fig4

Tyrosine kinases in KMT2A/MLL-rearranged acute leukemias as potential therapeutic targets to overcome cancer drug resistance

Figure 4. Gene Expression Levels for Tyrosine Kinases in Leukemic Cells from Pediatric Patients with KMT2A/MLL-R+ AML vs. Other subsets of AML without KMT2A/MLL rearrangements. Probeset level normalized signal values from the archived data sets GSE17855 and GSE19577 were examined in these comparisons. The cluster figure displays the expression levels in KMT2A/MLL-R+ AML cells mean centered to the reference group (non-KMT2A/MLL-R+ other AML subsets) for log2-transformed fold change values (blue to red color indicates under-expression to over-expression respectively in KMT2A/MLL-R+ samples). Co-regulated probesets are organized and depicted by dendrograms for both probesets (rows) and patients (columns). Comparing 190 cases of non-KMT2A/MLL-R+ other samples (GSE17855) with 89 cases of KMT2A/MLL-R+ pediatric AML samples [GSE17855 (N = 47) and GSE19577(N = 42)] exhibited 38 differentially expressed probesets, of which 25 probesets were significantly upregulated in pediatric KMT2A/MLL-R+ subset of cases. FGR_208438_s_at was the most significantly upregulated transcript (Fold Change = 4.31 P-value < 10-8) followed by SYK_207540_s_at (Fold Change = 4.01; P-value < 10-8) and HCK_208018_s_at (Fold Change = 3.97; P-value < 10-8)
[Supplementary Table 9]. SYK (3 probesets), JAK2 (2 probesets), JAK1, FGR and HCK formed a cluster of patients with significantly higher expression levels in KMT2A/MLL-R+ cases.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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