Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human T-cell leukaemia virus type-1 (HTLV-1) is known to cause adult T-cell leukaemia. The prevalence of anti-HTLV-1 antibody in haemodialysis patients has been reported to be higher than that in the general population. The anti-HTLV-1 antibody-positive rate in patients with primary glomerulonephritis in the Nagasaki district, an endemic area of HTLV-1, was evaluated. The antibody-positive rates in patients with primary glomerulonephritis (9.9%) and in haemodialysis patients (18.4%) were significantly higher than the rate in general blood donors (6.6%). Of 142 patients with primary glomerulonephritis, 14 (9.9%) were positive for the antibody; histological evaluation of these patients showed minor glomerular abnormality in one, mesangial proliferative glomerulonephritis in eight (IgA nephropathy in six and non-IgA nephropathy in two), membranous nephropathy in three, and crescentic glomerulonephritis in two. Evaluation of 10 antibody-positive patients by immunofluorescent microscopy showed immunocomplex-type nephritis in nine, suggesting the involvement of HTLV-1-associated antigen in the development and progression of glomerulonephritis.
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PMID:Evaluation of anti-HTLV-1 antibody in primary glomerulonephritis. 777 59

An etiologic agent directly linked to the development of IgA nephropathy (IgAN) has not been identified, despite the fact that various causes, including viral infections, have been implicated in the pathogenesis of this disease. Human immunodeficiency virus (HIV) infection has been linked with the development of IgAN in several clinical studies, and retroviral infection may be associated with the pathogenesis of IgAN in some patients. The incidence of IgAN has been found to possess distinct geographical distributions, and familial genetic clustering. To determine if retroviral infection is associated with IgAN in a large population of patients, genomic DNA from peripheral blood mononuclear cells from 90 patients seronegative for HIV and human T-cell leukemia virus type 1 (HTLV-1) (37 IgAN, 33 other glomerulonephritis, and 20 healthy controls) was evaluated by nested PCR using a pan-lentivirus-specific primer set (PLSPS), targeting the consensus sequence of the lentiviral pol gene. In 37.8% (14 of 37) of the patients with IgAN, the PCR products migrated in parallel with bands produced by PCR of simian immunodeficiency virus (SIV) infected cells. No products of the expected size were detected in the other patient groups (p < 0.0001, Chi-square). These results suggest that exposure to retroviral infection is more common in patients with IgAN, compared with patients with other proliferative glomerulonephritides, or patients without renal disease. These data demonstrate a possible association of IgAN with infection with non-HIV, non-HTLV-1 retrovirus.
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PMID:Retroviral infection in peripheral mononuclear cells in patients with IgA nephropathy. 912 86

We describe herein a case of nephrotic syndrome (NS) following allogeneic bone marrow transplantation (allo-BMT) for natural killer cell leukemia/lymphoma. Histologic studies defined the diagnosis as crescentic glomerulonephritis with massive immunoglobulin A (IgA) deposition, which has never been reported in NS cases following allo-BMT. Most of the massive infiltrated cells in the interstice were CD3(+)CD4(-)CD8(+) T cells derived from the donor. We observed mesangial deposition of Haemophilus parainfluenza outer membrane (OMHP) antigen and decreased glycosylation of the IgA1 hinge in the recipient's samples is consistent with the recently reported pathogenesis of IgA nephropathy. Further, the titer of IgA antibody against the donor serum was as high as other IgA nephropathy cases. These findings suggest that NS and crescentic glomerulonephritis in this case occurred as one of the forms of chronic graft-versus-host disease (GVHD), and that IgA deposition was associated with H parainfluenza and decreased glycosylation of the IgA1 hinge.
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PMID:Nephrotic syndrome with crescent formation and massive IgA deposition following allogeneic bone marrow transplantation for natural killer cell leukemia/lymphoma. 1254 67

IgA nephropathy (IgAN) associated with leukemia and lymphoma has not, to our knowledge, been reported in children. Two children suffering from these diseases are described here. One patient developed IgAN at the end of 5 years' chemotherapy for acute lymphocytic leukemia. The other had microscopic hematuria 3 years before the onset of non-Hodgkin lymphoma, and hematuria continued during chemotherapy. Each disease occurred after a long interval, and the clinical courses did not run parallel. The association was thought to be incidental in our cases. Chemotherapy with adrenocorticosteroids and immunosuppressants [6-mercaptopurine (6-MP) and cyclophosphamide (CY)] for leukemia and lymphoma did not affect the clinical course of IgAN.
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PMID:IgA nephropathy associated with leukemia and lymphoma: report of two cases. 1817 50

FcalphaR (CD89) is the Fc receptor for immunoglobulin A (IgA) and plays important roles in IgA-mediated immune responses. It is a heavily glycosylated protein with six potential N-linked glycosylation sites. Previous reports showed that abnormal glycosylation of FcalphaR was involved in some diseases, including human immunodeficiency virus infection, alcoholic liver cirrhosis and IgA nephropathy. In this study, we examined the effects of N-glycosylation on interaction between FcalphaR and IgA. We found that depletion of N-glycosylation of FcalphaR transfected in Chinese hamster ovary (CHO) cells by tunicamycin resulted in increased IgA binding. To identify which glycosylation site is responsible for increased IgA binding, we performed site-directed mutagenesis at each N-linked glycosylation site by changing asparagine to glutamine. Flow cytometry analysis of IgA binding to CHO cells transfected with mutated FcalphaR showed that deglycosylation of FcalphaR at individual N44, N120, N156, N165 or N177 site did not affect IgA binding but deglycosylation at N58 resulted in marked increase of IgA binding. Similar result was shown for N58Q-FcalphaR transfected RBL2H3, a rat basophilic leukemia cell line. Furthermore, increased IgA binding was also observed on desialylated FcalphaR after neuraminidase treatment and desialylation of N58 contributed most to the increased IgA binding. These data demonstrated that glycosylation at N58 site influenced FcalphaR binding to IgA.
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PMID:Deglycosylation of FcalphaR at N58 increases its binding to IgA. 2037 33

We encountered 2 immunocompromised children complicated by Raoultella ornithinolytica bacteremia. One had received methylprednisolone pulse therapy for IgA nephropathy, and the other had leukopenia because of chemotherapy for leukemia. Both children had no specific symptoms, and R. ornithinolytica bacteremia was identified by routine blood culture. Both patients were successfully treated with antibiotic treatment.
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PMID:Bacteremia Caused by Raoultella ornithinolytica in Two Children. 2697 50

Tris (dibenzylideneacetone) dipalladium (Tris DBA), a small-molecule palladium complex, can inhibit cell growth and proliferation in pancreatic cancer, lymphocytic leukaemia and multiple myeloma. Given that this compound is particularly active against B-cell malignancies, we have been suggested that it can alleviate immune complexes (ICs)-mediated conditions, especially IgA nephropathy (IgAN). The therapeutic effects of Tris DBA on glomerular cell proliferation and renal inflammation and mechanism of action were examined in a mouse model of IgAN. Treatment of IgAN mice with Tris DBA resulted in markedly improved renal function, albuminuria and renal pathology, including glomerular cell proliferation, neutrophil infiltration, sclerosis and periglomerular inflammation in the renal interstitium, together with (Clin J Am Soc Nephrol. 2011, 6, 1301-1307) reduced mitochondrial ROS generation; (Am J Physiol-Renal Physiol. 2011. 301, F1218-F1230) differentially regulated autophagy and NLRP3 inflammasome; (Clin J Am Soc Nephrol. 2012, 7, 427-436) inhibited phosphorylation of JNK, ERK and p38 MAPK signalling pathways, and priming signal of the NLRP3 inflammasome; and (Free Radic Biol Med. 2013, 61, 285-297) blunted NLRP3 inflammasome activation through SIRT1- and SIRT3-mediated autophagy induction, in renal tissues or cultured macrophages. In conclusion, Tris DBA effectively ameliorated the mouse IgAN model and targeted signalling pathways downstream of ICs-mediated interaction, which is a novel immunomodulatory strategy. Further development of Tris DBA as a therapeutic candidate for IgAN is warranted.
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PMID:Tris DBA ameliorates IgA nephropathy by blunting the activating signal of NLRP3 inflammasome through SIRT1- and SIRT3-mediated autophagy induction. 3313 20