Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The 25,000 dalton protein of Mason-Pfizer monkey virus (MPMV) was isolated by gel filtration chromatography. In agreement with results from other laboratories, antisera to type-C and the non-type-C bovine leukemia and equine infectious anemia viruses did not precipitate 125I-labelled MPMV p25. In addition, these viruses did not cross-react in a competition radioimmunoassay for MPMV p25. Twenty-one human tissues (15 breast carcinomas, 2 normal breasts, 3 acute myelogenous leukemias and 1 sarcoma) were fractionated by detergent solubilization, ammonium sulfate precipitation, and DE-52 anion exchange chromatography. These methods were shown to be highly effective for purification of MPMV p25. Under assay conditions which minimized incubation damage to the 125I-MPMV p25, all tissues failed to react in the competition radioimmunoassay (RIAT). Two hundred and two human sera or plasma specimens, including those from patients with breast cancer and 33 age-matched controls, from 50 patients with hematologic malignancies, from 12 patients with amyotrophic lateral sclerosis, and from 14 patients with systemic lupus erythematosis, were examined for antibodies to MPMV p25. With the exception of two multiple myeloma plasma which produced artifactual false positive reactions based on hypergammaglobulinemia, a known complication of salt precipitation radioimmunoassays, the remainder of the specimens were negative for evidence of MPMV p25 antibodies.
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PMID:Radioimmunoassay for the major structural protein of Mason-Pfizer monkey virus: Attempts to detect the presence of antigen or antibody in humans. 40 48

The systemic rheumatic diseases are commonly complicated by hematologic abnormalities. Five frequently encountered and clinically relevant complications are reviewed. They include the anemia of chronic disease, neutropenia, autoimmune thrombocytopenic purpura, the lupus inhibitor, and hematologic malignancies. The pathophysiology and treatment of each of these conditions are discussed in this review.
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PMID:Hematologic complications of rheumatic disease. 311 57

Markers of thrombotic risk--fibrinogen, factor VIII and immunoglobulin G (IgG) anticardiolipin titres--were measured, and the presence of lupus anticoagulant and factor V Leiden were assessed in 84 patients with a solid or haematological malignancy. These patients were monitored, following the insertion of an indwelling venous catheter, for thrombosis. Fifty-five were given prophylactic low-dose warfarin. Over a mean of 15 weeks there were 10 (12%) thrombotic events in 10 patients. Seven were on warfarin. Haemorrhagic problems occurred in three (5%), all on warfarin. Of the 84 patients, 86% had raised fibrinogen levels, 37% elevated factor VIII and 44% raised anticardiolipin levels. Lupus anticoagulant was present in five and three were heterozygous for factor V Leiden. A high prevalence of a range of prothrombotic changes was confirmed and the frequent presence of low-titre anticardiolipin antibody in subjects with malignancy demonstrated. However, none of these parameters predicted the development of thrombosis (P > 0.05).
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PMID:Thrombosis, markers of thrombotic risk, indwelling central venous catheters and antithrombotic prophylaxis using low-dose warfarin in subjects with malignant disease. 1064 78

Cancer has been reported in patients with systemic lupus erythematosus (SLE). A possible association of the development of hematologic malignancies in patients with SLE has been suggested. In some patients, subacute cutaneous lupus erythematosus, a distinct subset of lupus erythematosus, has appeared, resolved, or both as a solid tumor-related paraneoplastic syndrome. A woman in whom a meningioma was diagnosed 44 years following the onset of subacute cutaneous lupus erythematosus is described; her skin lesions improved after starting isotretinoin therapy. The relationship between lupus erythematosus and neoplasia is summarized and the management of subacute cutaneous lupus erythematosus with retinoids is reviewed.
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PMID:Subacute cutaneous lupus erythematosus: report of a patient who subsequently developed a meningioma and whose skin lesions were treated with isotretinoin. 1100 52

Cell death by apoptosis is exerted by the coordinated action of many different gene products. Mutations in some of them, acting at different levels in the apoptosis process, have been identified as cause or contributing factor for human diseases. Defects in the transmembrane tumor necrosis factor receptor 1 (TNF-R1) lead to the development of familial periodic fever syndromes. Mutations in the homologous receptor Fas (also named CD95; Apo-1) are observed in malignant lymphomas, solid tumors and the autoimmune lymphoproliferative syndrome type I (ALPS I). A mutation in the ligand for Fas (Fas ligand; CD95 ligand, Apo-1 ligand), which induces apoptosis upon binding to Fas, was described in a patient with systemic lupus erythematodes and lymphadenopathy. Perforin, an other cytotoxic protein employed by T- and NK-cells for target cell killing, is mutated in chromosome 10 linked cases of familial hemophagocytic lymphohistiocytosis. Caspase 10, a representative of the caspase family of proteases, which plays a central role in the execution of apoptosis, is defect in autoimmune lymphoproliferative syndrome type II (ALPS II). The intracellular pro-apoptotic molecule bcl-10 is frequently mutated in mucosa-associated lymphoid tissue (MALT) lymphomas and various non-hematologic malignancies. The p53, an executioner of DNA damage triggered apoptosis, and Bax, a pro-apoptotic molecule with the ability to perturb mitochondrial membrane integrity, are frequently mutated in malignant neoplasms. Anti-apoptotic proteins like bcl-2, cellular-inhibitor of apoptosis protein 2 (c-IAP2) and neuronal apoptosis inhibitory protein 1 (NAIP1) are often altered in follicular lymphomas, MALT lymphomas and spinal muscular atrophy (SMA), respectively. This article reviews the current knowledge on mutations of apoptosis genes involved in the pathogenesis of human diseases and summarises the gradual transformation of discoveries in apoptosis research into benefits for the clinical management of diseases.
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PMID:Mutations in apoptosis genes: a pathogenetic factor for human disease. 1139 50

Reactive angioendotheliomatosis (RAE) is a very rare disorder characterized by marked proliferation of endothelial cells. It is often associated with infections, such as subacute bacterial endocarditis, but has also been described as an early sign of a developing hematological malignancy. We report the case of a 71-year-old Caucasian female who developed lupus-like RAE lesions. A thorough diagnostic workup and subsequent 3-year clinical follow-up revealed no sign of an underlying infectious or neoplastic disorder. Repetitive serum immunofixations were only once consistent with a monoclonal gammopathy of undetermined significance. In lesional skin, the pronounced bud-like endothelial cell formation was associated with an increased epidermal expression of vascular endothelial growth factor (VEGF), a potent angiogenic mediator. In accordance with the paracrine action of epidermally derived VEGF, vascular endothelial cells in lesional skin revealed increased expression of the VEGF receptor VEGFR-2 (KDR). This case suggests a possible role of epidermally derived VEGF in endothelial cell proliferation in RAE.
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PMID:Increased expression of VEGF in glomeruloid reactive angioendotheliomatosis. 1465 35

As a result of increasing life expectancy of lupus patients, malignant disorders have become major determinants of morbidity and mortality. The objectives of this study were to analyze cancer-associated morbidity and mortality, the type of malignancies in Hungarian lupus patients, and to analyze association with immune-suppressive therapy, disease duration, and age of the patients. Data from 860 systemic lupus erythematosus (SLE) patients were retrospectively analyzed in a study period between 1970 and 2004. Results were compared to data from age- and sex-matched population obtained from the Health for All database, and also to literature data. A total of 37 patients presented with cancer, reflecting 4.3% cancer-associated morbidity. Patients were 47 (20-73) years old at the onset of malignancy, which appeared 13 (1-45) years later than SLE. Cancer prevalence was the highest in the first 5-10 years of lupus. Breast cancer was the most common malignancy (n = 11) followed by gastrointestinal tumors (n = 9), cervix cancer and hematologic malignancies (n = 5 for both), bronchial cancer (n = 4), bladder, skin, and ovarian cancer (n = 1 for each). Standardized incidence ratio was the highest for non-Hodgkin lymphoma (standardized incidence ratio [SIR] 3.5, 95% CI 0.4-12.5) and cervix cancer (SIR 1.7, 95% CI 0.6-4.1). Although 76% of patients with cancer received immune-suppressive therapy besides corticosteroids, no direct correlation could be confirmed between therapy and malignancy. Out of the 164 patients that expired during the study period, 18 were cancer-related. As such the cancer-associated mortality was 11% (18/164). This peaked during the last 4 years of the study period (8/24, 33%). Lupus patients are at high risk for particular types of malignant disorders, highlighting the importance of screening measures and focused patient examination.
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PMID:Occurrence of malignancies in Hungarian patients with systemic lupus erythematosus: results from a single center. 1789 72

The transmembrane receptor CD30 (TNFRSF8) and its ligand CD30L (CD153, TNFSF8) are members of the tumor necrosis factor (TNF) superfamily and display restricted expression in subpopulations of activated T-and B-cells in nonpathologic conditions. CD30 expression is upregulated in various hematological malignancies, including Reed-Sternberg cells in Hodgkin's disease (HD), anaplastic large cell lymphoma (ALCL) and subsets of Non-Hodgkin's lymphomas (NHLs). Increased CD30L expression was found on mast cells within HD tumors and preclinical and clinical studies with compounds targeting the CD30/ CD30L system in HD and ALCL demonstrated therapeutic benefit. Upregulation of CD30 and CD30L is also linked to leukocytes in patients with chronic inflammatory diseases, including lupus erythematosus, asthma, rheumatoid arthritis and atopic dermatitis (AD). Preclinical studies conducted with transgenic mice or biologic compounds suggested important regulatory functions of the CD30-CD30L system in various aspects of the immune system. Such key regulatory roles and their low expression in normal conditions combined with increased expression in malignant tissues provided a strong rationale to investigate CD30 and CD30L as therapeutic targets in hematologic malignancies, autoimmune and inflammatory diseases. In this report, we review the pharmacodynamic effects of specific therapeutic compounds targeting the CD30/CD30L system in preclinical- and clinical studies.
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PMID:Targeting CD30/CD30L in oncology and autoimmune and inflammatory diseases. 1976 74

Comorbidities make determining a patient's optimal treatment plan substantially more difficult. This article describes lupus cerebritis, a neuropsychiatric presentation of systemic lupus erythematosus, in a patient with a risk for hematologic malignancies. The patient's primary care team had to weigh the benefit versus potential harm of various therapies to find the best treatment.
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PMID:Suspected hematologic malignancy complicates lupus cerebritis treatment. 3091 46

Systemic lupus erythematosus is associated with a small overall increased cancer risk compared with the general population. This risk includes a 4-fold increased risk of non-Hodgkin lymphoma, but a decreased risk of other cancers (such as breast cancer). The pathophysiology underlying the increased risk of hematologic cancer is not fully understood, but many potential mechanisms have been proposed, including dysfunction of the tumor necrosis factor and other pathways. A decreased risk of breast, ovarian, and endometrial cancer might be driven by hormonal factors or lupus-related antibodies, but these links have not been proved.
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PMID:Cancer and Systemic Lupus Erythematosus. 3263 2


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