BCR-ABL1 mutations in K562 cells
| Construct transduced | Treatment | BCR-ABL1 sequence analysis | Number of clones/total | Amino acid change |
| GFP | Imatinib | Unmutated | 6/8 | No changes |
| 894 CTA to CTG | 1/8 | Silent | ||
| 1062 CTA to CTG | 1/8 | Silent | ||
| AID-ires-GFP | Control | Unmutated | 7/9 | No changes |
| 894 CTA to CTG | 1/9 | Silent | ||
| 1062 CTA to CTG | 1/9 | Silent | ||
| AID-ires-GFP | Imatinib | Unmutated | 2/10 | No changes |
| 894 CTA to CTG | 3/10 | Silent | ||
| 944 ACT to ATT | 4/10 | T315I | ||
| 1062 CTA to CTG | 2/10 | Silent | ||
| 1334/1335 CGT to CTG | 1/10 | R445L | ||
| 1356 CTA to CTG | 2/10 | Silent | ||
| 1375 GAG to AAG | 3/10 | E459K | ||
| AID-ires-GFP | Imatinib + 17-AAG | Unmutated | 6/9 | No changes |
| 894 CTA to CTG | 1/9 | Silent | ||
| 1062 CTA to CTG | 2/9 | Silent |
| Construct transduced | Treatment | BCR-ABL1 sequence analysis | Number of clones/total | Amino acid change |
| GFP | Imatinib | Unmutated | 6/8 | No changes |
| 894 CTA to CTG | 1/8 | Silent | ||
| 1062 CTA to CTG | 1/8 | Silent | ||
| AID-ires-GFP | Control | Unmutated | 7/9 | No changes |
| 894 CTA to CTG | 1/9 | Silent | ||
| 1062 CTA to CTG | 1/9 | Silent | ||
| AID-ires-GFP | Imatinib | Unmutated | 2/10 | No changes |
| 894 CTA to CTG | 3/10 | Silent | ||
| 944 ACT to ATT | 4/10 | T315I | ||
| 1062 CTA to CTG | 2/10 | Silent | ||
| 1334/1335 CGT to CTG | 1/10 | R445L | ||
| 1356 CTA to CTG | 2/10 | Silent | ||
| 1375 GAG to AAG | 3/10 | E459K | ||
| AID-ires-GFP | Imatinib + 17-AAG | Unmutated | 6/9 | No changes |
| 894 CTA to CTG | 1/9 | Silent | ||
| 1062 CTA to CTG | 2/9 | Silent |
Identity of the mutations indicated in the diagram in Fig. 7 E. The BCR-ABL1 (exon 13 of BCR and exon 9 of ABL1) was RT-PCR amplified from single cell clones, and a fragment of ∼700 bp in the ABL1 kinase domain was directly sequenced. The number to the left of the mutation indicates the mutated position with respect to the ABL1 open reading frame. The mutated base is underlined within the affected codon. Mutations at C:G pairs and amino acid substitutions previously described to confer clinical imatinib resistance (Branford and Hughes, 2006) are highlighted in bold.