ArticleLeukemia2005
Epigenetic changes in the repression and induction of asparagine synthetase in human leukemic cell lines.
Article in Leukemia, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Metabolism of asparagine in the physiological state and cancer.Cell communication and signaling : CCS · 2024Review
- Anticancer Activity of Extremely Effective Recombinant L-Asparaginase fromJournal of microbiology and biotechnology · 2022Article
- Targeting Nutrient Dependency in Cancer Treatment.Frontiers in oncology · 2022Review
- Mutant p53-reactivating compound APR-246 synergizes with asparaginase in inducing growth suppression in acute lymphoblastic leukemia cells.Cell death & disease · 2021Article
- Asparagine: A Metabolite to Be Targeted in Cancers.Metabolites · 2021Review
- Glutaminase Activity of L-Asparaginase Contributes to Durable Preclinical Activity against Acute Lymphoblastic Leukemia.Molecular cancer therapeutics · 2019Article
- Drugging the addict: non-oncogene addiction as a target for cancer therapy.EMBO reports · 2016Review
- Erythrocyte encapsulated l-asparaginase (GRASPA) in acute leukemia.International journal of hematologic oncology · 2016Review
- Glutaminase activity determines cytotoxicity of L-asparaginases on most leukemia cell lines.Leukemia research · 2015Article
- Differential mechanisms of asparaginase resistance in B-type acute lymphoblastic leukemia and malignant natural killer cell lines.Scientific reports · 2015Article
- Adipocytes cause leukemia cell resistance to L-asparaginase via release of glutamine.Cancer research · 2013Article
- Asparagine synthetase: regulation by cell stress and involvement in tumor biology.American journal of physiology. Endocrinology and metabolism · 2013Review
- Cell-cycle inhibition by Helicobacter pylori L-asparaginase.PloS one · 2010Article
- Mesenchymal cells regulate the response of acute lymphoblastic leukemia cells to asparaginase.The Journal of clinical investigation · 2007Article
- Methylation analysis of asparagine synthetase gene in acute lymphoblastic leukemia cells.Leukemia · 2006Article
- Accurate detection of asparagine synthetase (ASNS) using quantitative real-time PCR (qRT-PCR), without requiring DNaseI treatment.Leukemia · 2005Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In common with certain other lymphoid neoplasms, cells of the human lymphocytic leukemia lines 1873 and 1929 are asparagine (ASN) auxotrophs. Asparagine synthetase (ASY), which is a housekeeping gene, is repressed and the promoting region of the gene is highly methylated. We now demonstrate in these cells multiple levels in control of the expression of this gene, in a system of cocultivation with macrophages and other cell types. In this system, mediated by cell-to-cell contact, ASY becomes expressed by the leukemic cells and they become prototrophic. Demethylation of ASY occurs; it follows expression and is permanent over multiple cell generations, but the cells return to auxotrophy with rapid repression of ASY on removal from cell contact. With ASY expression, the associated histone H3 at lysine position 9 (H3K9) becomes acetylated and H3K4, methylated. In contrast to other systems, H3K9 methylation does not characterize the repressed state. The changes leading from repression to induction of ASY and demethylation parallel the physiological changes specific to functional maturation of normal lymphoid precursors. The lability of expression of ASY has potential significance in determining the sensitivity of leukemic cells to L-asparaginase.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.