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Measurable residual disease monitoring in acute myeloid leukemia with t(8;21)(q22;q22.1): results from the AML Study Group

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Measurable residual disease monitoring in acute myeloid leukemia with t(8;21)(q22;q22.1): results from the AML Study Group. / Rücker, Frank G; Agrawal, Mridul; Corbacioglu, Andrea; Weber, Daniela; Kapp-Schwoerer, Silke; Gaidzik, Verena I; Jahn, Nikolaus; Schroeder, Thomas; Wattad, Mohammed; Lübbert, Michael; Koller, Elisabeth; Kindler, Thomas; Götze, Katharina; Ringhoffer, Mark; Westermann, Jörg; Fiedler, Walter; Horst, Heinz A; Greil, Richard; Schroers, Roland; Mayer, Karin; Heinicke, Thomas; Krauter, Jürgen; Schlenk, Richard F; Thol, Felicitas; Heuser, Michael; Ganser, Arnold; Bullinger, Lars; Paschka, Peter; Döhner, Hartmut; Döhner, Konstanze.

In: BLOOD, Vol. 134, No. 19, 07.11.2019, p. 1608-1618.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Rücker, FG, Agrawal, M, Corbacioglu, A, Weber, D, Kapp-Schwoerer, S, Gaidzik, VI, Jahn, N, Schroeder, T, Wattad, M, Lübbert, M, Koller, E, Kindler, T, Götze, K, Ringhoffer, M, Westermann, J, Fiedler, W, Horst, HA, Greil, R, Schroers, R, Mayer, K, Heinicke, T, Krauter, J, Schlenk, RF, Thol, F, Heuser, M, Ganser, A, Bullinger, L, Paschka, P, Döhner, H & Döhner, K 2019, 'Measurable residual disease monitoring in acute myeloid leukemia with t(8;21)(q22;q22.1): results from the AML Study Group', BLOOD, vol. 134, no. 19, pp. 1608-1618. https://doi.org/10.1182/blood.2019001425

APA

Rücker, F. G., Agrawal, M., Corbacioglu, A., Weber, D., Kapp-Schwoerer, S., Gaidzik, V. I., Jahn, N., Schroeder, T., Wattad, M., Lübbert, M., Koller, E., Kindler, T., Götze, K., Ringhoffer, M., Westermann, J., Fiedler, W., Horst, H. A., Greil, R., Schroers, R., ... Döhner, K. (2019). Measurable residual disease monitoring in acute myeloid leukemia with t(8;21)(q22;q22.1): results from the AML Study Group. BLOOD, 134(19), 1608-1618. https://doi.org/10.1182/blood.2019001425

Vancouver

Rücker FG, Agrawal M, Corbacioglu A, Weber D, Kapp-Schwoerer S, Gaidzik VI et al. Measurable residual disease monitoring in acute myeloid leukemia with t(8;21)(q22;q22.1): results from the AML Study Group. BLOOD. 2019 Nov 7;134(19):1608-1618. https://doi.org/10.1182/blood.2019001425

Bibtex

@article{12b3572995634ed5b0a77bc5ef9dbf03,
title = "Measurable residual disease monitoring in acute myeloid leukemia with t(8;21)(q22;q22.1): results from the AML Study Group",
abstract = "We performed serial measurable residual disease (MRD) monitoring in bone marrow (BM) and peripheral blood (PB) samples of 155 intensively treated patients with RUNX1-RUNX1T1+ AML, using a qRT-PC-based assay with a sensitivity of up to 10-6. We assessed both reduction of RUNX1-RUNX1T1 transcript levels (TLs) and achievement of MRD negativity (MRD-) for impact on prognosis. Achievement of MR2.5 (>2.5 log reduction) after treatment cycle 1 and achievement of MR3.0 after treatment cycle 2 were significantly associated with a reduced risk of relapse (P = .034 and P = .028, respectively). After completion of therapy, achievement of MRD- in both BM and PB was an independent, favorable prognostic factor in cumulative incidence of relapse (4-year cumulative incidence relapse: BM, 17% vs 36%, P = .021; PB, 23% vs 55%, P = .001) and overall survival (4-year overall survival rate BM, 93% vs 70%, P = .007; PB, 87% vs 47%, P < .0001). Finally, during follow-up, serial qRT-PCR analyses allowed prediction of relapse in 77% of patients exceeding a cutoff value of 150 RUNX1-RUNX1T1 TLs in BM, and in 84% of patients exceeding a value of 50 RUNX1-RUNX1T1 TLs in PB. The KIT mutation was a significant factor predicting a lower CR rate and inferior outcome, but its prognostic impact was outweighed by RUNX1-RUNX1T1 TLs during treatment. Virtually all relapses occurred within 1 year after the end of treatment, with a very short latency from molecular to morphologic relapse, necessitating MRD assessment at short intervals during this time period. Based on our data, we propose a refined practical guideline for MRD assessment in RUNX1-RUNX1T1+ AML.",
author = "R{\"u}cker, {Frank G} and Mridul Agrawal and Andrea Corbacioglu and Daniela Weber and Silke Kapp-Schwoerer and Gaidzik, {Verena I} and Nikolaus Jahn and Thomas Schroeder and Mohammed Wattad and Michael L{\"u}bbert and Elisabeth Koller and Thomas Kindler and Katharina G{\"o}tze and Mark Ringhoffer and J{\"o}rg Westermann and Walter Fiedler and Horst, {Heinz A} and Richard Greil and Roland Schroers and Karin Mayer and Thomas Heinicke and J{\"u}rgen Krauter and Schlenk, {Richard F} and Felicitas Thol and Michael Heuser and Arnold Ganser and Lars Bullinger and Peter Paschka and Hartmut D{\"o}hner and Konstanze D{\"o}hner",
note = "{\textcopyright} 2019 by The American Society of Hematology.",
year = "2019",
month = nov,
day = "7",
doi = "10.1182/blood.2019001425",
language = "English",
volume = "134",
pages = "1608--1618",
journal = "BLOOD",
issn = "0006-4971",
publisher = "American Society of Hematology",
number = "19",

}

RIS

TY - JOUR

T1 - Measurable residual disease monitoring in acute myeloid leukemia with t(8;21)(q22;q22.1): results from the AML Study Group

AU - Rücker, Frank G

AU - Agrawal, Mridul

AU - Corbacioglu, Andrea

AU - Weber, Daniela

AU - Kapp-Schwoerer, Silke

AU - Gaidzik, Verena I

AU - Jahn, Nikolaus

AU - Schroeder, Thomas

AU - Wattad, Mohammed

AU - Lübbert, Michael

AU - Koller, Elisabeth

AU - Kindler, Thomas

AU - Götze, Katharina

AU - Ringhoffer, Mark

AU - Westermann, Jörg

AU - Fiedler, Walter

AU - Horst, Heinz A

AU - Greil, Richard

AU - Schroers, Roland

AU - Mayer, Karin

AU - Heinicke, Thomas

AU - Krauter, Jürgen

AU - Schlenk, Richard F

AU - Thol, Felicitas

AU - Heuser, Michael

AU - Ganser, Arnold

AU - Bullinger, Lars

AU - Paschka, Peter

AU - Döhner, Hartmut

AU - Döhner, Konstanze

N1 - © 2019 by The American Society of Hematology.

PY - 2019/11/7

Y1 - 2019/11/7

N2 - We performed serial measurable residual disease (MRD) monitoring in bone marrow (BM) and peripheral blood (PB) samples of 155 intensively treated patients with RUNX1-RUNX1T1+ AML, using a qRT-PC-based assay with a sensitivity of up to 10-6. We assessed both reduction of RUNX1-RUNX1T1 transcript levels (TLs) and achievement of MRD negativity (MRD-) for impact on prognosis. Achievement of MR2.5 (>2.5 log reduction) after treatment cycle 1 and achievement of MR3.0 after treatment cycle 2 were significantly associated with a reduced risk of relapse (P = .034 and P = .028, respectively). After completion of therapy, achievement of MRD- in both BM and PB was an independent, favorable prognostic factor in cumulative incidence of relapse (4-year cumulative incidence relapse: BM, 17% vs 36%, P = .021; PB, 23% vs 55%, P = .001) and overall survival (4-year overall survival rate BM, 93% vs 70%, P = .007; PB, 87% vs 47%, P < .0001). Finally, during follow-up, serial qRT-PCR analyses allowed prediction of relapse in 77% of patients exceeding a cutoff value of 150 RUNX1-RUNX1T1 TLs in BM, and in 84% of patients exceeding a value of 50 RUNX1-RUNX1T1 TLs in PB. The KIT mutation was a significant factor predicting a lower CR rate and inferior outcome, but its prognostic impact was outweighed by RUNX1-RUNX1T1 TLs during treatment. Virtually all relapses occurred within 1 year after the end of treatment, with a very short latency from molecular to morphologic relapse, necessitating MRD assessment at short intervals during this time period. Based on our data, we propose a refined practical guideline for MRD assessment in RUNX1-RUNX1T1+ AML.

AB - We performed serial measurable residual disease (MRD) monitoring in bone marrow (BM) and peripheral blood (PB) samples of 155 intensively treated patients with RUNX1-RUNX1T1+ AML, using a qRT-PC-based assay with a sensitivity of up to 10-6. We assessed both reduction of RUNX1-RUNX1T1 transcript levels (TLs) and achievement of MRD negativity (MRD-) for impact on prognosis. Achievement of MR2.5 (>2.5 log reduction) after treatment cycle 1 and achievement of MR3.0 after treatment cycle 2 were significantly associated with a reduced risk of relapse (P = .034 and P = .028, respectively). After completion of therapy, achievement of MRD- in both BM and PB was an independent, favorable prognostic factor in cumulative incidence of relapse (4-year cumulative incidence relapse: BM, 17% vs 36%, P = .021; PB, 23% vs 55%, P = .001) and overall survival (4-year overall survival rate BM, 93% vs 70%, P = .007; PB, 87% vs 47%, P < .0001). Finally, during follow-up, serial qRT-PCR analyses allowed prediction of relapse in 77% of patients exceeding a cutoff value of 150 RUNX1-RUNX1T1 TLs in BM, and in 84% of patients exceeding a value of 50 RUNX1-RUNX1T1 TLs in PB. The KIT mutation was a significant factor predicting a lower CR rate and inferior outcome, but its prognostic impact was outweighed by RUNX1-RUNX1T1 TLs during treatment. Virtually all relapses occurred within 1 year after the end of treatment, with a very short latency from molecular to morphologic relapse, necessitating MRD assessment at short intervals during this time period. Based on our data, we propose a refined practical guideline for MRD assessment in RUNX1-RUNX1T1+ AML.

U2 - 10.1182/blood.2019001425

DO - 10.1182/blood.2019001425

M3 - SCORING: Journal article

C2 - 31554635

VL - 134

SP - 1608

EP - 1618

JO - BLOOD

JF - BLOOD

SN - 0006-4971

IS - 19

ER -