Genetic alterations activating kinase and cytokine receptor signaling in high-risk acute lymphoblastic leukemia Journal Article

   

Authors:	Roberts, K.; Morin, R.; Zhang, J.; Hirst, M.; Zhao, Y.; Su, X.; Chen, S. C.; Payne-Turner, D.; Churchman, M. L.; Harvey, R.; Chen, X.; Kasap, C.; Yan, C.; Becksfort, J.; Finney, R.; Teachey, D.; Maude, S.; Tse, K.; Moore, R.; Jones, S.; Mungall, K.; Birol, I.; Edmonson, M.; Hu, Y.; Buetow, K.; Chen, I. M.; Carroll, W.; Wei, L.; Ma, J.; Kleppe, M.; Levine, R.; Garcia-Manero, G.; Larsen, E.; Shah, N.; Devidas, M.; Reaman, G.; Smith, M.; Paugh, S.; Evans, W.; Grupp, S.; Jeha, S.; Pui, C. H.; Gerhard, D.; Downing, J.; Willman, C.; Loh, M.; Hunger, S. P.; Marra, M.; Mullighan, C. G.
Article Title:	Genetic alterations activating kinase and cytokine receptor signaling in high-risk acute lymphoblastic leukemia
Abstract:	Genomic profiling has identified a subtype of high-risk B-progenitor acute lymphoblastic leukemia (B-ALL) with alteration of IKZF1, a gene expression profile similar to BCR-ABL1-positive ALL and poor outcome (Ph-like ALL). The genetic alterations that activate kinase signaling in Ph-like ALL are poorly understood. We performed transcriptome and whole genome sequencing on 15 cases of Ph-like ALL and identified rearrangements involving ABL1, JAK2, PDGFRB, CRLF2, and EPOR, activating mutations of IL7R and FLT3, and deletion of SH2B3, which encodes the JAK2-negative regulator LNK. Importantly, several of these alterations induce transformation that is attenuated with tyrosine kinase inhibitors, suggesting the treatment outcome of these patients may be improved with targeted therapy. © 2012 Elsevier Inc.
Journal Title:	Cancer Cell
Volume:	22
Issue:	2
ISSN:	1535-6108
Publisher:	Cell Press
Date Published:	2012-08-14
Start Page:	153
End Page:	166
Language:	English
DOI:	10.1016/j.ccr.2012.06.005
PROVIDER:	scopus
PMCID:	PMC3422513
PUBMED:	22897847
DOI/URL:	http://www.scopus.com/inward/record.url?eid=2-s2.0-84865118132&partnerID=40&md5=a513b6a1f3fb99a7d5e0946cbf280819
Notes:	--- - "Cited By (since 1996): 1" - "Export Date: 4 September 2012" - "CODEN: CCAEC" - "Source: Scopus"

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