory phenotype, drug sensitivity, growth, and engraftment behavior, as determined by RNA seq ...[more]

PMID: 30245083

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Project description:Myelodysplastic syndromes (MDS) are a group of clonal hematological disorders characterized by ineffective hematopoiesis with morphological evidence of marrow cell dysplasia resulting in peripheral blood cytopenia. Microarray technology has permitted a refined high-throughput mapping of the transcriptional activity in the human genome. Noncoding-RNAs (ncRNAs) transcribed from intronic regions of genes are involved in a number of processes related to post-transcriptional control of gene expression, and in the regulation of exon-skipping and intron retention. Characterization of ncRNAs in progenitor cells and stromal cells of MDS patients could be strategic for understanding gene expression regulation in this disease. In this study, gene expression profiles of CD34+ and stromal cells of MDS patients with refractory anemia with ringed sideroblasts (RARS) subgroup were compared those of healthy individuals, using 44k combined intron-exon oligoarrays, which included probes for protein-coding genes, for sense and antisense strands of totally intronic noncoding (TIN) and for partially intronic noncoding (PIN) RNAs. In CD34+ cells of MDS-RARS patients, 217 genes were significantly differentially expressed (q-value < 0.01) in comparison to healthy individuals, of which 68 (31%) were noncoding transcripts. In stromal cells of MDS-RARS, 13 genes were significantly differentially expressed (q-value < 0.05) in comparison to healthy individuals, of which 4 (30%) were noncoding transcripts. These results demonstrated, for the first time, in CD34+ cells and stromal cells the differential ncRNA expression profile between MDS-RARS and healthy individuals, suggesting that ncRNAs may play an important role during the development of myelodysplastic syndromes. Bone marrow (BM) CD34+ cell samples were collected from 4 healthy subjects and from 4 MDS patients. Stromal samples were collected from 4 healthy subjects and 3 MDS patients. All patients were diagnosed as RARS according to the French-American-British (FAB) classification and did not present chromosomal abnormalities; they received no growth factors or any further MDS treatment.