Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors have investigated the possibility of using sera with cold auto-lymphocytotoxic antibodies for the differential diagnosis of chronic lymphocytic leukemia (CLL) and malignant non-Hodgkin's disease (MNHD) at the stage of leukemization. The new rapid immunologic method was approved in the diagnosis of 40 CLL and 52 MNHD patients. The high informative value of this method has permitted the authors to recommend its use as an additional procedure for the differential diagnosis of the above lympho-proliferative diseases.
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PMID:[Autolymphocytotoxins in the differential immunodiagnosis of chronic lympholeukemia and malignant non-Hodgkin's lymphoma at the leukemization stage]. 134 83

Two t(14;18)-negative follicular B-non-Hodgkin's lymphomas with the same chromosomal abnormality, dup(12)(q13----qter), are presented. The absence of a BCL2 gene rearrangement was confirmed by molecular studies in both cases. Instead, duplication of a 12q segment was found. Further evidence for the presence of the dup(12)(q13----qter) was found using fluorescence in situ hybridization. dup(12q) may be equivalent to the trisomy 12 originally described in B-chronic lymphocytic leukemia. This chromosome anomaly has also been reported in B-non-Hodgkin's lymphomas, usually in association with other chromosome anomalies and a more aggressive tumor phenotype. Occurrence of dup(12q) in two histologically similar cases of follicular small cleaved-cell lymphoma without a typical t(14;18), suggests that this karyotypic change may play a critical role in some cases of follicle center-cell lymphomas.
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PMID:dup(12)(q13----qter) in two t(14;18)-negative follicular B-non-Hodgkin's lymphomas. 137 36

In search for a rationale for the use of interferons (IFNs) in treatment of non-Hodgkin lymphoma (NHL), we have investigated the IFN system of 13 patients with low-grade NHL, 15 patients with high-grade NHL, and 20 patients with chronic lymphocytic leukemia or leukemic immunocytoma (CLL/IC). Production of IFN induced by phytohemagglutinin (PHA), concanavalin A (Con A), pokeweed mitogen (PWM), Corynebacterium parvum, Herpes simplex virus (HSV), Newcastle disease virus (NDV), and interleukin 2 (IL-2) were studied in the peripheral leukocytes from the patients and from 21 control persons by means of a whole blood technique. All three groups of patients with NHL had significantly reduced production upon stimulation by NDV (p ranged between 0.0038 and less than 0.0001) compared to controls. Similarly, C. parvum also induced lower titers of IFN in the leukocytes of patients with non-leukemic NHL (p = 0.0015 for low-grade NHL and p = 0.0038 for high-grade NHL). When stimulated by PHA, the IFN response of all groups of patients was within normal range. With the exception in low-grade NHL, Con A also induced normal titers of IFN in the patients with NHL. The levels of IFN induced by PWM, HSV, and IL-2 were very low and no differences between controls and patients could be found. As NDV and C. parvum induce mainly IFN-alpha and the mitogens PHA and Con A mainly IFN-gamma, our results suggest that there is a deficiency in the IFN-alpha response in the patients with NHL but normal response in IFN-gamma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Deficiency in interferon production of peripheral blood leukocytes from patients with non-Hodgkin lymphoma. 137 88

The translocation t(11;14)(q13;q32) has been described in a spectrum of B-lymphoproliferative diseases and involves a putative oncogene, BCL1, which maps to chromosome band 11q13. Recent evidence indicates that this abnormality may delineate particular subtypes of lymphoma, such as intermediate lymphocytic and centrocytic lymphomas. Thus the possible significance of the t(11;14) within B-cell disorders should be reexamined in the light of a more objective approach to classifying these diseases by morphology, histology, and immunophenotype. We describe 16 patients with t(11;14)(q13;q32) from a series of 90 patients with chronic lymphoid disorders in whom clonal chromosome abnormalities were detected. All the cases were leukemic: prolymphocytic (B-PLL; 4/15 cases), chronic lymphocytic leukemia (CLL) with increase in prolymphocytes (2/9 cases), or non-Hodgkin lymphoma in leukemic phase, intermediate (3/4 cases), lymphoplasmacytic (2/2 cases), splenic lymphoma with villous lymphocytes (4/18 cases), and follicular (1 case). None of the CLL (25) or hairy cell leukemia cases (15) had t(11;14). Our findings showed that t(11;14) occurred in leukemias of mature B cells with lymphoplasmacytic features as judged by morphology and immunophenotype.
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PMID:Translocation t(11;14)(q13;q32) in chronic lymphoid disorders. 138 52

The pathogenesis of Reed-Sternberg cells and variants (RS-H cells) found in rare cases of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) is unknown. We studied 13 such cases by immunohistochemistry and in situ hybridization for identification of Epstein-Barr virus (EBV) RNA. The RS-H cells in five cases expressed the B-lineage marker CD20 and were negative for CD15. In two cases, the RS-H cells showed expression of both CD20 and CD15, whereas in another six cases, the cells were positive for CD15 but negative for CD20. Three of the cases expressing CD15 showed subsequent evidence of disseminated Hodgkin's disease. Regardless of the phenotype or clinical behavior, the RS-H cells in 12 of 13 cases were found to contain EBV RNA by in situ hybridization, but the surrounding neoplastic lymphocytes were invariably negative for EBV RNA. It is suggested that EBV has an important role in the pathogenesis of the RS-H cells in these rare cases.
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PMID:Chronic lymphocytic leukemia/small lymphocytic lymphoma with Reed-Sternberg-like cells and possible transformation to Hodgkin's disease. Mediation by Epstein-Barr virus. 839 5

Inv (1) antigen distribution was studied in 568 normal subjects and in 354 hematological patients in the Armenian population. Inv (1) antigen was detected in 16.7% of the normal Armenians studied. The incidence rate of Inv (1) factor does not depend on the distribution of phenotypes of ABO system, rhesus factor (D), and the sex of the subjects investigated. Inv (1) antigen incidence rate in patients with acute leukemia, chronic lymphocytic leukemia, iron deficiency anemia, lymphogranulomatosis, idiopathic thrombocytopenic purpura, autoimmune hemolytic anemia was similar to that in the control, and only patients with chronic myeloid leukemia had significantly decreased levels of Inv (1) antigen: 6.8% as compared to 16.7% in the population.
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PMID:[Antigenic composition of serum proteins of the Inv system in normal conditions and in patients with hematologic diseases among the Armenian population]. 138 57

This is a report on our attempt to use polymerase chain reaction (PCR) to detect rearrangement of the immunoglobulin gene in the tissue specimens obtained from 30 patients with non-Hodgkin's lymphomas. There were 20 B-cell lymphomas and 10 T-cell. All 20 B-cell lymphomas but none of the 10 T-cell lymphomas had JH rearrangement by Southern analysis. Two pairs of primers (V670/OL-4 and VH26/OL-4) were designed to amplify the CDR3 region of the immunoglobulin gene heavy chain. The PCR analysis was positive using either one or both pairs of primers in 11 of the the 20 cases (55 per cent) of B-cell lymphomas which all had positive rearrangement by Southern analysis. The two pairs of primers seemed to produce complementary results as the specimens may be positive to one pair but negative to the other. The false negative rate of 45 per cent is however much higher than the respective figures of 18 per cent and 0 per cent observed in our patients with acute lymphoblastic leukemia and chronic lymphocytic leukemia in a previous study. Peripheral blood and bone marrow biopsy specimens obtained at the time of initial diagnosis were available from 10 patients with B-cell lymphomas whose lymph node biopsy specimens at the time of diagnosis were positive by both Southern analysis and PCR. All these peripheral blood and marrow specimens had no microscopic evidence of involvement by lymphoma cells and JH rearrangement was not detected by Southern analysis. However, rearranged bands identical to that of the lymph node biopsy specimen were detected by PCR in the peripheral and marrow blood of one of them. This PCR technique has been shown to have a sensitivity of 0.1 per cent in our previous report and may be more useful than morphology alone or Southern analysis in detecting minimal lymphomatous involvement in the peripheral blood and bone marrow at the time of initial diagnosis. Further clinical correlation is required to confirm the finding.
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PMID:Detection of immunoglobulin gene rearrangement in B-cell lymphomas by polymerase chain reaction gene amplification. 139 11

Forty-five patients with low grade non-Hodgkin's lymphomas were studied with respect to the fraction of S-phase cells in fresh tumour material by flow cytometric analysis. Patients with stage I lymphomas were treated with radiotherapy, patients with stage II-IV lymphomas with Prednimustine (Sterecyt). Patients with lymphocytic lymphomas of CLL type were only treated if they had symptoms. Median S-phase fraction in the samples was 2.0 per cent. A significantly shorter survival was found for patients with lymphocytic lymphomas with S-phase fractions > 2.0 per cent compared with cases showing lower S-phase fractions. No significant difference in survival was found in the subgroups of immunocytic or follicular and follicular/diffuse centroblastic/centrocytic lymphomas. In a Cox multivariate analysis, in which also age, constitutional symptoms, stage and morphology were included, the fraction of S-phase cells was found to be a statistically significant, prognostic parameter for low grade lymphomas, mainly due to the result in the subgroup of lymphocytic lymphomas.
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PMID:'Aggressive' low grade lymphocytic lymphomas can be identified by flow cytometric S-phase determinations. 139 13

In this report the association of autoimmunity and autoimmune syndromes with lymphoproliferative disorders (LPD) is described in 15 patients. Non-Hodgkin's lymphoma (NHL) developed in 10 patients, Hodgkin's disease (HD) in 3 and chronic lymphocytic leukemia (CLL) in two. In most instances clinical and laboratory phenomena preceded the development/diagnosis of these disorders. Manifestations ranged from the presence of autoantibodies in the serum to the presence of both ill defined or incomplete autoimmune syndromes including cold urticaria, Raynaud's phenomenon, cold agglutinin disease, thyroiditis, nephrotic syndrome and vasculitis to typical systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and even one of scleroderma. It is suggested that in some patients (in)complete clinical manifestations of autoimmunity may precede the development of lymphoid neoplasias. The link between autoimmunity and lymphoproliferative disorders is briefly discussed.
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PMID:Autoimmunity and auto-immune syndromes associated with and preceding the development of lymphoproliferative disorders. 143 18

While Hodgkin's disease (HD) and non-Hodgkin's lymphoma (NHL) have long been regarded as distinct disease entities, recent observations suggest a closer association. The analysis of cases in which these diagnoses are made in the same anatomic site (composite lymphomas) or in separate sites (simultaneous or sequential HD and NHL) indicates that this phenomenon occurs more frequently than would be expected by chance alone. The most common form of composite lymphoma is coexistent nodular lymphocyte-predominant Hodgkin's disease (NLPHD) and large cell lymphoma (LCL) of B cell phenotype. This finding is consistent with a B cell origin for the abnormal cells in NLPHD, suggesting that LCL represents a form of histologic progression, with the existence of a clonal relationship between the two components. The association of other forms of HD (nodular sclerosis or mixed-cellularity) and NHL is less common, but still significant. As with NLPHD and LCL, one may observe composite lymphomas, or the diagnosis of HD may precede or follow the diagnosis of NHL. The vast majority of NHLs associated with HD are of B cell origin, most commonly follicular lymphomas. An association between HD and B cell chronic lymphocytic leukemia (CLL) is also observed. In selected cases, Reed-Sternberg (RS) cells are seen in a background of otherwise typical CLL, and some of these patients have progressed to disseminated HD. These findings suggest that, at least in some cases, HD may be clonally related to an underlying B cell malignancy, and that the RS cell may be an altered B lymphocyte.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The interrelationship of Hodgkin's disease and non-Hodgkin's lymphomas--lessons learned from composite and sequential malignancies. 148 Aug 52


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