Figure 5
Figure 5. Detection of mutant ATP1A1 transcripts in CD34+ cells from IM nonresponders. (A) Structure of the ATP1A1 gene and location of 3 forward and reverse primer pairs used to generate 3 overlapping fragments for PCR amplification of the entire ATP1A1 transcript cDNA (3.7 kb). Frameshift mutations (in red) that generate new amino acid sequences and premature stop codons (*) within the ATP1A1 gene were identified in CD34+ CML cells from all 3 IM nonresponders studied. (B) Specific ATP1A1 mutations identified in the pretreatment CD34+ cells from the 3 IM nonresponders studied. The mutations detected within the BCR-ABL tyrosine kinase domain from the same patients' cells are also indicated.

Detection of mutant ATP1A1 transcripts in CD34+ cells from IM nonresponders. (A) Structure of the ATP1A1 gene and location of 3 forward and reverse primer pairs used to generate 3 overlapping fragments for PCR amplification of the entire ATP1A1 transcript cDNA (3.7 kb). Frameshift mutations (in red) that generate new amino acid sequences and premature stop codons (*) within the ATP1A1 gene were identified in CD34+ CML cells from all 3 IM nonresponders studied. (B) Specific ATP1A1 mutations identified in the pretreatment CD34+ cells from the 3 IM nonresponders studied. The mutations detected within the BCR-ABL tyrosine kinase domain from the same patients' cells are also indicated.

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