Kinase rearrangement and therapeutic targets in Ph-like ALL. The TKIs shown are known or predicted to be active against rearrangements involving the listed kinase in experimental models but, with the exception of imatinib/dasatinib in EBF1-PDGFRB ALL, have not been shown to be effective in ALL [data from Roberts et al. (2014) and adapted from Mullighan (2014)].
Kinase | TKI | No. of Partners | No. of Cases | 5′ Genes |
---|---|---|---|---|
ABL1 | Dasatinib | 6 | 14 | ETV6, NUP214, RCSD1, RANBP2, SNX2, ZMIZ1 |
ABL2 | Dasatinib | 3 | 7 | PAG1, RCSD1, ZC3HAV1 |
CSF1R | Dasatinib | 1 | 4 | SSBP2 |
PDGFRB | Dasatinib | 4 | 11 | EBF1, SSBP2, TNIP1, ZEB2 |
CRLF2 | JAK2 Inhibitor | 2 | 30 | IGH, P2RY8 |
JAK2 | JAK2 Inhibitor | 10 | 19 | ATF7IP, BCR, EBF1, ETV6, PAX5, PPFIBP1, SSBP2, STRN3, TERF2, TPR |
EPOR | JAK2 Inhibitor | 2 | 9 | IGH, IGK |
DGKH | Unknown | 1 | 1 | ZFAND3 |
IL2RB | JAK1/3 inhibitor | 1 | 1 | MYH9 |
NTRK3 | Crizotinib, LOXO-101 | 1 | 1 | ETV6 |
PTK2B | FAK inhibitor | 2 | 1 | KDM6A |
TSLP | JAK2 Inhibitor | 1 | 1 | IQGAP2 |
TYK2 | TYK2 inhibitor | 1 | 1 | MYB |