Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA112367PRJNA132313PRJNA208363PRJNA96045
INSTRUMENT(S): TripleTOF 5600
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Blood Cell, Blood
DISEASE(S): Chronic Myeloid Leukemia
SUBMITTER: Andrew Williamson
LAB HEAD: Anthony David Whetton
PROVIDER: PXD001504 | Pride | 2016-06-03
REPOSITORIES: Pride
Action | DRS | |||
---|---|---|---|---|
5600CML_Cyto_1_MGFPeaklist.mgf | Mgf | |||
CML_Cyto_1.mzXML | Mzxml | |||
CML_Cyto_1.xml | Xml | |||
CML_Cyto_10.mzXML | Mzxml | |||
CML_Cyto_11.mzXML | Mzxml |
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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]