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Sensitivity to L-asparaginase is not associated with expression levels of asparagine synthetase in t(12;21)+ pediatric ALL
Open accessAbstract
The (12;21) translocation resulting in TEL/AML1 gene fusion is present in about 25% of childhood precursor B-lineage acute lymphoblastic leukemia (ALL) and is associated with a good prognosis and a high cellular sensitivity to L-asparaginase (L-Asp). ALL cells are thought to be sensitive to L-Asp due to lower asparagine synthetase (AS) levels. Resistance to L-Asp may be caused by an elevated cellular level of AS or by the ability of resistant cells to rapidly induce the expression of the AS gene on L-Asp exposure. AS may be a target regulated by t(12;21). We studied the relationship between t(12;21) and the mRNA level of AS to investigate a possible mechanism underlying L-Asp sensitivity. Real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis surprisingly revealed that 30 patients positive for t(12;21) expressed 5-fold more AS mRNA compared with 17 patients negative for t(12;21) (P =.008) and 11 samples from healthy controls (P =.016). The mRNA levels of AS between t(12;21)(-) ALL and healthy controls did not differ. No difference was found between ALL patients positive or negative for t(12;21) in the capacity to up-regulate AS after in vitro L-Asp exposure, excluding a defective capacity for t(12;21) cells in up-regulating AS on L-Asp exposure. Moreover, no correlation was observed between AS mRNA expression and sensitivity to L-Asp. We conclude that the sensitivity of t(12;21)(+) childhood ALL to L-Asp is not associated with the expression level of the AS gene. Furthermore, we contradict the general thought that leukemic cells specifically lack AS compared with normal bone marrow and blood cells.
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“Though the mechanism of asparagine auxotrophy in ALL cells was assumed to be genetically defined, studies have shown that clinical response to L-asparaginase treatment is independent of asparagine synthase (ASNS) expression, the enzyme that converts aspartate to asparagine (Figure 7) (Appel et al., 2006; Stams et al., 2003).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Stams et al., 2003
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The t(12;21) Translocation Converts AML-1B from an Activator to a Repressor of Transcription
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TEL-AML1 Fusion Transcript in Relapsed Childhood Acute Lymphoblastic Leukemia
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Pharmacological and clinical evaluation of l-asparaginase in the treatment of leukemia
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Metadata
- Authors
- Stams, W. A. G.
- Affiliations
- Erasmus MC (NL)
- Corresponding author
- Stams, W. A. G.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2002-11-14
- Volume
- 101
- Issue
- 7
- Pages
- 2743-2747
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2149324701
- Cited by
- 149
- References
- 35
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 5 · 2023: 8 · 2022: 6 · 2021: 6 · 2020: 3 · 2019: 7 · 2018: 7 · 2017: 10 · 2016: 6 · 2015: 4 · 2014: 7 · 2013: 6 · 2012: 11
- FWCI
- 6.97
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion, other-oa)
- RePub (Erasmus University Rotterdam) (submittedVersion, other-oa)
- RePub (Erasmus University Rotterdam) (submittedVersion)
- Funders
- Fondation pour la Recherche Médicale
- Topics
- Health Sciences › Medicine › Hematology › Acute Lymphoblastic Leukemia research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Keywords
- L-asparaginase, asparagine synthetase, TEL-AML1 fusion, childhood acute lymphoblastic leukemia, B-lineage ALL, drug sensitivity, gene expression, chemoresistance
- MeSH terms
- Asparaginase, Aspartate-Ammonia Ligase, Child, Child, Preschool, Chromosomes, Human, Pair 12, Chromosomes, Human, Pair 21, Humans, Infant, RNA, Messenger, Translocation, Genetic, Leukemia, Lymphocytic, Chronic, B-Cell, Up-Regulation, Case-Control Studies, Precursor Cell Lymphoblastic Leukemia-Lymphoma
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