Fig. 1.
Fig. 1. Response of individual subclones from TEL/AML1-positive leukemias to treatment. / The presence of the dominant leukemic clones and the relapse clones was analyzed by quantitative clone-specific PCR in diagnostic, follow-up (indicated by the months after diagnosis at which samples were obtained), and relapse bone marrow MNCs as described (see “Patients, materials, and methods”). ● indicates the dominant leukemic clone at diagnosis as detected by immune receptor rearrangements (patient 1 [pt 1]: IgH, TCRD; pt 2: IgHb, TCRDa, TCRGa); ▴ shows the relapse clone detected by immune receptor rearrangements (pt 1: TCRGa and b; pt 2: IgHd, TCRDb, TCRGb); filled symbols indicate a quantifiable amount of the clone (more than 5 × 10−5); open symbols indicate lack of detection; * indicates the amount of the TEL/AML1 genomic fusion gene as determined by patient-specific breakpoint PCRs.

Response of individual subclones from TEL/AML1-positive leukemias to treatment.

The presence of the dominant leukemic clones and the relapse clones was analyzed by quantitative clone-specific PCR in diagnostic, follow-up (indicated by the months after diagnosis at which samples were obtained), and relapse bone marrow MNCs as described (see “Patients, materials, and methods”). ● indicates the dominant leukemic clone at diagnosis as detected by immune receptor rearrangements (patient 1 [pt 1]: IgH, TCRD; pt 2: IgHb, TCRDa, TCRGa); ▴ shows the relapse clone detected by immune receptor rearrangements (pt 1: TCRGa and b; pt 2: IgHd, TCRDb, TCRGb); filled symbols indicate a quantifiable amount of the clone (more than 5 × 10−5); open symbols indicate lack of detection; * indicates the amount of the TEL/AML1 genomic fusion gene as determined by patient-specific breakpoint PCRs.

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