Figure 2.
Figure 2. Distribution of kinase subtypes in Ph-like ALL within each age group.18,19,30,31 Combined prevalence of Ph-like ALL subtypes in childhood NCI standard risk (SR; age 1-9.99 years and white blood cells <50 000/μL), NCI high risk (HR; age 10-15 years or white blood cells ≥50 000/μL), AYAs (16-39 years), and adults (older than or equal to 40 years). Genomic subtypes include IGH-CRLF2, P2RY8-CRLF2, ABL-class fusions (ABL1, ABL2, CSF1R, LYN, PDGFRA, and PDGFRB), JAK2 and EPOR rearrangements, other mutations in JAK-STAT signaling (JAK1/3, IL7R, SH2B3, TYK2, and IL2RB), other kinase alterations (FLT3, FGFR1, and NTRK3,), Ras mutations (KRAS, NRAS, NF1, PTPN11, BRAF, and CBL), and unknown alterations.

Distribution of kinase subtypes in Ph-like ALL within each age group.18,19,30,31  Combined prevalence of Ph-like ALL subtypes in childhood NCI standard risk (SR; age 1-9.99 years and white blood cells <50 000/μL), NCI high risk (HR; age 10-15 years or white blood cells ≥50 000/μL), AYAs (16-39 years), and adults (older than or equal to 40 years). Genomic subtypes include IGH-CRLF2, P2RY8-CRLF2, ABL-class fusions (ABL1, ABL2, CSF1R, LYN, PDGFRA, and PDGFRB), JAK2 and EPOR rearrangements, other mutations in JAK-STAT signaling (JAK1/3, IL7R, SH2B3, TYK2, and IL2RB), other kinase alterations (FLT3, FGFR1, and NTRK3,), Ras mutations (KRAS, NRAS, NF1, PTPN11, BRAF, and CBL), and unknown alterations.

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