ArticleLeukemia2005
Differential gene expression in hematopoietic progenitors from paroxysmal nocturnal hemoglobinuria patients reveals an apoptosis/immune response in 'normal' phenotype cells.
Article in Leukemia, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 49 citations in OpenAlex.
- Imputing causality and clonal dynamics from single-cell transcriptomics in paroxysmal nocturnal hemoglobinuria.Leukemia · 2026Article
- Identifying Genes Associated With Proliferation, Immunity and Thrombosis in Paroxysmal Nocturnal Haemoglobinuria.Journal of cellular and molecular medicine · 2024Article
- Single-cell sequencing reveals alterations in the differentiation of bone marrow haematopoietic cells in patients with paroxysmal nocturnal haemoglobinuria.Clinical and translational medicine · 2024Article
- Paroxysmal Nocturnal Hemoglobinuria: Biology and Treatment.Medicina (Kaunas, Lithuania) · 2023Review
- Insights Into the Emergence of Paroxysmal Nocturnal Hemoglobinuria.Frontiers in immunology · 2021Review
- Coombs-positive Paroxysmal Nocturnal Haemoglobinuria.Oxford medical case reports · 2020Article
- Whole transcriptome sequencing identifies increased CXCR2 expression in PNH granulocytes.British journal of haematology · 2017Article
- The mutational landscape of paroxysmal nocturnal hemoglobinuria revealed: new insights into clonal dominance.The Journal of clinical investigation · 2014Article
- Potential link between MHC-self-peptide presentation and hematopoiesis; the analysis of HLA-DR expression in CD34-positive cells and self-peptide presentation repertoires of MHC molecules associated with paroxysmal nocturnal hemoglobinuria.Cell biochemistry and biophysics · 2013Article
- Phenotypic and functional characterization of a mouse model of targeted Pig-a deletion in hematopoietic cells.Haematologica · 2010Article
- Paroxysmal nocturnal hemoglobinuria and myelodysplastic syndromes: clonal expansion of PIG-A-mutant hematopoietic cells in bone marrow failure.Haematologica · 2009Article
- Glycosylphosphatidylinositol-anchored protein deficiency confers resistance to apoptosis in PNH.Experimental hematology · 2009Article
- Paroxysmal nocturnal hemoglobinuria: pathophysiology, natural history and treatment options in the era of biological agents.Biologics : targets & therapy · 2008Article
- Clonality of the stem cell compartment during evolution of myelodysplastic syndromes and other bone marrow failure syndromes.Leukemia · 2007Review
- Review
- Recent advances in biological and clinical aspects of paroxysmal nocturnal hemoglobinuria.International journal of hematology · 2006Review
- Heterogeneity in the molecular pathogenesis of paroxysmal nocturnal hemoglobinuria (PNH) syndromes and expansion mechanism of a PNH clone.International journal of hematology · 2006Review
- Immune pathogenesis of paroxysmal nocturnal hemoglobinuria.International journal of hematology · 2006Review
- The GOD of hematopoietic stem cells: a clonal diversity model of the stem cell compartment.Cell cycle (Georgetown, Tex.) · 2006Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired stem cell disorder characterized clinically by intravascular hemolysis, venous thrombosis, and bone marrow failure. Despite elucidation of the biochemical and molecular defects in PNH, the pathophysiology of clonal expansion of glycosylphosphatidylinositol-anchored protein (GPI-AP)-deficient cells remains unexplained. In pursuit of evidence of differences between GPI-AP-normal and -deficient CD34 cells, we determined gene expression profiles of isolated marrow CD34 cells of each phenotype from PNH patients and healthy donors, using DNA microarrays. Pooled and individual patient samples revealed consistent gene expression patterns relative to normal controls. GPI-AP-normal cells from PNH patients showed upregulation of genes involved in apoptosis and the immune response. Conversely, genes associated with antiapoptotic function and hematopoietic cell proliferation and differentiation were downregulated in these cells. In contrast, the PNH clone of GPI-AP-deficient cells appeared more similar to CD34 cells of healthy individuals. Gene chip data were confirmed by other methods. Similar gene expression patterns were present in PNH that was predominantly hemolytic as in PNH associated with aplastic anemia. Our results implicate an environmental influence on hematopoietic cell proliferation, in which the PNH clone evades immune attack and destruction, while normal cells suffer a stress response followed by programmed cell death.
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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.