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Relapse risk following truncation of pegylated asparaginase in childhood acute lymphoblastic leukemia

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Harvard

Gottschalk Højfeldt, S, Grell, K, Abrahamsson, J, Lund, B, Vettenranta, K, Jonsson, OG, Frandsen, TL, Wolthers, BO, Marquart, HVH, Vaitkeviciene, G, Lepik, K, Heyman, M, Schmiegelow, K & Albertsen, BK 2021, 'Relapse risk following truncation of pegylated asparaginase in childhood acute lymphoblastic leukemia', Blood, bind 137, nr. 17, s. 2373-2382. https://doi.org/10.1182/blood.2020006583

APA

Gottschalk Højfeldt, S., Grell, K., Abrahamsson, J., Lund, B., Vettenranta, K., Jonsson, O. G., Frandsen, T. L., Wolthers, B. O., Marquart, H. V. H., Vaitkeviciene, G., Lepik, K., Heyman, M., Schmiegelow, K., & Albertsen, B. K. (2021). Relapse risk following truncation of pegylated asparaginase in childhood acute lymphoblastic leukemia. Blood, 137(17), 2373-2382. https://doi.org/10.1182/blood.2020006583

CBE

Gottschalk Højfeldt S, Grell K, Abrahamsson J, Lund B, Vettenranta K, Jonsson OG, Frandsen TL, Wolthers BO, Marquart HVH, Vaitkeviciene G, Lepik K, Heyman M, Schmiegelow K, Albertsen BK. 2021. Relapse risk following truncation of pegylated asparaginase in childhood acute lymphoblastic leukemia. Blood. 137(17):2373-2382. https://doi.org/10.1182/blood.2020006583

MLA

Vancouver

Gottschalk Højfeldt S, Grell K, Abrahamsson J, Lund B, Vettenranta K, Jonsson OG o.a. Relapse risk following truncation of pegylated asparaginase in childhood acute lymphoblastic leukemia. Blood. 2021 apr 29;137(17):2373-2382. https://doi.org/10.1182/blood.2020006583

Author

Gottschalk Højfeldt, Sofie ; Grell, Kathrine ; Abrahamsson, Jonas ; Lund, Bendik ; Vettenranta, Kim ; Jonsson, Olafur G ; Frandsen, Thomas Leth ; Wolthers, Benjamin Ole ; Marquart, Hanne Vibeke Hansen ; Vaitkeviciene, Goda ; Lepik, Kristi ; Heyman, Mats ; Schmiegelow, Kjeld ; Albertsen, Birgitte Klug. / Relapse risk following truncation of pegylated asparaginase in childhood acute lymphoblastic leukemia. I: Blood. 2021 ; Bind 137, Nr. 17. s. 2373-2382.

Bibtex

@article{5d608fc34c4c4b1f9600869a2b583fcf,
title = "Relapse risk following truncation of pegylated asparaginase in childhood acute lymphoblastic leukemia",
abstract = "Truncation of asparaginase treatment due to asparaginase-related toxicities or silent inactivation (SI) is common and may increase relapse risk in acute lymphoblastic leukemia (ALL). We investigated relapse risk following suboptimal asparaginase exposure among 1401 children aged 1 to 17 years, diagnosed with ALL between July 2008 and February 2016, treated according to the Nordic Society of Pediatric Hematology and Oncology (NOPHO) ALL2008 protocol (including extended asparaginase exposure [1000 IU/m2 intramuscularly weeks 5-33]). Patients were included with delayed entry at their last administered asparaginase treatment, or detection of SI, and followed until relapse, death, secondary malignancy, or end of follow-up (median, 5.71 years; interquartile range, 4.02-7.64). In a multiple Cox model comparing patients with (n = 358) and without (n = 1043) truncated asparaginase treatment due to clinical toxicity, the adjusted relapse-specific hazard ratio (HR; aHR) was 1.33 (95% confidence interval [CI], 0.86-2.06; P = .20). In a substudy including only patients with information on enzyme activity (n = 1115), the 7-year cumulative incidence of relapse for the 301 patients with truncation of asparaginase treatment or SI (157 hypersensitivity, 53 pancreatitis, 14 thrombosis, 31 other, 46 SI) was 11.1% (95% CI, 6.9-15.4) vs 6.7% (95% CI, 4.7-8.6) for the 814 remaining patients. The relapse-specific aHR was 1.69 (95% CI, 1.05-2.74, P=.03). The unadjusted bone marrow relapse-specific HR was 1.83 (95% CI, 1.07-3.14, P=.03) and 1.86 (95% CI, 0.90- 3.87, P=.095) for any central nervous system relapse. These results emphasize the importance of therapeutic drug monitoring and appropriate adjustment of asparaginase therapy when feasible. This trial was registered at www.clinicaltrials.gov as #NCT03987542.",
author = "{Gottschalk H{\o}jfeldt}, Sofie and Kathrine Grell and Jonas Abrahamsson and Bendik Lund and Kim Vettenranta and Jonsson, {Olafur G} and Frandsen, {Thomas Leth} and Wolthers, {Benjamin Ole} and Marquart, {Hanne Vibeke Hansen} and Goda Vaitkeviciene and Kristi Lepik and Mats Heyman and Kjeld Schmiegelow and Albertsen, {Birgitte Klug}",
note = "{\textcopyright} 2021 by The American Society of Hematology.",
year = "2021",
month = apr,
day = "29",
doi = "10.1182/blood.2020006583",
language = "English",
volume = "137",
pages = "2373--2382",
journal = "Blood",
issn = "0006-4971",
publisher = "American Society of Hematology",
number = "17",

}

RIS

TY - JOUR

T1 - Relapse risk following truncation of pegylated asparaginase in childhood acute lymphoblastic leukemia

AU - Gottschalk Højfeldt, Sofie

AU - Grell, Kathrine

AU - Abrahamsson, Jonas

AU - Lund, Bendik

AU - Vettenranta, Kim

AU - Jonsson, Olafur G

AU - Frandsen, Thomas Leth

AU - Wolthers, Benjamin Ole

AU - Marquart, Hanne Vibeke Hansen

AU - Vaitkeviciene, Goda

AU - Lepik, Kristi

AU - Heyman, Mats

AU - Schmiegelow, Kjeld

AU - Albertsen, Birgitte Klug

N1 - © 2021 by The American Society of Hematology.

PY - 2021/4/29

Y1 - 2021/4/29

N2 - Truncation of asparaginase treatment due to asparaginase-related toxicities or silent inactivation (SI) is common and may increase relapse risk in acute lymphoblastic leukemia (ALL). We investigated relapse risk following suboptimal asparaginase exposure among 1401 children aged 1 to 17 years, diagnosed with ALL between July 2008 and February 2016, treated according to the Nordic Society of Pediatric Hematology and Oncology (NOPHO) ALL2008 protocol (including extended asparaginase exposure [1000 IU/m2 intramuscularly weeks 5-33]). Patients were included with delayed entry at their last administered asparaginase treatment, or detection of SI, and followed until relapse, death, secondary malignancy, or end of follow-up (median, 5.71 years; interquartile range, 4.02-7.64). In a multiple Cox model comparing patients with (n = 358) and without (n = 1043) truncated asparaginase treatment due to clinical toxicity, the adjusted relapse-specific hazard ratio (HR; aHR) was 1.33 (95% confidence interval [CI], 0.86-2.06; P = .20). In a substudy including only patients with information on enzyme activity (n = 1115), the 7-year cumulative incidence of relapse for the 301 patients with truncation of asparaginase treatment or SI (157 hypersensitivity, 53 pancreatitis, 14 thrombosis, 31 other, 46 SI) was 11.1% (95% CI, 6.9-15.4) vs 6.7% (95% CI, 4.7-8.6) for the 814 remaining patients. The relapse-specific aHR was 1.69 (95% CI, 1.05-2.74, P=.03). The unadjusted bone marrow relapse-specific HR was 1.83 (95% CI, 1.07-3.14, P=.03) and 1.86 (95% CI, 0.90- 3.87, P=.095) for any central nervous system relapse. These results emphasize the importance of therapeutic drug monitoring and appropriate adjustment of asparaginase therapy when feasible. This trial was registered at www.clinicaltrials.gov as #NCT03987542.

AB - Truncation of asparaginase treatment due to asparaginase-related toxicities or silent inactivation (SI) is common and may increase relapse risk in acute lymphoblastic leukemia (ALL). We investigated relapse risk following suboptimal asparaginase exposure among 1401 children aged 1 to 17 years, diagnosed with ALL between July 2008 and February 2016, treated according to the Nordic Society of Pediatric Hematology and Oncology (NOPHO) ALL2008 protocol (including extended asparaginase exposure [1000 IU/m2 intramuscularly weeks 5-33]). Patients were included with delayed entry at their last administered asparaginase treatment, or detection of SI, and followed until relapse, death, secondary malignancy, or end of follow-up (median, 5.71 years; interquartile range, 4.02-7.64). In a multiple Cox model comparing patients with (n = 358) and without (n = 1043) truncated asparaginase treatment due to clinical toxicity, the adjusted relapse-specific hazard ratio (HR; aHR) was 1.33 (95% confidence interval [CI], 0.86-2.06; P = .20). In a substudy including only patients with information on enzyme activity (n = 1115), the 7-year cumulative incidence of relapse for the 301 patients with truncation of asparaginase treatment or SI (157 hypersensitivity, 53 pancreatitis, 14 thrombosis, 31 other, 46 SI) was 11.1% (95% CI, 6.9-15.4) vs 6.7% (95% CI, 4.7-8.6) for the 814 remaining patients. The relapse-specific aHR was 1.69 (95% CI, 1.05-2.74, P=.03). The unadjusted bone marrow relapse-specific HR was 1.83 (95% CI, 1.07-3.14, P=.03) and 1.86 (95% CI, 0.90- 3.87, P=.095) for any central nervous system relapse. These results emphasize the importance of therapeutic drug monitoring and appropriate adjustment of asparaginase therapy when feasible. This trial was registered at www.clinicaltrials.gov as #NCT03987542.

UR - http://www.scopus.com/inward/record.url?scp=85105617052&partnerID=8YFLogxK

U2 - 10.1182/blood.2020006583

DO - 10.1182/blood.2020006583

M3 - Journal article

C2 - 33150360

VL - 137

SP - 2373

EP - 2382

JO - Blood

JF - Blood

SN - 0006-4971

IS - 17

ER -

ID: 61695792