Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA112367PRJNA132313PRJNA208363PRJNA96045
INSTRUMENT(S): QSTAR
ORGANISM(S): Mus Musculus (mouse)
TISSUE(S): B Cell, Blood
DISEASE(S): Acute Leukemia
SUBMITTER: Andrew Williamson
LAB HEAD: Prof. Tony Whetton
PROVIDER: PXD002782 | Pride | 2016-05-26
REPOSITORIES: Pride
Action | DRS | |||
---|---|---|---|---|
012111_AP_Scope4.4_Cyto_17.mzML | Mzml | |||
012111_AP_Scope4.4_Cyto_17.wiff | Wiff | |||
012111_AP_Scope4.4_Cyto_17.wiff.scan | Wiff | |||
012111_AP_Scope4.4_Cyto_18.mzML | Mzml | |||
012111_AP_Scope4.4_Cyto_18.wiff | Wiff |
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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]