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L‐asparaginase treatment in acute lymphoblastic leukemia: A focus on Erwinia asparaginase
Open accessAbstract
Asparaginases are a cornerstone of treatment protocols for acute lymphoblastic leukemia (ALL) and are used for remission induction and intensification treatment in all pediatric regimens and in the majority of adult treatment protocols. Extensive clinical data have shown that intensive asparaginase treatment improves clinical outcomes in childhood ALL. Three asparaginase preparations are available: the native asparaginase derived from Escherichia coli (E. coli asparaginase), a pegylated form of this enzyme (PEG-asparaginase), and a product isolated from Erwinia chrysanthemi, ie, Erwinia asparaginase. Clinical hypersensitivity reactions and silent inactivation due to antibodies against E. coli asparaginase, lead to inactivation of E. coli asparaginase in up to 60% of cases. Current treatment protocols include E. coli asparaginase or PEG-asparaginase for first-line treatment of ALL. Typically, patients exhibiting sensitivity to one formulation of asparaginase are switched to another to ensure they receive the most efficacious treatment regimen possible. Erwinia asparaginase is used as a second- or third-line treatment in European and US protocols. Despite the universal inclusion of asparaginase in such treatment protocols, debate on the optimal formulation and dosage of these agents continues. This article provides an overview of available evidence for optimal use of Erwinia asparaginase in the treatment of ALL.
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“Depletion of plasma asparagine by a recombinant form of bacterial L-Asparaginase is an effective anticancer intervention for this cancer type (Hill et al., 1967; Pieters et al., 2011).”
From The emerging hallmarks of cancer metabolism (2016) · cites this paper as Pieters et al., 2011
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Self-citationTreating Childhood Acute Lymphoblastic Leukemia without Cranial Irradiation
Pui, C.-H., Campana, D., Pei, D., Bowman, W. P., Sandlund, J. T., Kaste, S. C., Ribeiro, R. C., Rubnitz, J. E., Raimondi, S. C., Onciu, M., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0900386 · Cited by 1,215
Self-citationSilverman, L. B. (2001) · Blood · doi:10.1182/blood.v97.5.1211 · Cited by 869
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Self-citationBoissel, N., Auclerc, M.-F., Lhéritier, V., Pérel, Y., Thomas, X., Leblanc, T. M., Rousselot, P. H., Cayuela, J., Gabert, J. A., Fegueux, N., et al. (2003) · Journal of Clinical Oncology · doi:10.1200/jco.2003.02.053 · Cited by 606
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Pui, C., Sandlund, J. T., Pei, D., Campana, D., Rivera, G. K., Ribeiro, R. C., Rubnitz, J. E., Razzouk, B. I., Howard, S. C., Hudson, M. M., et al. (2004) · Blood · doi:10.1182/blood-2004-04-1616 · Cited by 461
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The emerging hallmarks of cancer metabolism
Pavlova, N. N., & Thompson, C. B. (2016) · Cell Metabolism · doi:10.1016/j.cmet.2015.12.006 · Cited by 5,926
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Childhood Acute Lymphoblastic Leukemia: Progress Through Collaboration
Pui, C., Yang, J. J. J., Hunger, S. P., Pieters, R., Schrappe, M., Biondi, A., Vora, A. J., Baruchel, A., Silverman, L. B., Schmiegelow, K., et al. (2015) · Journal of Clinical Oncology · doi:10.1200/jco.2014.59.1636 · Cited by 1,016
Self-citationSurviving Stress: Modulation of ATF4-Mediated Stress Responses in Normal and Malignant Cells
Wortel, I. M. N., van der Meer, L. T., Kilberg, M. S., & van Leeuwen, F. N. (2017) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2017.07.003 · Cited by 630
Metadata
- Authors
- Pieters, R., Hunger, S. P., Boos, J., Rizzari, C., Silverman, L., Baruchel, A., Goekbuget, N., Schrappe, M., & Pui, C.
- Affiliations
- St. Jude Children's Research Hospital (US)
- Children's Hospital Colorado (US)
- University of Münster (DE)
- Azienda Ospedaliera San Gerardo (IT)
- Boston Children's Hospital (US)
- University Hospital Frankfurt (DE)
- University Hospital Schleswig-Holstein (DE)
- Corresponding author
- Pieters, Rob
- Pui, Ching‐Hon
- ORCID
- Venue
- Cancer
- Publisher
- Wiley
- Published
- 2010-09-07
- Volume
- 117
- Issue
- 2
- Pages
- 238-249
- ISSN
- 0008-543X (ISSN-L)
- 1097-0142
- PMC
- PMC3000881
- OpenAlex
- W1965542498
- Cited by
- 569
- References
- 74
- Citations by year
- 2026: 17 · 2025: 25 · 2024: 35 · 2023: 38 · 2022: 49 · 2021: 53 · 2020: 56 · 2019: 43 · 2018: 41 · 2017: 41 · 2016: 39 · 2015: 37 · 2014: 42 · 2013: 28 · 2012: 18
- FWCI
- 2.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cancer (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- RePub (Erasmus University Rotterdam) (submittedVersion, other-oa)
- Funders
- National Cancer Institute (CA21765, P01CA020180, P30CA021765)
- Topics
- Health Sciences › Medicine › Hematology › Acute Lymphoblastic Leukemia research
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Keywords
- L-asparaginase, acute lymphoblastic leukemia, PEG-asparaginase, pediatric leukemia, treatment protocols, dose optimization
- MeSH terms
- Asparaginase, Drug Combinations, Drug Hypersensitivity, Erwinia, Humans, Spironolactone, Sulfonamides, Drug Monitoring, Precursor Cell Lymphoblastic Leukemia-Lymphoma
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