fig1
![Tyrosine kinases in KMT2A/MLL-rearranged acute leukemias as potential therapeutic targets to overcome cancer drug resistance](https://image.oaes.cc/12d553d7-8198-4683-b906-4a3c019ec275/5221.fig.1.jpg)
Figure 1. Gene Expression Levels for Tyrosine Kinases in Leukemic Cells from infants with KMT2A/MLL-R+ B-ALL vs. Other Types of B-ALL without KMT2A/MLL Rearrangements. Probeset level normalized, robust multi-array analysis (RMA) signal values from the archived data for infant ALL (GSE68720) were examined in these comparisons. Infant KMT2A/MLL-R+ B-ALL gene partners for KMT2A were AF4 (N = 48), ENL (N = 16), AF9 (N = 6), ASAH3 (N = 1), EPS15 (N = 3), Unknown (N = 6) (GSE68720; Total N = 80). The cluster figure displays the expression levels in KMT2A/MLL-R+ ALL cells mean centered to the reference group [KMT2A/MLL germline/WT gene (KMT2A/MLL-R-)] represented by 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). The log2-transformed RMA values for leukemic cells from 80 infants with KMT2A/MLL-R+ B-ALL compared to that from leukemia cells obtained from 17 infants with MLL-germline/WT ALL (MLL-R negative) showed 19 probesets that were upregulated in KMT2A/MLL-R+ infant ALL cells. FLT3_206674_at was the most significantly upregulated probeset (Fold Change = 11.23; P-value < 10-8) followed by BLK_206255_at (Fold Change = 3.98; P-value < 10-8) and HCK_208018_s_at (Fold Change = 2.46; P-value < 10-8)