Asparagine synthetase activity in paediatric acute leukaemias: AML-M5 subtype shows lowest activity
British Journal of Haematology, ISSN: 0007-1048, Vol: 109, Issue: 2, Page: 427-429
2000
- 46Citations
- 34Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations46
- Citation Indexes46
- 46
- CrossRef34
- Captures34
- Readers34
- 34
Article Description
Lack of sufficient cellular activity of asparagine synthetase (AS) in blast cells compared with normal tissue is thought to be the basis of the antileukaemic effect of L-asparaginase in acute lymphoblastic leukaemia (ALL). Although L-asparaginase is routinely used in ALL, its role and value in the treatment of acute myelogenous leukaemia (AML) is still being discussed. To evaluate the pharmacological basis for L-asparaginase treatment, we established pretreatment monitoring of the intracellular AS activity in blast cells of patients with AML and ALL. There was no general difference in AS activity between ALL and AML samples. Significantly lower AS activity, however, was found in the B-lineage ALL subgroups as well as AML- M5.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0034039017&origin=inward; http://dx.doi.org/10.1046/j.1365-2141.2000.02015.x; http://www.ncbi.nlm.nih.gov/pubmed/10848836; https://onlinelibrary.wiley.com/doi/10.1046/j.1365-2141.2000.02015.x; https://dx.doi.org/10.1046/j.1365-2141.2000.02015.x; https://onlinelibrary.wiley.com/doi/full/10.1046/j.1365-2141.2000.02015.x
Wiley
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