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. Author manuscript; available in PMC: 2015 Mar 11.
Published in final edited form as: N Engl J Med. 2014 Sep 11;371(11):1005–1015. doi: 10.1056/NEJMoa1403088

Figure 2. Recurring Kinase Alterations in Ph-like ALL.

Figure 2

Data are shown for 154 patients with Ph-like ALL who underwent detailed genomic analysis, including transcriptome sequencing (RNA-seq), whole-genome sequencing (WGS), whole-exome sequencing (WES), and reverse-transcriptase polymerase chain reaction (RT-PCR). The cohort is divided into patients with ABL-class fusions (ABL1, ABL2, CSF1R, PDGFRB) responsive to dasatinib, EPOR or JAK2 rearrangements, CRLF2 rearrangements, other JAK–STAT–activating mutations (IL7R, FLT3, SH2B3, JAK1, JAK3, TYK2, IL2RB, and TSLP), other kinase fusions (miscellaneous group, including NTRK3 and DGKH), alterations in the Ras pathway (KRAS, NRAS, PTPN11, NF1, and BRAF), and no kinase alteration. For details of specific alterations, see Tables S9 and S12 in Supplementary Appendix 1 and Table S20 in Supplementary Appendix 3.