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)

Using routine histology, resin embedded sections and immunohistochemical techniques on formalin-fixed, paraffin processed tissue, 66 cases of primary gastrointestinal lymphoma have been classified. This study necessitated the development of reliable criteria to separate lymphomas of true histiocytic origin from those of lymphocytic origin. Among the morphologic properties of malignant histiocytes were complex pleomorphic nuclei, abundant well delineated cytoplasm and phagocytosis. These cells were shown to contain all major immunoglobulin chains, C3, lysozyme and in some cases alpha 1 antitrypsin. Malignant lymphomas derived from histiocytes could be divided into two groups: malignant histiocytosis of the intestine (MHI), a recently described diffuse pleomorphic lymphoma associated with villous atrophy of the small intestine, and histiocytic lymphoma (HL) which forms solid tumor masses in a similar manner to lymphocyte derived tumors. Immunohistochemical studies of lymphocyte derived tumors were negative apart from one case with plasmacytoid differentiation. Of the 66 cases, 50% were of histiocytic origin (33% MHI, 17% HL) and 41% of lymphocyte origin, there was one case of Hodgkin's disease and five cases were unclassified. The role of the histiocyte in gastrointestinal mucosa deserves further study.
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PMID:Primary gastrointestinal lymphomas: a classification of 66 cases. 37 99

Lag time (the interval between symptom onset and diagnosis) was described for 2665 children with lymphoma or a solid tumor who participated in Pediatric Oncology Group therapeutic protocols from 1982 until 1988. Median lag time ranged from 21 days for neuroblastoma to 72 days for Ewing sarcoma. Significant differences in lag time were found among diagnostic groups (p less than 0.001), even after adjustment for age, gender, and race. Age was significantly associated with lag time for all diagnoses (p less than 0.05) except Hodgkin disease. Girls had increased lag times for non-Hodgkin lymphoma (p = 0.02) but decreased lag times for Ewing sarcoma (p = 0.02). Differences in lag time related to race were significant only for children with osteosarcoma (p = 0.02), for which white children had longer lag times. Type of tumor and age were strongly associated with lag time. Within diagnostic groups, age, gender, and race failed to explain more than 16% of the variance in lag time, suggesting that other factors may play more prominent roles. Further study is necessary to identify these factors and to assess the relationship between lag time, stage of disease at diagnosis, and prognosis, especially before designing early-detection interventions for childhood cancer.
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PMID:Interval between symptom onset and diagnosis of pediatric solid tumors. 194 78

The risk of second primary cancer (SPC) was evaluated in 947 patients treated for Hodgkin's disease (HD) during the period January 1969 to December 1979. The median follow-up of this series was 10.5 years (range, 9 to 19). Treatment categories included radiotherapy (RT) alone (115 patients, 12%), chemotherapy (CHT) alone (161 patients, 17%), combined RT plus CHT (381 patients, 40%), and salvage treatment for resistant or relapsing HD (290 patients, 30.6%). Fifty-six SPCs were observed, occurring between 1 and 17 years from initial treatment. Among these, secondary acute nonlymphoid leukemia (s-ANLL) was the most frequent SPC (23 cases). Secondary non-Hodgkin's lymphoma (s-NHL) occurred in 5 patients, whereas a secondary solid tumor (s-ST) was observed in 28 patients. The calculated actuarial risk (+/- SE) of developing SPC was 5.0% (+/- 0.9%) and 23.1% (+/- 5.8%) at 10 and 19 years, respectively. Concerning treatment modalities and s-ANLL risk, no cases were observed in the radiotherapy group, whereas CHT plus RT and salvage groups showed the highest actuarial risk. This was, in fact, at 10 and 19 years, 3.1% (+/- 0.9%) and 8.1% (+/- 4.0%) in the former group, and 1.8% (+/- 1.0%) and 16% (+/- 9.0%) in the latter. A statistically significant difference was observed when the CHT plus RT group was compared with CHT and RT groups (P = .04). Concerning the relationships with chemotherapeutic regimens, 12 s-ANLL cases occurred in the mechlorethamine, vincristine, procarbazine, and prednisone (MOPP) plus RT group, and only one case in the group receiving doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) plus RT. A statistically significant difference of s-ANLL actuarial risk was found comparing patients receiving MOPP plus RT to all other treatment groups (P = .04). With respect to s-ST, the actuarial risk at 10 and 19 years was 2.0% (+/- 0.6%) and 13.0% (+/- 3.8%), respectively. No significant differences were found among groups treated with different modalities. These data were confirmed by a multivariate analysis, which indicated treatment modality and age as independent variables for s-ANLL and s-ST development, respectively. Based on the prolonged follow-up analysis, the actuarial SPC risk at 10 years hereby reported should reflect the real SPC incidence in our series.
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PMID:Second primary cancer following Hodgkin's disease: updated results of an Italian multicentric study. 199 12

Primary central nervous system (CNS) lymphomas were studied in fifteen autopsied patients with the acquired immunodeficiency syndrome (AIDS). Using the working formulation for non-Hodgkin's lymphomas, the tumors were classified as large cell (7 patients), mixed large and small cell (6 patients), small cleaved cell (1 patient), and unclassifiable (1 patient). The mixed lymphomas displayed unusual features characterized by a high mitotic rate and the presence of numerous medium-sized cells (5 to 10 mus), not classifiable using the working formulation. Focal T cell and lymphoplasmacytoid B cell infiltrates accompanied lymphoma cells at the periphery of and remote from solid tumor masses in 9 cases. Immunohistochemical analysis of the lymphomas suggested B cell neoplasms. All of these patients had concurrent CNS and systemic cytomegalovirus (CMV) infections. The CNS infections were of both viral (CMV, human immunodeficiency virus (HIV), varicella zoster virus (VZV), progressive multifocal leukoencephalopathy (PML) and non-viral (toxoplasmosis, candidiasis) etiology. In the general AIDS population at our institution, the autopsy incidence of CNS infections and systemic CMV was 63% and 60%, respectively. In contrast, the incidence for both these entities was 0% in otherwise healthy, non-AIDS patients with CNS lymphoma supports the hypothesis that viral infection plays a role in the pathogenesis of CNS lymphoma in the immunocompromised. Polyclonal lymphoplasmacytoid B and T cell infiltrates accompanying lymphoma may produce diagnostic difficulties on surgical biopsy. As these infiltrates were a frequent feature in this study, we caution that their recognition does not argue against the presence of CNS lymphoma.
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PMID:Central nervous system lymphoma in the acquired immunodeficiency syndrome. 217 24

The risk of a second malignancy was determined for 999 patients given primary treatment using chemotherapy only, radiation therapy only, or both for Hodgkin's Disease or a non-Hodgkin's lymphoma at Duke University Medical Center between 1970 and 1981. The incidence, 10-year actuarial risk, and relative risk of developing an acute leukemia, solid tumor, or second lymphoma were determined by treatment modality and initial lymphoma type. Among the 313 Hodgkin's disease patients, the acute leukemia actuarial risk was 2.0% after chemotherapy, 1.4% after radiation therapy, and 0.9% after combined treatment with chemotherapy and radiation therapy. Their relative risk for acute leukemia was 51.3 overall (95% confidence interval [CI] 13.8 to 131.8) and was elevated in each treatment group. Among the 686 non-Hodgkin's lymphoma patients, the acute leukemia actuarial risk was zero after radiation therapy, 4.6% after chemotherapy, and 4.5% after the combined treatment, again not significantly different between treatment groups. The leukemia relative risk was 10.6 (95% CI 3.4 to 24.8) in the chemotherapy and 11.9 (95% CI 3.2 to 30.6) in the combined treatment group. Among both the Hodgkin's disease and non-Hodgkin's lymphoma populations, the combined treatment group had a lower actuarial risk for solid tumors than either the chemotherapy or radiation therapy group (P less than 0.02). Solid tumor actuarial risk did not differ significantly between the chemotherapy and radiation therapy groups. Hodgkin's disease patients had a solid tumor relative risk that was elevated significantly after radiation therapy (6.5; 95% CI 2.4 to 14.0) and to a lesser extent after chemotherapy (2.6; 95% CI 0.8 to 6.1) or combined treatment (1.7; 95% CI 0.2 to 6.0). Solid tumor relative risk among non-Hodgkin's lymphoma patients was 0.3 for the combined treatment, 0.8 for the chemotherapy, and 1.0 for the radiation therapy group. None of the Hodgkin's disease patients developed a non-Hodgkin's lymphoma. This study found no significant difference in leukemia risk among lymphoma patients treated with chemotherapy and the combined treatment. It also found that the overall risk of a second malignancy is no higher after treatment with the combined therapy than with chemotherapy or radiation therapy alone.
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PMID:Impact on second malignancy risk of the combined use of radiation and chemotherapy for lymphomas. 235 13

The risk of second malignant neoplasm (SMN) was evaluated in 979 children with Hodgkin's disease. This cohort was diagnosed between 1955 and 1979 at one of the institutions of the Late Effects Study Group. Solid tumors, non-lymphocytic leukemia, and non-Hodgkin's lymphoma (NHL) developed in 18, 17, and 3 patients, respectively. The estimated cumulative probability of developing any SMN was 2% at 5 years from diagnosis, 5% at 10 years, and 9% at 15 years. The incidence is ninefold greater than the risk of acquiring cancer in 19 year-olds, the median age at which the diagnosis of SMN was made in this study population. For leukemia and NHL the corresponding probabilities were 1%, 3%, and 4% for the group as a whole but were increased (2%, 6%, and 8%) in patients who had suffered one or more recurrences. In order to analyze the risk of leukemia and NHL associated with alkylating agent chemotherapy, each patient was assigned a score of one for each alkylating agent administered for a 6-month period. Scores of 2, 4, 6, and 8 were associated with probabilities of leukemia or NHL of 2%, 3%, 6%, and 10%, respectively. In a multivariate analysis for leukemia/lymphoma that included AAD score, stage, and splenectomy, the effect of AAD score and splenectomy did not change substantially compared to the univariate results. AAD score remained statistically significant (P = .0001), and splenectomy was of borderline significance (P = .09). Of the 18 solid tumor SMNs, 15 developed within the field of radiation, and one other developed in tissue irradiated 34 years earlier for hemangioma. This study of a large and unselected group of children with Hodgkin's disease who received a variety of therapies demonstrates that children are as likely as adults to develop acute leukemia after alkylating agents and solid tumors in the field of radiation therapy.
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PMID:Second malignant neoplasms following childhood Hodgkin's disease: treatment and splenectomy as risk factors. 258 62

Modern multidisciplinary treatment of childhood cancer has made extent of disease evaluation important for proper treatment planning. Accurate staging is essential to cooperative group studies and for comparing treatment modalities at different centers. Operative staging plays an important role where clinical or imaging methods are limited, as in abdominal Hodgkin's disease or regional nodal metastasis. Operative staging is carried out either as a special diagnostic procedure, as in lymphoma, or as part of a planned surgical resection of a solid tumor. For lymphomas: Operative staging of abdominal Hodgkin's disease is required where protocols include involved field irradiation and sparing of normal growing tissue in the child. In non-Hodgkin's lymphoma, bulky abdominal tumor may be surgically evaluated after intensive chemotherapy either in delayed primary surgery or in second look procedures. Residual tumor may be excised or tagged with clips for localized irradiation to the tumor sparing normal abdominal organs. For solid tumors: During surgical resection of neuroblastoma, Wilms' tumor and rhabdomyosarcoma, the correct procedure involves regional staging either by formal node dissections or by multiple biopsies to determine extent of spread. Regional node dissections are often part of a correct cancer operation for cure, but also give staging information unobtainable by other methods. The surgeon must plan every procedure carefully with the aim of curing the patient and also deriving maximum information from the operation to enable correct planning of further treatment.
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PMID:The objectives and importance of operative staging of children with cancer. 301 92

To determine the significance of 67Ga localization in the thymus of children, 142 67Ga photoscans from 45 children with various tumors were studied. Sixty-nine photoscans were taken for 17 cases of lymphoma, 73 photoscans were made for 28 cases of nonlymphoid tumors. Thymic localization of 67Ga was positive in 16 (36%) of the 45 patients and in 30 (21%) of the 142 photoscans. Positive thymus scans were seen in five (29%) of the 17 cases of lymphoma and 11 (39%) of the 28 solid tumors. The positive incidence was highest (90%) in ages 1-2 yr old. Of the eight grade 2 (strong positive) patients, the thymus in one case of Hodgkin's disease was diagnosed as malignant and the other seven solid tumor cases were nonmalignant. Most of the latter seven cases became positive after beginning of treatment (surgery and/or chemotherapy). Although the precise mechanism is not well understood, thymic localization of 67Ga may represent immunologic response to tumors, especially in infants with nonlymphoid neoplasms.
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PMID:Thymic localization of gallium-67 in pediatric patients with lymphoid and nonlymphoid tumors. 310

A monoclonal antibody, designated BM-1, which is reactive in B5 formalin-fixed, paraffin-embedded tissues, has been generated against a cytoplasmic and nuclear antigen expressed in human myeloid precursor cells and derived leukemias. Using the avidin-biotin-complex immunoperoxidase procedure, BM-1 was found to stain selectively myeloid precursor cells in normal bone marrow and mature granulocytes in the blood. In a screen of 26 normal adult and fetal human organs fixed in B5 formalin, BM-1 was negative in all nonhematopoietic tissues with the exception of tissue granulocytes and scattered cells in the peripheral cortex of the thymus. Likewise a screen of 30 solid tumor cell lines including a spectrum of carcinomas, sarcomas, and neural-derived tumors was negative. BM-1 was also negative with 21 T and B cell lymphomas and 11 Hodgkin's disease tumors. A preliminary study of tumors of the hematopoietic system revealed that BM-1 was reactive with M2 and M3 acute myelogenous leukemias (AML), chronic myelogenous leukemias (CML) and myelomonocytic leukemias, and granulocytic sarcomas. M1, M4, M5, and M6 AML clot preparations were negative in this study, indicating that BM-1 may have a role in the histopathologic diagnosis of myelogenous leukemia. Myeloid leukemic cell lines HL-60, ML-2, KG1, and TPH-1-O showed BM-1 nuclear and/or cytoplasmic reactivity in a subpopulation of cells, but erythroid and lymphoid leukemias and all lymphoma cell lines were negative. Immunoperoxidase studies of a panel of fetal tissues showed BM-1 positive cells in the peripheral cortex of the thymus and portal myelopoietic regions of the liver at 18 weeks gestation. Finally, DNA-cellulose and solid phase radioimmunoassay (RIA) techniques developed in our laboratory demonstrate that the BM-1 antigenic domain is reactive only after binding to eukaryotic but not prokaryotic single- or double-stranded DNA. Immunoblot techniques using a DNA-cellulose purified protein sample revealed that BM-1 recognizes a 183 kD protein. These studies indicate that BM-1 is recognizing a myeloid-specific antigen that, because of its DNA binding characteristics, may have an important role in the differentiation of myeloid cells at the molecular level.
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PMID:Immunohistochemical characterization of a 183 KD myeloid-specific-DNA-binding protein in B5 fixed, paraffin-embedded tissues, and bone marrow aspirates by monoclonal antibody BM-1. 330 47

13 patients with Hodgkin's disease (HD) previously treated, 9 of whom were long-time (more than 2 yr) off-therapy, were studied for peripheral blood lymphocyte response to interleukin 2 and for lymphocyte subpopulations by means of in vitro cultures and monoclonal antibodies. The aim of the study was to ascertain the role played by interleukin 2 in the impaired cell-mediated immunity of HD patients. The results show a response of peripheral blood mononuclear cells of HD patients to either the T cell-specific polyclonal mitogens PHA and Con A or to the T cell-dependent, although B cell-specific, PWM, most significantly decreased compared to the normal response. As far as the interleukin 2 involvement in HD is concerned, our study suggests: an impaired endogenous interleukin 2 production by T lymphocytes, a most probable deficiency of the interleukin 2 receptor (Tac) expression and 3) a decrease of the number and/or of the function of NK cells no longer responsive in vitro to interleukin 2. The phenotypic analysis of peripheral blood mononuclear cells showed a slight decrease of total T cells (T3+), of the helper/inducer subset (T4+) and of the T4+/T8+ cells ratio. Our data seem to support the rationale for a therapeutical approach with interleukin 2 in controlled clinical trials also in HD patients, according to the experiments in progress in solid tumor patients.
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PMID:Peripheral blood lymphocyte response to recombinant and non-recombinant interleukin 2 in previously treated patients with Hodgkin's disease, long-time off-therapy. 349 36


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