Journal
CANCER CELL
Volume 22, Issue 2, Pages 153-166Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2012.06.005
Keywords
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Categories
Funding
- NCI
- NIH, Therapeutically Applicable Research to Generate Effective Treatments initiative [N01-C0-12400]
- Children's Oncology Group Chair's award [CA098543]
- National Cancer Institute Strategic Partnering to Evaluate Cancer Signatures Program [CA114762]
- NIH Cancer Center Core Grant [CA21765]
- St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project
- Stand Up To Cancer Innovative Research Grant
- American Lebanese Syrian Associated Charities of St. Jude Children's Research Hospital
- National Health and Medical Research Council (Australia)
- Haematology Society of Australia
- New Zealand Novartis New Investigator Scholarship
- MSFHR
- [U10 CA98543]
- [U10 CA98413]
- [U24 CA114766]
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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.
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