Herein, gene expression analysis identified a significant loss of the SWI/SNF core component SMARCC1, along with ARID1B, ACTL6A, and SMARCD1, in human AA BM CD34<sup>+</sup> HSCs and hematopoietic stem and progenitor cells (HSPCs) compared with normal HSPCs.
Our results indicate that genetic ATG5 variants contributed to AA, which may facilitate further clarifying the underlying mechanisms of AA and making a patient-tailored medical decision.
The gene expression profile of primary human CD34 hematopoietic stem cells from AA was consistent with a stressed, dying, and immunologically activated target cell population.
We quantified CD55-CD59- granulocytes and red blood cells (RBCs) in peripheral blood from 122 patients with recently diagnosed AA and correlated numbers of PNH-type cells and responses to immunosuppressive therapy (IST).
We quantified CD55-CD59- granulocytes and red blood cells (RBCs) in peripheral blood from 122 patients with recently diagnosed AA and correlated numbers of PNH-type cells and responses to immunosuppressive therapy (IST).
Deep sequencing and flow cytometric characterization of expanded effector memory CD8<sup>+</sup>CD57<sup>+</sup> T cells frequently reveals T-cell receptor Vβ oligoclonality and CDR3 homology in acquired aplastic anemia.
We report on a female patient with acquired aplastic anemia whose bone marrow cells showed DNA rearrangement of the immunoglobulin-JH region that disappeared after 1 month with recovery of hematopoiesis through treatment with granulocyte colony-stimulating factor (G-CSF) and immunosuppressive drugs.
We have investigated the expression of RNA transcripts of hematopoiesis regulatory molecules, viz., macrophage inflammatory protein (MIP)-1<i>α</i>, tumor necrosis factor (TNF)-<i>α</i>, granulocyte colony-stimulating factor (G-CSF), stromal cell-derived factor (SDF)-1<i>α</i>, stem cell factor (SCF), and transforming growth factor (TGF)-<i>β</i> in lipopolysaccharide-induced bone marrow mesenchymal stem cells (BM-MSCs) and levels of their soluble forms in the culture supernatants of BM-MSCs and BM plasma of patients with acquired aplastic anemia (AA) (<i>n</i> = 29) and controls (<i>n</i> = 29).
Altered metabolism of benzo(a)pyrene due to the polymorphism in the CYP1A1 gene might be an etiologic factor in the increased incidence of AA in these patients.
The aim of the study was to characterize the genetic polymorphism of biotransforming phase I (p450-cyp2E1) and phase II [microsomal epoxide hydrolase (mEh), glutathione S-transferase (GST)] enzymes in pediatric patients with acquired aplastic anemia.
Diazepam-binding inhibitor-related protein 1: a candidate autoantigen in acquired aplastic anemia patients harboring a minor population of paroxysmal nocturnal hemoglobinuria-type cells.
Thus, the GST θ1-null genotype and the 139A--G mEh gene polymorphism may enhance the susceptibility to AA and provide an evidence of gene-environmental interaction.
Both mEPHXTyr113His and His139Arg gene polymorphisms were associated with increased risk of developing AA, and have a significant impact of bad prognosis (p value < 0.01).