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Expression of chromosome 21-localized genes in acute myeloid leukemia: differences between Down syndrome and non-Down syndrome blast cells and relationship to in vitro sensitivity to cytosine arabinoside and daunorubicin.

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TLDR
Examining the expression of chromosome 21-localized genes in myeloblasts from newly diagnosed AML patients found increased CBS transcripts could result in elevated CBS activity, which modulates ara-C metabolism by altering reduced folate pools, deoxycytidine triphosphates pools, S-adenosylmethionine levels, and/or methylation of the deoxy Cystathionine-beta-synthase gene.
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This article is published in Blood.The article was published on 1999-08-15 and is currently open access. It has received 171 citations till now. The article focuses on the topics: Deoxycytidine triphosphate & Cytarabine.

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SULFUR AMINO ACID METABOLISM: Pathways for Production and Removal of Homocysteine and Cysteine

TL;DR: The regulation of the metabolism of methionine andCys is discussed from the standpoint of maintaining low levels of Hcy and Cys while, at the same time, ensuring an adequate supply of these thiols for their essential functions.
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Endogenous hydrogen sulfide overproduction in Down syndrome.

TL;DR: The cystathionine beta synthase (CBS) gene is localized on chromosome 21 (21q22.3) and this overproduction is potentially able to induce some of the clinical signs of Down syndrome such as hypotonia and mental retardation.
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Expression profiling reveals fundamental biological differences in acute myeloid leukemia with isolated trisomy 8 and normal cytogenetics

TL;DR: It is concluded that the clinical and cytogenetic heterogeneity of AML is due to fundamental biological differences and apoptosis-regulating genes were significantly down-regulated in AML+8 compared with AML-CN.
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A prospective study of the natural history of transient leukemia (TL) in neonates with Down syndrome (DS): Children's Oncology Group (COG) study POG-9481.

TL;DR: Ongoing collaborative clinical studies are needed to determine the optimal role of chemotherapy for infants at risk for increased mortality or disease recurrence and to further the knowledge of the unique biologic features of this transient leukemia in newborns with Down syndrome.
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l-Cysteine Inhibits Insulin Release From the Pancreatic β-Cell : Possible Involvement of Metabolic Production of Hydrogen Sulfide, a Novel Gasotransmitter

TL;DR: It is suggested here that L-cysteine inhibits insulin release via multiple actions on the insulin secretory process through H(2)S production, which may participate in the deterioration of insulin release in this disease.
References
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Journal ArticleDOI

Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction

TL;DR: A new method of total RNA isolation by a single extraction with an acid guanidinium thiocyanate-phenol-chloroform mixture is described, providing a pure preparation of undegraded RNA in high yield and can be completed within 4 h.
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The Importance of Diagnostic Cytogenetics on Outcome in AML: Analysis of 1,612 Patients Entered Into the MRC AML 10 Trial

TL;DR: Subgroup analysis demonstrated that the three cytogenetically defined prognostic groups retained their predictive value in the context of secondary as well as de novo AML, within the pediatric age group and furthermore were found to be a key determinant of outcome from autologous or allogeneic bone marrow transplantation (BMT) in first CR.
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Cancer statistics, 1998

TL;DR: The Surveillance Research Program of the American Cancer Society's Department of Epidemiology and Surveillance reports its 32nd annual compilation of cancer incidence, mortality, and survival data for the United States and around the world.
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Apoptosis and increased generation of reactive oxygen species in Down's syndrome neurons in vitro

TL;DR: It is reported that cortical neurons from fetal DS and age-matched normal brain differentiate normally in culture, but DS neurons subsequently degenerate and undergo apoptosis whereas normal neurons remain viable, suggesting that DS neurons have a defect in the metabolism of reactive oxygen species that causes neuronal apoptosis.
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