Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002874 (aplastic anemia)
 5,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Benzene is a well-known environmental pollutant that can induce hematotoxicity, aplastic anemia, acute myelogenous leukemia, and lymphoma. Benzene toxicity is likely mediated through metabolites induced by means of multiple pathways. Although benzene metabolites are known to induce oxidative stress and disrupt the cell cycle, the mechanism underlying leukemogenesis is not fully understood. The aim of this study was to analyze the genome-wide expression profiles of human promyelocytic leukemia HL-60 cells that had been exposed to benzene and its metabolites. This was carried out using whole human genome oligonucleotide microarrays to ascertain potential biomarkers. Genes that were differentially expressed (>1.5-fold and p-values <0.05) after exposure to benzene (BZ), hydroquinone (HQ), and 1,4-benzoquinone (BQ) were then classified with GO, KEGG and GSEA pathway annotation. All genes that were identified were then functionally categorized as being involved in the cell cycle, the p53 signaling pathway, apoptosis, the MAPK signaling pathway, or the T cell receptor signaling pathway. Functionally important genes were further validated by means of real-time RT-PCR. The results showed that EGR1, PMAIP1, AR, CCL2, CD69, HSPA8, SLC7A11, HERPUD1, ELK1, and MKI57 genes altered their expression profiles. Similar expression profiles were also found in human erythromyeloblastoid leukemia K562 cells and in human leukemic monocyte lymphoma U937 cells. In conclusion, gene expression profiles along with GO, KEGG and GSEA pathway annotation analysis have provided an insight into the leukemogenesis as well as highlighted potential gene-based biomarkers of human leukemia cell lines when they are exposed to benzene and its metabolites.
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PMID:Differential gene expression profiles of human leukemia cell lines exposed to benzene and its metabolites. 2184 10

Th1/Th17/Th2-related chemokines (CXCL10/CCL20/CCL2) and their receptors (CXCR3/CCR6/CCR2) have rarely been studied in acquired bone marrow failure syndromes (BMFs). We evaluated the concentrations of CXCL10, CCL20 and CCL2 in plasma and BM fluid from aplastic anemia (AA), paroxysmal nocturnal hemoglobinuria (PNH), and myelodysplastic syndromes (MDS) patients by enzyme-linked immunosorbent assay (ELISA). Real-time quantitative polymerase chain reaction (RT-PCR) was performed to determine mRNA expressions of those chemokines and their receptors. CCL20 levels in both plasma and BM fluid from AA, PNH and MDS patients were significantly higher than those in the corresponding samples from healthy controls; there were no differences in terms of CXCL10 and CCL2 levels. Significantly higher expressions of CXCR3 and CCL20 mRNA, meanwhile significantly lower expression of CCR2 mRNA in both peripheral blood mononuclear cells (PBMNCs) and bone marrow MNCs (BMMNCs) from AA and PNH patients were observed, with no differences in terms of CXCL10, CCL2 and CCR6 mRNA expressions. CCR6 mRNA expressions in both PBMNCs and BMMNCs from MDS patients were significantly higher than of the corresponding samples from controls. Our study implicated that CXCL10-CXCR3, CCL20-CCR6 and CCL2-CCR2 interaction might play important roles in Th1 and Th17 (but not for Th2) cells trafficking toward BM in acquired bone marrow failure syndromes.
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PMID:Differential expression profile of Th1/Th17/Th2-related chemokines and their receptors in patients with acquired bone marrow failure syndromes. 2320 Jul 57