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)

Spontaneous reticulum cell sarcoma in SJL/J mice has been proposed as an animal tumor model for Hodgkin's lymphoma. The relationship of tumor progression and immune function is not clear, however, and has prompted a systematic evaluation of SJL/J immune competence. It was found that the ability to generate cell-mediated immunity and antibody response to allografts was not impaired in 2- to 12-month-old mice, regardless of their tumor status. All animals were capable of generating in vivo cytotoxic effector T-cells and both IgG and IgM classes of cytotoxic antibody to a tumor allograft. In addition to being able to respond, older mice showed an unexpected hyperresponsiveness to alloantigens, which suggested that escape from feedback control might be a characteristic of SJL/J mice. Loss of immune regulation was further indicated by the failure to induce tolerance to human gamma-globulin in mice 4 months and older, while 3-week-old SJL/J mice could be rendered unresponsive. Coincident with this apparent loss of regulation, circulating antibodies to synthetic double-stranded RNA, polyinosinis - polycytidylic acid, were first detected in unimmunized mice at 4 months of age, and titers remained elevated regardless of tumor status. It is suggested that tumor development as well as autoimmunity may result from an effective amplification of the immune response.
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PMID:Immune functions characteristic of SJL/J mice and their association with age and spontaneous reticulum cell sarcoma. 76 61

The cases are presented of 4 hydantreated epileptic patients developing malignant lymphomas (1 Hodgkin's lymphoma). The duration of the hydantoin therapy ranged from 7 to 23 years. There was no evidence of an allergic drug reaction, with the exception of slight blood eosinophilia. Prior to the lymphoma one patient exhibited leukopenia and a second thrombocytopenia. Hydantoins were discontinued in 3 cases but the lymphomas never disappeared spontaneously and only once did tumor progression came to a stillstand. Two patients were successfully treated with either chemo- or radiotherapy. Possible correlations between the documented immunosuppressive action of hydantoin derivatives and tumor induction are discussed. Malignant lymphomas may be sequelae of long-term hydantoin therapy and are not always preceded by the well-known reversible hydantoin lymphadenopathy.
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PMID:[Malignant lymphoma following years of hydantoin treatment for epilepsy]. 121 68

In this study we examined the P170-expression (mdr-phenotype) in 42 non-Hodgkin's Lymphomas with variant entities immunohistochemically with the mab JSB1. The mdr-phenotype was related to the tumor proliferation as measured by Ki67-expression and AgNOR numbers. Furthermore the mdr-phenotype was related to the tumor associated T-lymphocytes. The mdr-phenotype showed no relation to histological type and the proliferation of the tumor. There was a positive correlation between the mdr-phenotype and CD2-reactive lymphocytes. There was also a significant positive correlation between CD4-reactive lymphocytes and the mean number of AgNOR's. Possibly P170-expression and proliferation of the tumor cells have a lymphotactic effect on T-lymphocytes. The latter could promote tumor progression by means of paracrine mechanisms.
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PMID:[Tumor proliferation, MDR phenotype and tumor associated t-lymphocytes in non-Hodgkin's lymphomas]. 128 69

Cytokines are potent modulators of the physiological immune response. A number of reactive processes are associated with a deregulation of this cytokine expression. Animal models with transgenic mice or transfection experiments have shown that an autocrine or paracrine pathway might be involved in tumor progression and/or tumorigenesis. The study of cytokine expression in malignant lymphomas showed a heterogeneous expression pattern with a number of cases which quantitatively show indications for a marked deregulation of the cytokine expression. The expression od IL-7 and IL-9 seem to be special features of Hodgkin's disease and large cell anaplastic lymphomas. Transfection experiment with IL-9 into mouse T cells results in an autocrine loop and tumorigenesis of the transfected cells. These tumors share a number of similarities to Hodgkin's disease and large cell anaplastic lymphomas in human.
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PMID:[Cytokines and malignant lymphomas]. 128 79

p53 is a tumor suppressor gene that commonly undergoes mutations in human tumors, including lymphomas. Because p53 mutations are not restricted to a single locus, immunohistochemistry is useful to detect p53 expression and correlate this finding with lymphoma phenotype. Cryostat sections from 125 cases of lymphoma were analyzed for p53 expression using three different monoclonal antibodies (pAb 421, 1801, 240) which react with human cellular p53 and a common conformational epitope on mutant p53. A control antibody (pAb 246) reacts only with wild type p53 of murine origin and was negative in all cases. Tissue from 29 cases of lymphoid hyperplasia, including six from human immunodeficiency virus-positive (HIV+) patients, were negative for p53. p53 was predominantly localized in nuclei of high-grade lymphomas, including 14 of 46 cases of B cell immunoblastic lymphomas and two of five T cell immunoblastic lymphomas. p53 expression was relatively common in lymphomas from HIV+ patients, and unusual in intermediate and low-grade lymphomas of follicular center cell type. Low-grade lymphoma of small lymphocytic type disclosed p53+ large cells (paraimmunoblasts) that may play a role in tumor progression in this lymphoma subtype. p53 was also strongly expressed in the nuclei of Reed Sternberg cells from 19 of 37 cases of Hodgkin's disease, including six cases of mixed cellularity, and 13 cases of nodular sclerosing type. Immunohistochemical staining is a rapid method to identify p53 expression in lymphomas.
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PMID:Immunohistochemical analysis of p53 expression in malignant lymphomas. 146 98

The sonographic appearances of primary non-Hodgkin lymphoma developing in the porta hepatis in three patients soon after hepatic transplantation were reviewed. The lymphomas appeared as large hypoechoic masses encasing vital portal structures--the hepatic artery and the common bile duct--in all three cases and displacing the portal vein in two. The liver was only locally involved. All patients presented with jaundice soon after transplantation (average interval, 6.3 months). Rapid tumor progression caused hepatic infarction, necessitating retransplantation in two patients. The third patient died shortly after diagnosis. The authors believe this complication will be seen increasingly as liver transplantation becomes more common. Non-Hodgkin lymphoma should be considered when an obstructing mass is found in the porta hepatis, even when the time interval since transplantation is short.
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PMID:Non-Hodgkin lymphoma in the porta hepatis after orthotopic liver transplantation: sonographic findings. 153 10

This prospective study was designed to determine the efficacy of iodized talc pleurodesis in patients with pleural effusions. Thirty-four patients underwent this treatment (three bilaterally) between October 1, 1989, and March 31, 1991. All patients had to have complete or nearly complete lung reexpansion after tube thoracostomy with fluid drainage less than 100 ml in 24 hours. A slurry containing 5 gm of talc and 3 gm of thymol iodide was instilled into the pleural space through the chest tube. Chest tubes were removed after complete reexpansion and clearing of the effusions, usually in 3 to 5 days. The patients' ages ranged from 26 to 88 years (average 50 years). Eighteen patients had lung carcinoma, two had mesothelioma, and one each had carcinoma of the ovary, breast, or anorectum, multiple myeloma, schwannoma, or Hodgkin's lymphoma. Two patients had an unknown adenocarcinoma primary and five other patients had acquired immunodeficiency syndrome. One patient had congestive heart failure. Nineteen patients had left, 12 had right, and three had bilateral pleural effusions. The effusion was serosanguineous in 26 and serofibrinous in eight patients. Serial chest radiography showed complete response in all patients. The period of follow-up ranged from 1 to 21 (average 4.9) months, with no recurrences. Twenty-three patients have died during the follow-up period, and there was no sign that reaccumulated pleural effusion existed in any, despite clinical evidence of systemic tumor progression. These observations indicate that intrapleural instillation of a slurry of iodized talc is a safe, adequate, and effective treatment for control of neoplastic or benign pleural effusions.
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PMID:Iodized talc pleurodesis for the treatment of pleural effusions. 156 70

Cytogenetic abnormalities in non-Hodgkin's Lymphoma (NHL) provide a model system for the analysis of the role of multiple genomic aberrations in human malignancy. In order to define correlations with histology, tumor evolution, and the effects of genotoxic exposure, cytogenetic analysis was performed on 434 specimens of NHL derived from 423 patients consecutively ascertained over a 5-year period (1984-1989). Six recurring translocations (RT) were observed: t(14;18)(q32;q21), t(8;14)(q24;q32), t(11;14)(q13;q32), t(3;22)(q27;11), t(2;5)(p23;q35), and t(1;6)(q21;q25). No translocation was specific to a single histologic subtype. Other structural chromosome abnormalities were analyzed according to break site; groups of related breaks were considered together for statistical analysis. Recurring other structural and numerical aberrations (ROA) encountered in greater than 10% of specimens included rearrangements with breaks at bands 1p32-36, 1q21-23, 6q21-25, and trisomies of chromosomes 7 and 12. ROA with one of these breaks or numerical abnormalities were the sole abnormalities in at least two cases. Correlations were observed among ROA and between ROA and histologic subtypes. Trisomy 7, breaks at 1q21-23, 1p32-36, 6q21-25, and 7q32 were associated with t(14;18); trisomy 18 was associated with trisomy 3; and structural abnormalities of chromosome 17 were associated with breaks at 1p32-36 and 6q21-25. Trisomy 7 and trisomy 12 were more frequent in t(14;18)-bearing intermediate to high grade tumors compared to low grade tumors. Trisomy 12 and breaks at band 1p22 were associated with large cell diffuse lymphomas. Incidence rates of reciprocal translocations, ROA, and measures of karyotypic complexity, including number of breakpoints and marker chromosomes were compared in pretreatment and posttreatment samples. Karyotypic complexity was greater in the posttreatment samples, reflecting an increased frequency of nonrecurring and low incidence aberrations. These results better define the association of genomic aberrations and tumorigenesis, histologic transformation, and tumor progression.
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PMID:Cytogenetic analysis of 434 consecutively ascertained specimens of non-Hodgkin's lymphoma: correlations between recurrent aberrations, histology, and exposure to cytotoxic treatment. 186 33

We describe 4 patients with Hodgkin's disease who developed neuralgic amyotrophy in the setting of radiation therapy. In contrast to tumor progression or radiation plexopathy, the symptom onset was abrupt and occurred within days to weeks of receiving radiation treatments. There is an association between Hodgkin's disease, radiation therapy, and neuralgic amyotrophy.
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PMID:Neuralgic amyotrophy in association with radiation therapy for Hodgkin's disease. 200 16

We have investigated the frequency of p53 mutations in B- and T-cell human lymphoid malignancies, including acute lymphoblastic leukemia, the major subtypes of non-Hodgkin lymphoma, and chronic lymphocytic leukemia. p53 exons 5-9 were studied by using genomic DNA from 197 primary tumors and 27 cell lines by single-strand conformation polymorphism analysis and by direct sequencing of PCR-amplified fragments. Mutations were found associated with (i) Burkitt lymphoma (9/27 biopsies; 17/27 cell lines) and its leukemic counterpart L3-type B-cell acute lymphoblastic leukemia (5/9), both of which also carry activated c-myc oncogenes, and (ii) B-cell chronic lymphocytic leukemia (6/40) and, in particular, its stage of progression known as Richter's transformation (3/7). Mutations were not found at any significant frequency in other types of non-Hodgkin lymphoma or acute lymphoblastic leukemia. In many cases, only the mutated allele was detectable, implying loss of the normal allele. These results suggest that (i) significant differences in the frequency of p53 mutations are present among subtypes of neoplasms derived from the same tissue; (ii) p53 may play a role in tumor progression in B-cell chronic lymphocytic leukemia; (iii) the presence of both p53 loss/inactivation and c-myc oncogene activation may be important in the pathogenesis of Burkitt lymphoma and its leukemic form L3-type B-cell acute lymphoblastic leukemia.
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PMID:p53 mutations in human lymphoid malignancies: association with Burkitt lymphoma and chronic lymphocytic leukemia. 205 20


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