ArticleHaematologica2012
The small population of PIG-A mutant cells in myelodysplastic syndromes do not arise from multipotent hematopoietic stem cells.
Article in Haematologica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Burst-forming unit-erythroid assays to distinguish cellular bone marrow failure disorders.Experimental hematology · 2013Trial
- Minor GPI(-) granulocyte populations in aplastic anemia and healthy individuals derived from a few PIGA-mutated hematopoietic stem progenitor cells.Blood cancer journal · 2023Article
- The spectrum of paroxysmal nocturnal hemoglobinuria clinical presentation in a Brazilian single referral center.Annals of hematology · 2022Article
- Clonal Cell Proliferation in Paroxysmal Nocturnal Hemoglobinuria: Evaluation ofAnnals of laboratory medicine · 2019Article
- Paroxysmal nocturnal hemoglobinuria testing in patients with myelodysplastic syndrome in clinical practice-frequency and indications.Current oncology (Toronto, Ont.) · 2018Article
- Independent Paroxysmal Nocturnal Hemoglobinuria and Myelodysplastic Syndrome Clones in a Patient With Complete Bone Marrow Failure.HemaSphere · 2018Article
- Paroxysmal nocturnal haemoglobinuria.Nature reviews. Disease primers · 2017Review
- PIGN gene expression aberration is associated with genomic instability and leukemic progression in acute myeloid leukemia with myelodysplastic features.Oncotarget · 2017Article
- Paroxysmal nocturnal hemoglobinuria.Blood · 2014Review
- The challenging world of cytopenias: distinguishing myelodysplastic syndromes from other disorders of marrow failure.The oncologist · 2014Review
- Last marrow standing: bone marrow transplantation for acquired bone marrow failure conditions.Current hematologic malignancy reports · 2012Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPatients with paroxysmal nocturnal hemoglobinuria harbor clonal glycosylphosphatidylinositol-anchor deficient cells arising from a multipotent hematopoietic stem cell acquiring a PIG-A mutation. Many patients with aplastic anemia and myelodysplastic syndromes also harbor small populations of glycosylphosphatidylinositol-anchor deficient cells. Patients with aplastic anemia often evolve into paroxysmal nocturnal hemoglobinuria; however, myelodysplastic syndromes seldom evolve into paroxysmal nocturnal hemoglobinuria. Here, we investigate the origin and clonality of small glycosylphosphatidylinositol-anchor deficient cell populations in aplastic anemia and myelodysplastic syndromes. DESIGN AND
methodsWe used peripheral blood flow cytometry to identify glycosylphosphatidylinositol-anchor deficient blood cells, a proaerolysin-resistant colony forming cell assay to select glycosylphosphatidylinositol-anchor deficient progenitor cells, a novel T-lymphocyte enrichment culture assay with proaerolysin selection to expand glycosylphosphatidylinositol-anchor deficient T lymphocytes, and PIG-A gene sequencing assays to identify and analyze PIG-A mutations in patients with aplastic anemia and myelodysplastic syndromes.
resultsTwelve of 15 aplastic anemia patients were found to harbor a small population of glycosylphosphatidylinositol-anchor deficient granulocytes; 11 of them were found to harbor a small population of glycosylphosphatidylinositol-anchor deficient erythrocytes, 10 patients were detected to harbor glycosylphosphatidylinositol-anchor deficient T lymphocytes, and 3 of them were detected only after T-lymphocyte enrichment in proaerolysin selection. PIG-A mutation analyses on 3 patients showed that all of them harbored a matching PIG-A mutation between CFU-GM and enriched T lymphocytes. Two of 26 myelodysplastic syndromes were found to harbor small populations of glycosylphosphatidylinositol-anchor deficient granulocytes and erythrocytes transiently. Bone marrow derived CD34(+) cells from 4 patients grew proaerolysin-resistant colony forming cells bearing PIG-A mutations. No glycosylphosphatidylinositol-anchor deficient T lymphocytes were detected in myelodysplastic syndrome patients.
conclusionsIn contrast to aplastic anemia and paroxysmal nocturnal hemoglobinuria, where PIG-A mutations arise from multipotent hematopoietic stem cells, glycosylphosphatidylinositol-anchor deficient cells in myelodysplastic syndromes appear to arise from more committed progenitors.
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