Hematogones are markedly reduced in pediatric acquired aplastic anemia: multiparametric flow cytometric analysis
| Autor: | Courtney Baker, Adriana I. Colovai, Nike T. Beaubier, Deborah W. Sevilla, Monica Bhatia, Bachir Alobeid, Govind Bhagat, Foxwell Emmons |
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| Rok vydání: | 2009 |
| Předmět: |
Male
Cancer Research Pathology medicine.medical_specialty Adolescent Antigens CD19 Antigens CD34 Bone Marrow Cells Biology Flow cytometry Pathogenesis medicine Humans Cytotoxic T cell Aplastic anemia Child In Situ Hybridization Fluorescence B-Lymphocytes medicine.diagnostic_test Myelodysplastic syndromes Hematopoietic Stem Cell Transplantation Anemia Aplastic Hematology Flow Cytometry Hematopoietic Stem Cells medicine.disease Pathophysiology Haematopoiesis Treatment Outcome medicine.anatomical_structure Oncology Child Preschool Immunology Leukocyte Common Antigens Female Neprilysin Bone marrow |
| Zdroj: | Leukemia & Lymphoma. 50:1951-1957 |
| ISSN: | 1029-2403 1042-8194 |
| DOI: | 10.3109/10428190903156737 |
| Popis: | Acquired aplastic anemia (AA) and myelodysplastic syndromes (MDS) are bone marrow (BM) failure syndromes with overlapping clinical features, and at least a subset appears to share common pathophysiologic mechanisms. Recent studies of MDS have shown down-regulation of genes involved in B-cell development and decreased B-cell precursors (hematogones). We explored the possibility that AA, similar to MDS, might also be associated with defects in development of lymphoid cells, especially B-cells, by using flow cytometry to assess the presence of hematogones and mature lymphocytes in BM samples from 25 children with AA and 41 age-matched controls. We observed that the percentage of total and early (stage I) hematogones were significantly decreased in AA compared to controls, and they returned to normal numbers after hematopoietic stem-cell transplant. This demonstrates early B-cell lineage involvement in AA, similar to recent findings in MDS. Our findings suggest dysfunction of an early multilineage progenitor in the pathogenesis of AA. |
| Databáze: | OpenAIRE |
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