Figure 1
Figure 1. Distribution of mutations in tested genes in 10 patients with CML. Schematic representation shows the main domains, primarily the tyrosine kinase binding (TKB) domain, linker sequence (L), RING finger domain (RF), proline-rich region (PPP), and leucine zipper (LZ)/ubiquitin-associated domain (UBA) of the CBL family, cysteine (C)–rich domain, and double-stranded β helix (DSBH) domain of TET2, additional sex comb (ASX) N-terminal (ASXN) domain, ASX-middle (ASXM) domain, nuclear receptor coregulator binding (NR box) motif, plant homeo domain (PHD) of ASXL1, and isocitrate dehydrogenase superfamily (IDS) region of IDH1/2. Genomic sequencing of protein-coding regions and splice sites showed missense (black), nonsense (orange), and frameshift mutations (blue) in CBL, CBLB, TET2, ASXL1, IDH1, and IDH2 genes. All base pair changes identified occurred in a heterozygous constellation.

Distribution of mutations in tested genes in 10 patients with CML. Schematic representation shows the main domains, primarily the tyrosine kinase binding (TKB) domain, linker sequence (L), RING finger domain (RF), proline-rich region (PPP), and leucine zipper (LZ)/ubiquitin-associated domain (UBA) of the CBL family, cysteine (C)–rich domain, and double-stranded β helix (DSBH) domain of TET2, additional sex comb (ASX) N-terminal (ASXN) domain, ASX-middle (ASXM) domain, nuclear receptor coregulator binding (NR box) motif, plant homeo domain (PHD) of ASXL1, and isocitrate dehydrogenase superfamily (IDS) region of IDH1/2. Genomic sequencing of protein-coding regions and splice sites showed missense (black), nonsense (orange), and frameshift mutations (blue) in CBL, CBLB, TET2, ASXL1, IDH1, and IDH2 genes. All base pair changes identified occurred in a heterozygous constellation.

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