Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunohistochemical investigations were performed on decalcified, paraffin-embedded iliac crest trephine biopsy specimens from 30 cases of acute myeloid leukemia (AML, as defined by the FAB classification) with antibodies against B cells (L26, 4KB5, MB1, Ki-B3), T cells (UCHL1, MT1), myeloid/histiocytic cells (anti-neutrophil elastase, MAC387, anti-S-100 protein, anti-alpha 1-antichymotrypsin, DAKO-M1), natural killer/killer cells (anti-Leu-7), and megakaryocytes (anti-factor VIII-related antigen). (1) The blast cells of all the cases reacted with from at least two to at most eight different antibodies. Each antibody reacted with blast cells in a minimum of two (maximum 30) cases. (2) MT1, Ki-B3, anti-alpha 1-antichymotrypsin anti-neutrophil elastase, anti-S-100 protein, and MAC387 stained blast cells in more than 50% of the cases; MB1, L26, UCHL1, 4KB5, and DAKO-M1 in 20% to 50% of the cases; and anti-Leu-7 and anti-factor VIII-related antigen in less than 20% of the cases. (3) In the majority of cases many T lymphocytes, a small-to-moderate number of B lymphocytes, and a few Leu-7-positive lymphoid cells were intermingled with the blast cells. In some cases, especially where only a minor proportion of the blast cells was immunostained, it was nearly impossible to distinguish the lymphocytes of the tumor's stromal reaction from small blast cells. Thus, AML exhibits a heterogeneous immunophenotype in trephine biopsy specimens. Immunohistologic diagnosis of this disease in such specimens may be extremely difficult. Since staining of the blast cells with one or more of the antibodies generally used to define B cells, T cells, or their neoplastic derivatives is not uncommon, misinterpretation as non-Hodgkin's lymphoma of high-grade malignancy could easily occur. These findings also suggest that mixed-type (hybrid) acute leukemias with coexpression of myeloid and lymphoid cell markers could be more common than generally realized.
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PMID:Acute myeloid leukemia: immunohistologic findings in paraffin-embedded bone marrow biopsy specimens. 169 93

Immunologic abnormalities resembling those seen in patients with the acquired immunodeficiency syndrome (AIDS) are frequently observed in multitransfused but otherwise healthy individuals with hemophilia. To determine whether there was clinical or laboratory evidence to suggest an abnormality of immunoregulation in persons with hemophilia before the recognition of AIDS, we examined data collected by the Hemophilia Study Group from 1975 to 1979 on 1,551 patients with factor VIII deficiency. The prevalence of lymphocytopenia and thrombocytopenia in patients over 5 years of age on entry was found to be 9.3% (94/1,013) and 5.0% (26/518), respectively. These rates were significantly different from a normal population (P less than .00001 and less than .0003). No cases meeting the definition of AIDS were noted during the study. However, on follow-up in 1984 of a cohort of 79 patients with thrombocytopenia or lymphocytopenia on two or more occasions during the study, eight patients (10%) with AIDS-related abnormalities, including idiopathic thrombocytopenic purpura, non-Hodgkin's lymphoma, generalized lymphadenopathy, and oral moniliasis without obvious cause were identified. Of the 79 patients, liver disease accounted for five of the ten deaths (12.6% mortality) observed during a minimum follow-up of five years after detection of cytopenia. Only one death was attributed to bleeding in the absence of liver disease. We conclude that (a) the frequency of lymphocytopenia and thrombocytopenia was increased in multitransfused factor VIII-deficient hemophiliacs before the advent of AIDS, and (b) persistent lymphocytopenia and thrombocytopenia appear to be strongly associated with liver disease, which was the leading cause of death in a cohort of hemophiliacs followed five or more years.
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PMID:Long-term follow-up of hemophiliacs with lymphocytopenia or thrombocytopenia. 406 24

A questionnaire concerning the occurrence of acquired immunodeficiency syndrome (AIDS) and possible related clinical syndromes in treated haemophiliacs was sent to directors of 201 European haemophilia centres. 135 replies were received from eighteen countries, covering 8928 patients with haemophilia A, 1889 with haemophilia B, and 2330 with von Willebrand's disease treated with blood products per year; 8 cases of AIDS were identified, one of which was in a patient with haemophilia B; 7 suffered from infections and 1 from pleomorphic non-Hodgkin's lymphoma. 3 other patients with lymphoma were recorded. The median age was 20 years with range 12-57 years and 3 were aged 14 years or less; 3 of the patients had died. 179 patients with other possible immunological disorders were recorded including 86 with lymphadenopathy but 70 of these occurred at one centre. At least 48 patients with thrombocytopenia were identified, suggesting that this condition is more common in treated haemophiliacs than is "idiopathic thrombocytopenic purpura" in the general population. None of the abnormalities could be related to use of any particular type of factor VIII concentrates. These results, together with 3 cases of AIDS previously reported and not returned in this study, point to an incidence of 11 cases in 13 000 treated haemophiliacs.
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PMID:Acquired immunodeficiency syndrome and other possible immunological disorders in European haemophiliacs. 614 88

Pulmonary microvascular tumor embolization is a recognized cause of respiratory distress in cancer patients that is rarely diagnosed antemortem. Previous studies with relatively few patients have reported high diagnostic yield using wedged pulmonary artery catheter-derived blood samples to evaluate dyspneic cancer patients for possible microembolization. From 1991 to 1993, 21 cancer patients with respiratory distress of relatively acute onset and varying severity who required pulmonary artery catheterization for hemodynamic monitoring were evaluated using this technique. Pulmonary microvascular cytology (PMC) was interpreted as positive for malignant cells in nine of 21 patients presenting with a range of tumor types, including carcinomas of the breast, colon, and pancreas as well as non-Hodgkin's lymphoma. In 11 patients the PMC was interpreted as negative. One case was considered nondiagnostic. Megakaryocytes, noted in most PMC specimens as well as in several samples of simultaneously drawn peripheral blood, may mimic epithelial tumor cells. Immunocytochemical stains for factor VIII and cytokeratins were used to resolve occasional diagnostic dilemmas. Clinical and/or pathologic follow-up information was available for all patients. Diagnostic accuracy was highest for epithelial malignancies. Two false-negative results occurred in patients with metastatic choriocarcinoma and breast carcinoma. Circulating malignant cells in the peripheral blood of a patient with non-Hodgkin's lymphoma led to one false-positive diagnosis. Benign lymphoid elements in PMC generally have a reactive and variable appearance that should not be misinterpreted as lymphoma. We conclude that PMC is a useful tool in the evaluation of dyspneic cancer patients requiring pulmonary artery catheterization for hemodynamic monitoring and its use potentially avoids additional diagnostic procedures.
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PMID:Diagnosis of pulmonary microvascular metastases by cytologic evaluation of pulmonary artery catheter-derived blood specimens. 751 73

An 82-year-old patient with acquired von Willebrand's disease in association with a non-Hodgkin's lymphoma and a benign IgG-lambda monoclonal paraproteinemia is described with severe recurring nasopharyngeal bleedings, who responded poorly to desmopressin (DDAVP) and factor VIII/von Willebrand factor concentrates but was successfully treated with high-dose e intravenous gamma-globulin therapy.
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PMID:Effectiveness of high-dose intravenous gamma globulin therapy in acquired von Willebrand's disease. 797 45

We report here a case of an HIV-uninfected, anti-hepatitis C virus (HCV) positive haemophiliac, who was transfused with blood and intermediate purity factor VIII concentrates. Since 1988, a progressive decline in the CD4+ T-cell count was recorded, and in 1993 a B-cell non-Hodgkin's lymphoma (B-NHL) was diagnosed. The morphological appearance of the tumor with features of intermediate/mantle zone lymphoma, and the absence of EBV sequences within the tumor, ruled out the occurrence of a typical "opportunistic" lymphoma. However it is possible that the blood product therapy and its infectious complications may have played a role on immune function impairment.
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PMID:B non-Hodgkin's lymphoma in a haemophilia patient with idiopathic CD4+ T-lymphocytopenia. 890 87

We report the development of a high titre antibody to factor VIII in a patient with previous high grade B cell non-Hodgkin's lymphoma treated with fludarabine. Unlike previous reports of factor VIII inhibitors and lymphoproliferative disease this patient's lymphoma was in remission. We speculate that the occurrence of the inhibitor is another manifestation of the increasingly recognized autoimmune side-effects of fludarabine.
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PMID:Acquired haemophilia complicating the remission of a patient with high grade non-Hodgkin's lymphoma treated by fludarabine. 1093 Nov 66

Acquired von Willebrand syndrome (AVWS) associated with hypothyroidism is of type I, results from a decreased synthesis of factor VIII and von Willebrand factor (VWF), responds to desmopressin with normal half-life times for factor VIII and VWF parameters, and disappears after treatment with I-thyroxine. AVWS type I or III, which occurs in a minority of patients with Wilms' tumour in the complete absence of an inhibitor against VWF and no absorption of factor VIII or VWF onto nephroblastoma cells, responds to chemotherapy and/or tumour resection. Hyaluronic acid produced by nephroblastoma cells may be the causative factor in atypical AVWS in Wilms' tumour. AVWS associated with thrombocythaemia of various myeloproliferative disorders is characterized by normal factor VIII and von Willebrand factor antigen (VWF: Ag) levels and a selective deficiency of functional ristocetin co-factor activity (VWF: RCo) and collagen-binding activity (VWF: CBA). AVWS type II in thrombocythaemia is caused by a platelet-dependent proteolysis of large VWF multimers, given the inverse relationship between platelet count and large VWF multimers in plasma and specific increases in the number of proteolytic VWF fragments in plasma. The laboratory findings of AVWS associated with systemic lupus erythematosus or IgG benign monoclonal gammopathy are characterized by a prolonged bleeding time and activated partial thromboplastin time, decreased or absent ristocetin-induced platelet activity, low to very low levels of factor VIII coagulant activity (mean 15%), VWF: Ag (mean 10.7%) and VWF: RCo (mean 6.2%), and a type II multimeric pattern of VWF. Neutralizing and non-neutralizing anti-VWF autoantibodies, usually IgG, have been detected in patient plasma either free or tightly bound to the intermediate and high molecular weight VWF factor VIII particles. The bound auto antibody-antigen complex is rapidly cleared from the circulation, resulting in low levels of factor VIII, VWF parameters as documented by a poor response to desmopressin and VWF factor VIII concentrate. High-dose intravenous immunoglobulin transiently corrects the factor VIII coagulant and VWF levels, lasting for a few weeks in AVWS type II associated with systemic lupus erythematosus or IgG benign monoclonal gammopathy. Prednisolone is effective in AVWS associated with autoimmune disorder. Prednisolone and chemotherapy will not affect AVWS associated with IgG benign monoclonal gammopathy because the monoclonal IgG protein remains to act as an anti-VWF autoantibody. An absorption of VWF to malignant cells has been documented in a few patients with various lymphoproliferative disorders or adrenal carcinoma and suggested to result in a depletion of VWF. The clinical picture of AVWS associated with early-stage IgG multiple myeloma, chronic lymphocytic leukaemia or non-Hodgkin's lymphoma without a paraprotein or no detectable underlying disorder is similar to that of AVWS type II in IgG benign monoclonal gammopathy but poorly documented with regard to the underlying immune mechanism of AVWS. The mechanical destruction of large VWF multimers may be of relevance in conditions in which the shear rate of flowing blood is increased, as may occur in cases of aortic stenosis, other heart valve defects or stenosed vessels. Drug-induced AVWS has been described in association with the use of pesticides valproic acid, ciprofloxacin, griseofulvin, tetracycline, thrombolytic agents and hydroxyethyl starch.
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PMID:Acquired von Willebrand syndromes: clinical features, aetiology, pathophysiology, classification and management. 1168 7

We describe a patient with non-Hodgkin's lymphoma who developed a lupus anticoagulant (LA) detectable by activated partial thromboplastin time (APTT), dilute Russell's viper venom time (DRVVT) and kaolin clotting time (KCT). IgM anticardiolipin antibodies (ACA) were elevated. At a later admission, and following treatment for the lymphoma, routine coagulation screening showed an elevated prothrombin time (PT) without correction in mixing tests using a recombinant thromboplastin. Routine APTT was below the reference range and ACA levels were normal. Raw data for one-stage factor assays demonstrated the presence of an inhibitor. Analysis for LA was undertaken by DRVVT, KCT, activated seven lupus anticoagulant assay, Taipan snake venom time, platelet neutralisation procedures (PNP), Ecarin time and PT using rabbit brain thromboplastin. The results revealed a LA capable of prolonging the clotting times of the PNPs and PT using recombinant thromboplastin, but that was corrected using Ecarin venom, modified PNP and brain thromboplastin. The antibody also demonstrated the lupus anticoagulant co-factor effect. The factor VIII: C was markedly raised which may have masked the LA in the APTT. The changing laboratory profile over time demonstrates the effects of LA heterogeneity and variations in sensitivity and specificity of assays for the detection of antiphospholipid antibodies.
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PMID:Alteration in the laboratory profile of a lupus anticoagulant in a patient with non-Hodgkin's lymphoma. 1559 3

This study investigated stromal changes in expression of tenascin and vasculogenesis in lymphoma. Documenting the dynamic nature of the stromal changes in lymphoma in relation to response to therapy is helpful in planning new therapies directed at these targets. Two hundred and sixty one samples from 111 patients with varying types of non-Hodgkin's lymphoma were reviewed and examined using immunohistochemistry techniques. Samples were stained for factor VIII - related antigen for microvessel density (MVD) analysis and anti-tenascin antibody for qualitative assessment of the stromal expression. Multiple samples from the same patient were taken at the same point in time to assess whether stromal changes were limited to sites of disease. Multiple samples were examined over the course of a patient's illness to assess whether the stromal changes were modulated according to disease activity. There was a significant increase in tenascin expression and MVD in the sites of disease compared with uninvolved sites (p = 0.01 and p < 0.0001, respectively). In patients who responded to therapy, there was a decrease in the expression of tenascin (p = 0.0049) and MVD (p < 0.0001), and in those with disease progression there was an increase in the tenascin expression (p = 0.0050) and MVD (p < 0.0001). Our results suggest stromal changes are isolated to the sites of disease within patients, allowing targeted therapies to be developed. Further, stromal changes correlate with disease response over the course of the patient's disease. This new finding may have implications for the timing of anti-stromally directed therapies.
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PMID:Tenascin and microvessel stromal changes in patients with non-Hodgkin's lymphoma are isolated to the sites of disease and vary in correlation to disease activity. 1619 91


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