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l asparagine/leukemia
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Levels of L-asparagine in CSF after intramuscular administration of asparaginase from Erwinia in children with acute lymphoblastic leukemia.
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OBJECTIVE
As part of a study on the pharmacokinetics associated with the administration of asparaginase (ASNase) from Erwinia to the CNS, we determined the levels of asparagine in the CSF of children with acute lymphoblastic leukemia (ALL).
METHODS
Twenty children received eight standard doses of
L-Asparagine depletion in plasma and cerebro-spinal fluid of children with acute lymphoblastic leukemia during subsequent exposures to Erwinia L-asparaginase.
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BACKGROUND
Monitoring L-asparagine (L-ASN) plasma levels could provide information useful for determining whether the dosage or schedule of L-asparaginase (L-ASE) administration is adequate. Very few data are available on depletion caused by the Erwinia chrysanthemi (E. chrysanthemi) product. Since
L-asparagine depletion and L-asparaginase activity in children with acute lymphoblastic leukemia receiving i.m. or i.v. Erwinia C. or E. coli L-asparaginase as first exposure.
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OBJECTIVE
The present study was aimed at investigating L-asparaginase (L-ASE) activity (in plasma) and L-asparagine (L-ASN) depletion (in plasma and CSF) in children with newly diagnosed acute lymphoblastic leukemia (ALL) exposed for the first time to different L-ASE products.
METHODS
During the
An isocratic fluorescence HPLC assay for the monitoring of l-asparaginase activity and l-asparagine depletion in children receiving E. colil-asparaginase for the treatment of acute lymphoblastic leukaemia.
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A novel assay for the determination of l-asparaginase activity in human plasma is described that is based on the HPLC quantitation of l-aspartic acid produced during enzyme incubation. Methods for monitoring l-asparagine depletion are also described. Chromatography of l-aspartic acid, l-asparagine
L-Asparagine depletion levels and L-asparaginase activity in plasma of children with acute lymphoblastic leukemia under asparaginase treatment.
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OBJECTIVE
To determine the minimum levels of L-asparaginase (ASNase) activity necessary to maintain L-asparagine (Asn) depletion under ASNase treatment in acute lymphoblastic leukemia (ALL).
METHODS
We measured ASNase activity using an enzyme coupling method with a limit of detection of 2 U/l and
The anti-asparagines antibodies correlate with L-asparagines activity and may affect clinical outcome of childhood acute lymphoblastic leukemia.
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The primary aim of the study was to evaluate the importance of anti-asparaginase antibodies for l-asparaginase activity in children with standard and medium risk acute lymphoblastic leukemia (ALL). Forty-seven children with newly diagnosed ALL were included into the prospective study. Enzyme
L-asparagine and leukemia.
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Amino acid dependent cancers: L-asparagine in leukemia.
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The requirement for L-asparagine of mouse leukemia cells L5178Y in culture.
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Depletion of L-asparagine supply and apoptosis of leukemia cells induced by human glycosylasparaginase.
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Characterization of polyethylene glycol-modified L-asparaginase from Escherichia coli and its application to therapy of leukemia.
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For the purpose of clinical application to the therapy of human leukemia and lymphosarcoma, L-asparaginase from Escherichia coli was modified with 2,4-bis(O-methoxypolyethylene glycol)-6-chloro-s-triazine (activated PEG2) by an improved method, which involves a purification step of activated PEG2 by
L-Asparagine synthetase in serum as a marker for neoplasia.
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L-Asparagine synthetase appears in serum approximately 7 days after the s.c. implantation of 1 X 10(5) cells of Leukemia 5178Y/AR (resistant to L-asparaginase) and increases in activity as the neoplasm grows and metastasizes. The principal source of the enzyme is the primary tumor. After
Determination of L-asparagine in biological samples in the presence of L-asparaginase.
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The antileukaemic efficacy of L-asparaginase is related to the ability of the enzyme to induce the complete disappearance from plasma of L-asparagine, an amino acid essential to lymphoblastic leukaemia cells. It is not feasible to monitor L-asparagine plasma levels in patients under L-asparaginase
L-asparagine requirements of human T-lymphocytes and B-lymphocytes in culture.
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The characterization of two human T-lymphocyte lines revealed that they required exogenous L-asparagine for cell growth, whereas all four B-cell lines studied were L-asparagine independent. T-cells were 800-2,000 times more sensitive to Escherichia coli L-asparaginase than were B-cells. The
A sulfoximine-based inhibitor of human asparagine synthetase kills L-asparaginase-resistant leukemia cells.
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An adenylated sulfoximine transition-state analogue 1, which inhibits human asparagine synthetase (hASNS) with nanomolar potency, has been reported to suppress the proliferation of an l-asparagine amidohydrolase (ASNase)-resistant MOLT-4 leukemia cell line (MOLT-4R) when l-asparagine is depleted in
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