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Table 1 List of the non-clonal mutations identified in the BCR-ABL1 fusion gene from imatinib-resistant K562 clones

From: The RNA editing enzyme APOBEC1 induces somatic mutations and a compatible mutational signature is present in esophageal adenocarcinomas

Samples Position AA change Codon change Sequence context
  1,503 E495G GAA > GGA  
Control 1,472 R491Q CGG > CAG GCCGG
  1,503 Silent TTT > TTC  
  633 G100C GGC > TGC GCCTA
AID 395 Silent AAA > AAG  
  568 G190D GGC > GAC TGCCA
  633 T212A ACG > GCG  
  987 G155D GGC > GAC GGCCA
  607 L203M CTG > ATG CCCTG
Rat APOBEC1 613 E205K GAG > AAG CTCGG
  764 K255T AAG > ACG  
  987 Silent GGG > GGT TTCCC
  1,245 silent AGC > AGT AGCCG
  758 R253H CGC > CAC TGCGC
  841* silent CTG > TTG AGCTG
  697 H233D CAT > GAT TTCAT
Human APOBEC1 699 H233D CAT > GAC  
  1,149* Silent GCC > GCA GCCAT
  1,245* F415L TTT > TTG  
  1. The region analyzed (encompassing exon 13 of BCR and exon 9 of ABL1) includes the imatinib-binding region of the fusion gene. The asterisk indicates mutations found in the same clone. The local sequence context for the mutations at cytosines is shown. Compared to the AID-induced mutations found in previous reports (mutations in approximately 30% of the sequences) [41],[42], we found approximately one mutation in each of the clones analyzed. This is explained by the different procedures we used to select resistant clones: whereas the other studies focused on competing bulk populations of AID-transfected GFP(+) cells and control GFP(−) cells, we analyzed individual clones arising from the same number of cells plated in the presence of imatinib.