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)

Five patients with Hodgkin's disease (IV stage) were implanted with fetal human thymus. Implantation were performed under the fascia of rectus abdominis muscle. Thymuses were obtained from fetuses 4-5 month old in aseptic condition and stored in tissue culture medium 199, before implantation. Immunological studies carried out during 4-6 months, revealed the elevation of the number of the lymphocyte in the peripheral blood, normalization of the number of rosete forming cells (RFC) as well as the response of peripheral blood lymphocytes to phytohaemagglutinin (PHA) stimulation. Two patients had long improvement of immunological responsiveness, but the other 3 only a transitient one during the first month after implantation. The possibility of the immunologic treatment in the early stages of Hodgkin's disease is discussed.
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PMID:[Case of implantation of human fetal thymus on the immunological reactivity in patients with Hodgkin's disease]. 122 9

A series of 22 consecutive cases of thymic tumour was collected and the tumours were reclassified according to a modified classification scheme. Two-thirds of them were benign lympho-epitheliomas, though in one case pleural implants were noted. One-third of the tumours were clearly malignant (carcinomas, lymphomas and seminomas). In one of the seminomas and in a case of Hodgkin's disease of the thymus no signs of recurrence or metastases have been observed in 10 and 8 years respectively. The sex distribution was fairly equal except that all three seminomas were detected in young men. The malignant tumours usually gave rise to symptoms, while the benign ones did not. Four of the lympho-epitheliomas were associated with myasthenia gravis. No other associated syndrome was observed. The possibility that lympho-epitheliomas may be malignant is discussed.
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PMID:Tumours of the thymus. 124 6

The immunologic deficiency of Hodgkin's disease includes skin anergy, delay in homograft rejection, negative transformation response of blood lymphocytes, and susceptibility to infections, particularly those of fungal or viral etiology (1, 3, 5). Since thymus-derived lymphocytes normally mediate these functions, a disturbance of this cell system would account for the observed immunological deficiencies in Hodgkin's disease. The majority, if not all of thymus-derived lymphocytes belong to the pool of recirculating, long-lived, small lymphocytes and an unimpeded circulation of these cells between lymph and blood is considered essential for a complete expression of their immunocompetence. Blockage and alteration of this circulation at the level of the lymph node is likely to occur in patients with Hodgkin's disease because of the characteristic infiltration of the lymph nodes by neoplastic cells. The question arises, therefore, whether the immunological deficiencies of Hodgkin's disease are due to intrinsically incompetent lymphocytes or the result of a faulty circulation of intrinsically competent lymphocytes. To answer this question the thoracic duct lymphocytes as well as blood lymphocytes of a patient with Hodgkin's disease have been studied with regard to re-circulation and immunocompetence.
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PMID:Lymphocyte function in Hodgkin's Disease. 126 73

P53 is a tumour suppressor gene, located in the short arm of chromosome 17, which encodes for a nuclear protein involved in the control of cellular growth, regulating the entry of the cell into the S-phase. P53 mutations have been identified in a progressively increasing number of human malignancies. Nuclear p53 protein is usually present in non-tumour cells in minute concentrations, due to its short half-life. In contrast, tumours with p53 mRNA mutations show a higher nuclear protein concentration, detectable by immunohistological techniques, due to stabilization by complexing with other proteins such as heat-shock protein or wild-type p53 protein. Levels of nuclear p53 protein detected by immunohistochemistry with the monoclonal antibody PAb 1801 were measured with the aid of an image analysis system in 83 non-Hodgkin's lymphomas (NHLs) and 13 cases of Hodgkin's disease, as well as in 14 cases of normal thymus, reactive tonsils, and lymphadenitis. High levels of p53 protein (greater than 5 per cent of the cells) were present only in high-grade lymphomas (in the proportion 13/55), with a peak incidence in Burkitt's lymphoma (5/8 cases). Lower levels (less than 5 per cent) of p53 protein were detected in low-grade B- and T-cell lymphomas, as well as in most of the cases of Hodgkin's disease, where p53 protein was selectively present in Hodgkin and Reed-Sternberg cells. In 5/14 reactive tonsils or lymph nodes, occasional p53-positive cells were identified. These results suggest a relationship between levels of p53 protein and the aggressiveness of NHL.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:P53 protein expression in lymphomas and reactive lymphoid tissue. 138 24

Epstein-Barr viral DNA (EBV DNA) has been detected in 20 to 58% of Hodgkin's disease tumors analyzed by Southern blotting or polymerase chain reaction (PCR). Because patients with Hodgkin's disease are generally immunodepressed, it is possible that the EBV is not directly involved in the pathogenesis of Hodgkin's disease but is merely detectable by molecular techniques because of reactivation of a latent infection. The purpose of this study was to determine if EBV DNA could be detected in an even higher percentage of cases of Hodgkin's disease, including acquired immunodeficiency syndrome (AIDS)-related Hodgkin's disease, by using newly designed, PCR amplification primers, and to compare the incidence of EBV DNA with the incidence of another common, latent virus (cytomegalovirus) in Hodgkin's disease tissue. The PCR was performed on DNA extracted from cells from 15 benign hyperplastic lymph nodes and from 15 cryopreserved cases of Hodgkin's disease, including 2 cases of AIDS-related Hodgkin's disease. For negative controls, PCR was also performed without template DNA and on genomic DNA from E. coli, calf thymus, a murine myeloma, and from a human cell line. After 32 cycles of amplification, a 225 base-pair amplification product comigrating with an EBV-positive control was detected in none of the negative controls but was present in 14 out of 15 cases (93%) of Hodgkin's disease, including both cases of AIDS-related Hodgkin's disease, and in 2 out of 15 cases of benign lymphoid hyperplasia. By contrast, cytomegalovirus DNA was undetectable by PCR in any of our specimens. We conclude that in our study set, the PCR procedure detected EBV-DNA but not cytomegalovirus DNA in a high percentage of cases of Hodgkin's disease, including two cases of AIDS-related Hodgkin's disease. These findings strengthen the hypothesis that EBV may be involved in the pathogenesis of Hodgkin's disease and AIDS-related Hodgkin's disease.
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PMID:Frequent detection of Epstein-Barr viral deoxyribonucleic acid and absence of cytomegalovirus deoxyribonucleic acid in Hodgkin's disease and acquired immunodeficiency syndrome-related Hodgkin's disease. 166 51

A monoclonal antibody (MAb), OPT1, reactive with T cells in formalin-fixed, paraffin-embedded tissue sections, has been identified through immunization with activated T cells from peripheral blood lymphocytes (PBL). The antibody is an IgG1 antibody as demonstrated by the Ouchterlony technique. By cytofluorometric analysis, almost all CD3+ lymphocytes and only a few CD20+ lymphocytes of peripheral blood expressed the OPT1 antigen. Nonhematolymphoid cell lines were negative for OPT1 by the immunoperoxidase staining using acetone-fixed cell lines. On the contrary, peripheral T cells, cells of two T cell lines out of four and a part of the cells of one B cell line out of two were positive for OPT1. The immunoperoxidase staining of paraffin-embedded tissue sections revealed that most of lymphocytes in T cell areas of lymph nodes expressed OPT1 antigen. Some lymphocytes in both cortex and medulla of the thymus and erythroid precursors of the bone marrow were OPT1+. In the malignant lymphoma series, approximately 90% of T cell lymphomas and 6% of B cell lymphomas reacted with OPT1. None of the Reed-Sternberg cells nor Hodgkin cells in Hodgkin's disease were positive. Consequently, OPT1 may be useful for the diagnosis and study of malignant lymphomas and other related lesions.
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PMID:A monoclonal antibody (OPT1) to T cells which is available for paraffin-embedded materials. 189 74

To evaluate the morphologic characteristics and frequency of thymic enlargement in Hodgkin disease, the initial and follow-up computed tomographic (CT) scans of 43 patients with newly diagnosed Hodgkin lymphoma were retrospectively analyzed. Sonograms of the thymic region in 21 patients were also available and were compared with the CT scans. Initial CT scans showed thymic enlargement in 17 of the 43 patients, no evidence of thymic enlargement in 15 patients, and equivocal findings in 11 patients. Analysis of follow-up CT scans indicated that seven of the 11 patients with initially equivocal findings had had thymic enlargement. In all seven patients, the anterior mediastinal tumor shrank with therapy and adopted a typical tongue-shaped thymic configuration. In nine of the 24 patients with thymic enlargement, the thymus remained enlarged after therapy and full clinical remission. The comparison of sonograms and CT scans showed that sonography could not help differentiate the normal-size thymus from surrounding fatty tissue. All thymic glands that were considered diseased because of enlargement at CT were sonographically visible due to an abnormal, hypoechoic structure. The results of the study show that thymic enlargement presumed to be due to involvement by Hodgkin disease seems to occur more frequently than previously reported.
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PMID:Thymic involvement in Hodgkin disease: CT and sonographic findings. 192 75

109 malignant lymphomas were surveyed by Southern blot analysis and polymerase chain reaction (PCR) for Epstein-Barr virus (EBV) DNA and compared with 16 examples of non-neoplastic lymphadenopathy and 4 normal thymuses. In specimens positive by the method of Southern and PCR, in situ hybridization studies were performed on formalin-fixed, paraffin-embedded sections. By Southern blot analysis, two of seven Hodgkin's disease samples (29%) (one of mixed cellularity and the other of lymphocyte predominance type), three of 56 B-cell lymphomas (5.6%) and five of 46 T-cell lymphomas (11%) demonstrated EBV DNA. However, the 16 examples of lymphadenitis and the 4 normal thymuses showed no EBV DNA. With PCR, EBV DNA was identified in one B-cell lymphoma, nine T-cell lymphomas, ten lymphadenitis specimens and two of the normal thymus, in addition to the positive specimens determined by the Southern blotting method. These results indicate that the presence of EBV DNA is not related to lymphoid malignancy, but enhancement of the DNA is demonstrated in some neoplastic conditions. By in situ hybridization, EBV genomes were not detected in all PCR-positive cases, but only in those positive by Southern blot analysis.
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PMID:Analysis of Epstein-Barr viral genomes in lymphoid malignancy using Southern blotting, polymerase chain reaction and in situ hybridization. 198 7

Immunization of BALB/c mice with EBV-CLL-1 cells, derived from Epstein-Barr virus transformed B lymphocytes from a chronic lymphocytic leukemia (CLL) patient, yielded 2 monoclonal antibodies (IgG1 Kappa and IgG2a Kappa) against a membrane antigen on a subset of normal B lymphocytes and non-Hodgkin's lymphomas. Immunofluorescence revealed strong reactivity of the antibodies with EBV-CLL-1 cells and with most lymphocytes in tonsil follicles, in the intestinal wall, around splenic arterioles and near Hassall's corpuscles in the neonatal thymus as well as with a small proportion of lymphocytes in some large reactive lymph node follicles, weak reactivity with 1/5 of peripheral blood B lymphocytes (PBL), and no reactivity with platelets, granulocytes and non-lymphoid tissues. PBL from 3 CLL patients showed weak staining of only larger cells. Intense fluorescence was observed in several non-Hodgkin's lymphomas of various histological types and in Burkitt's lymphoma lines but not in the 3 T lymphoblastoid and 12 nonlymphoid tumor lines examined. The antibodies precipitated Mr 22,000 and 33,000 bands from surface labeled RAJI or EBV-CLL-1 cells and cross-competed in a binding inhibition assay. The antibodies had approximately 6 million binding sites per EBV-CLL-1 or RAJI cell but were not cytotoxic. This high antigen-density and limited expression in normal cells may permit their use for immunocytological diagnosis and targeting cytotoxic agents and radionuclides against appropriate lymphoma cells.
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PMID:Monoclonal antibodies against Epstein-Barr virus transformed B lymphocytes from a CLL patient. 216 3

Frozen biopsy specimens taken from 30 cases with T cell tumors (8 with T cell acute lymphoblastic leukemia, 8 with T cell lymphoblastic lymphoma, and 14 with peripheral T cell lymphomas), and from 12 with Hodgkin's disease, were investigated using a direct immunohistochemical method to detect alpha-, beta- and gamma-enolases. Normal thymus and lymph node specimens with reactive lymphadenitis were also investigated. Subcortical thymocytes and the majority of deep cortical thymocytes showed reactivity of alpha-/beta-/gamma- approximately +/- -enolases, and medullary thymocytes and small lymphocytes in T zone areas of lymph node showed reactivity of alpha-/beta+/gamma- approximately +/- -enolases. Seven of the 8 cases with T cell acute lymphoblastic leukemia showed reactivity of alpha-/beta-/gamma(-)-enolases or alpha+/beta-/gamma(-)-enolases in leukemic lymphocytes, 7 of the 8 cases with T cell lymphoblastic lymphoma showed reactivity of beta(+)-enolase, and all 14 cases with peripheral T-cell lymphomas showed reactivity of alpha-/beta- approximately +/gamma(+)-enolases in lymphoma cells. All the 12 cases with Hodgkin's disease showed reactivity of alpha-/beta+/gamma(+)-enolases in Reed-Sternberg and Hodgkin's cells. These results indicate the following: (a) The neoplastic cells of T cell acute lymphoblastic leukemia, T cell lymphoblastic lymphoma and peripheral T cell lymphomas present different expressions in each of these three categories. This may imply a difference of maturation and differentiation or activation among neoplastic T lymphocytes. (b) T lymphocytes may switch from alpha- to beta-enolase and from alpha- to gamma-enolase in the course of differentiation and activation. (c) It is worth noting that the Reed-Sternberg and Hodgkin's cells of Hodgkin's disease present an identical expression of enolases.
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PMID:Expression of enolases in T cell tumors and Hodgkin's disease. 225 87


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