作者
Kathryn G Roberts, Ryan D Morin, Jinghui Zhang, Martin Hirst, Yongjun Zhao, Xiaoping Su, Shann-Ching Chen, Debbie Payne-Turner, Michelle L Churchman, Richard C Harvey, Xiang Chen, Corynn Kasap, Chunhua Yan, Jared Becksfort, Richard P Finney, David T Teachey, Shannon L Maude, Kane Tse, Richard Moore, Steven Jones, Karen Mungall, Inanc Birol, Michael N Edmonson, Ying Hu, Kenneth E Buetow, I-Ming Chen, William L Carroll, Lei Wei, Jing Ma, Maria Kleppe, Ross L Levine, Guillermo Garcia-Manero, Eric Larsen, Neil P Shah, Meenakshi Devidas, Gregory Reaman, Malcolm Smith, Steven W Paugh, William E Evans, Stephan A Grupp, Sima Jeha, Ching-Hon Pui, Daniela S Gerhard, James R Downing, Cheryl L Willman, Mignon Loh, Stephen P Hunger, Marco A Marra, Charles G Mullighan
发表日期
2012/8/14
期刊
Cancer cell
卷号
22
期号
2
页码范围
153-166
出版商
Elsevier
简介
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.
引用总数
2012201320142015201620172018201920202021202220232024116186103849783575280544727