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Late relapses evolve from slow-responding subclones in t(12;21)-positive acute lymphoblastic leukemia: evidence for the persistence of a preleukemic clone.

Published byΑελλα Δημητρίου Modified over 5 years ago

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Presentation on theme: "Late relapses evolve from slow-responding subclones in t(12;21)-positive acute lymphoblastic leukemia: evidence for the persistence of a preleukemic clone."— Presentation transcript:

1 Late relapses evolve from slow-responding subclones in t(12;21)-positive acute lymphoblastic leukemia: evidence for the persistence of a preleukemic clone by Marianne Konrad, Markus Metzler, Simon Panzer, Iris Östreicher, Martina Peham, Reinald Repp, Oskar A. Haas, Helmut Gadner, and E. Renate Panzer-Grümayer Blood Volume 101(9): May 1, 2003 ©2003 by American Society of Hematology

2 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 diagno... 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. Marianne Konrad et al. Blood 2003;101: ©2003 by American Society of Hematology

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