Dataset Information

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

ABSTRACT: The label-free quantitative proteome was generated for 30 primary AML patient samples enriched for CD34+ cells or CKIT+ cells in the case of NPMcyt samples. As controls 3 mobilized peripheral blood CD34+ cells were included.

INSTRUMENT(S): LTQ Orbitrap

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: PXD030487 | Pride | 2025-01-07

REPOSITORIES: pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	Sample_and_Data_relationship_Format_SDRF_file.txt	Txt
	Schuringa_AML_proteome_normalized_dataset.xlsx	Xlsx
	Schuringa_AML_proteome_result_intensities_output_2020.xlsx	Xlsx

Items per page:

1 - 3 of 3

Publications

Bleximenib, the novel menin-KMT2A inhibitor JNJ-75276617, impairs long-term proliferation and immune evasion in acute myeloid leukemia.

Hogeling Shanna M SM Lê Duy Minh DM La Rose Nikita N Kwon Min Chul MC Wierenga Albertus T J ATJ Van den Heuvel Fiona A J FAJ Van den Boom Vincent V Kuchnio Anna A Philippar Ulrike U Huls Gerwin G Schuringa Jan Jacob JJ

Haematologica 20241219

Acute myeloid leukemia (AML) remains challenging to treat, which in part relates to genetic heterogeneity of the disease, to the protective tumor microenvironment driving resistance to therapy, and also to immune evasion characteristics of leukemic cells. Targeting epigenetic programs in AML provides an attractive opportunity to impair long-term proliferation and induce differentiation. The novel inhibitor JNJ- 75276617 (bleximenib) targets the menin-KMT2A interaction and provides preclinical ef ...[more]

PMID: 39704147

Publication: 1/2

Similar Datasets

Project description:Murine bronchioalveolar stem cells play a key role in pulmonary epithelial maintenance and repair but their molecular profile is poorly described so far. In this study, we used antibodies directed against Sca-1 and CD34, two markers originally ascribed to pulmonary cells harboring regenerative potential, to isolate single putative stem cells from murine lung tissue. The mean detection rate of positive cells was 8 per 106 lung cells. We then isolated and globally amplified the mRNA of positive cells to analyze gene expression in single cells. The resulting amplicons were then used for molecular profiling by transcript specific polymerase chain reaction (PCR) and global gene expression analysis using microarrays. Single marker-positive cells displayed a striking heterogeneity for the expression of epithelial and mesenchymal transcripts on the single cell level. Nevertheless, they could be subdivided into two cell populations: Sca-1+/CD34- and Sca-1+/CD34+ cells. In these subpopulations, transcripts of the epithelial marker Epcam (CD326) were exclusively detected in Sca-1+/CD34- cells (p = 0.03), whereas mRNA of the mesenchymal marker PdgfrM-NM-1 (CD140a) was detected in both subpopulations and more frequently in Sca-1+/CD34+ cells (p = 0.04). FACS analysis confirmed the existence of a PdgfrM-NM-1 positive subpopulation within Epcam+/Sca-1+/CD34- epithelial cells. Gene expression analysis by microarray hybridization identified transcripts differentially expressed between the two cell types as well as between epithelial reference cells and Sca-1+/CD34+ single cells, and selected transcripts were validated by quantitative PCR. Our results suggest a more mesenchymal commitment of Sca-1+/CD34+ cells and a more epithelial commitment of Sca-1+/CD34- cells. In summary, the study shows that single cell analysis enables the identification of novel molecular markers in yet poorly characterized populations of rare cells. Our results could further improve our understanding of Sca-1+/CD34+,- cells in the biology of the murine lung. Single cells of 10 Sca-1+/CD34+/CD31-/CD45-, 7 Sca-1+/CD34-/CD31-/CD45-, and 12 Sca-1-/CD34-/CD31-/CD45- were analyzed. Although the raw data are two channel only Cy5 signal of each file as analyzed. The Cy5 channel for each gene is normalized to the average Cy5 intensity of the gene across all samples.