Dataset Information

CML proteome analysis, LTQ Orbitrap Velos

ABSTRACT: Using mass spectrometry the proteomes of CML were compared to normal tissue.

OTHER RELATED OMICS DATASETS IN: PRJNA112367PRJNA132313PRJNA208363PRJNA96045

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Cell, Blood

DISEASE(S): Chronic Myeloid Leukemia

SUBMITTER: Andrew Williamson

LAB HEAD: Prof. Anthony David Whetton

PROVIDER: PXD001502 | Pride | 2016-06-03

REPOSITORIES: pride

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Dataset's files

Source:

			Action	DRS
	030211_CML_Glasgow_Cyto_01.raw	Raw
	030211_CML_Glasgow_Cyto_02.raw	Raw
	030211_CML_Glasgow_Cyto_03.raw	Raw
	030211_CML_Glasgow_Cyto_04.raw	Raw
	030211_CML_Glasgow_Cyto_05.raw	Raw

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Publications

Dual targeting of p53 and c-MYC selectively eliminates leukaemic stem cells.

Abraham Sheela A SA Hopcroft Lisa E M LE Carrick Emma E Drotar Mark E ME Dunn Karen K Williamson Andrew J K AJ Korfi Koorosh K Baquero Pablo P Park Laura E LE Scott Mary T MT Pellicano Francesca F Pierce Andrew A Copland Mhairi M Nourse Craig C Grimmond Sean M SM Vetrie David D Whetton Anthony D AD Holyoake Tessa L TL

Nature 20160608 7607

Chronic myeloid leukaemia (CML) arises after transformation of a haemopoietic stem cell (HSC) by the protein-tyrosine kinase BCR-ABL. Direct inhibition of BCR-ABL kinase has revolutionized disease management, but fails to eradicate leukaemic stem cells (LSCs), which maintain CML. LSCs are independent of BCR-ABL for survival, providing a rationale for identifying and targeting kinase-independent pathways. Here we show--using proteomics, transcriptomics and network analyses--that in human LSCs, ab ...[more]

PMID: 27281222

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Project description:Background MicroRNAs are important regulators of transcription in hematopoiesis. Their expression deregulations were described in association with pathogenesis of some hematological malignancies. This study provides integrated microRNA expression profiling at different phases of chronic myeloid leukemia (CML) with the aim to select CML specific miRNAs and find new possible biomarkers. The functions of in silico filtered targets are in this report annotated and discussed in relation to CML pathogenesis. Results Using microarrays we identified differential expression profiles of 49 miRNAs in CML patients at diagnosis, in hematological relapse, therapy failure, blast crisis and major molecular response. The expression deregulation of miR-150, miR-20a, miR-17, miR-19a, miR-103, miR-144, miR-155, miR-181a, miR-221 and miR-222 in CML was confirmed by real-time quantitative PCR and in silico analyses identified targeted genes of these miRNAs encoding proteins that are involved in cell cycle, growth inhibition, MAPK, ErBb, transforming growth factor beta and p53 signaling pathways that are related to CML. Validated miR-150 decreased levels were detected in patients at diagnosis, in blast crisis and 67% of hematological relapses and showed significant negative correlation with miR-150 proved target MYB and with BCR-ABL transcript level. Conclusions This study revealed microRNAs that may be related to the CML pathogenesis and may reflect transformation from chronic to accelerated phases. The obtained expression patterns in peripheral blood total leukocytes during the course of CML suggest specific miRNAs as possible biomarkers. The annotated functions of in silico filtered targets of selected miRNAs outline mechanisms whereby microRNAs may be involved in CML pathogenesis. Twenty four patient samples of total leukocytes from peripheral blood were used to prepare pools representing different CML phases for microarray analysis: diagnosis (n=5, Dg), major molecular response (n=5, MMR), therapy failure (n=5, TF), hematological relapse (n=5, Hr), and blast crisis (n=4, BC). Eleven healthy donors of age median 60 (range 45 - 78) and man/woman ratio 3/2 following CML incidence were used to create a control pool.