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 aim of the present study is to evaluate the stimulatory capacity of chronic lymphatic leukemia (CLL) and Hodgkin's disease (HD) lymphocytes in the one-way mixed lymphocyte reaction (MLR) and to investigate whether, in patients with these diseases, a correlation exists between the degree of stimulatory capacity and production of a blastogenic factor. These studies might help to resolve the controversy about the nature of the stimulating cells and to offer some insight into the mechanism of the stimulation in the MLR. The significant observations from this study are summarized as follows: (1) Stimulatory capacity of CLL lymphocytes was intact or increased, while their responding capacity was markedly depressed. (2) In our group of patients with advanced Hodgkin's disease, both stimulating and responding capacities were imparied. (3) In these patients a correlation existed between the degree of stimulatory capacity and production of a blastogenic factor. This observation would raise the possibility that the production of a blostogenic factor may in some way be involved in the stimulation of responding lymphocytes in mixed cultures. Our results, which show a dichotomy between MLC stimulatory and responding capacities of CLL lymphocyte, may suggest that different factors are involved in stimulation and response.
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PMID:MLC stimulatory capacity and production of blastogenic factor in patients with chronic lymphatic leukemia and Hodgkin's disease. 12 1

Cellular immunity was evaluated in 15 untreated patients with Hodgkin's disease before and about 10 days after splenectomy. Skin test-reactivity was not affected by the operation. The number of lymphocytes was moderately increased in patients with pathologic stage I and II disease. The relative proportion of E-binding lymphocytes in the peripheral blood diminished significantly (p = .001) in patients with splenic weights of 240 g and more, whereas the PHA-stimulated thymidine incorporation increased significantly (p = .015) and the proportion of EAC-binding lymphocytes increased significantly (p = .023). The PHA-stimulation of peripheral lymphocytes in patients with pathologic stage I and II disease was at the same level before and after operation, but increased significantly (less than 0.02) in the more disseminated forms. The stimulation of the lymphocytes in vitro by a cocktail of antigens, and by allogeneic cells (MLC) remained unchanged. Although the number of cases studied is rather small, it is concluded that about 10 days after, splenectomy has no demonstrable untoward effect on the cellular immunologic potency.
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PMID:The influence of splenectomy on cellular immunologic parameters in Hodgkin's disease. 13 Sep 68

Peripheral blood lymphocytes and their in vitro reactivity have been recorded prior to treatment in 18 patients with Hodgkins disease, 11 with lymposarcoma, 13 with reticulosarcoma, 20 with various solid tumors and 37 normal control persons. The mean total numbers of lymphocytes, those of T lymphocytes,and the mean reactivity to PHA and ConA were reduced in all groups except lymphosarcoma, although with varying degrees of statistical significance. The percentages of T and B lymphocytes appeared to be normal in all groups, but the ranges of values were somewhat greater than among the normal controls. The mean total numbers of B lymphocytes were normal in all patient groups. All reductions seemed to be more pronounced in patients with disseminated than in those with localized disease, but none of these differences was statistically significant. All patient groups appeared to have reduced reactivity in MLC, while the ability to stimulate control lymphocytes was nearly normal. The results fail to indicate an in vitro immunological abberation specific to Hodgkin's disease. It seems that human malignant, neoplastic diseases are associated with a relatively selective reduction of the total numbers and reactivity of blood T lymphocytes. Various explanations of the reactivity impairment are proposed. The pathogenesis of the reduction of the total number of blood T lymphocytes remains obscure.
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PMID:Blood B and T lymphocytes and in vitro cellular immune reactivity in untreated human malignant lymphomas and other malignant tumors. 13 31

HLA typing for 27 A and B locus antigens was performed in 137 Caucasian patients with Hodgkin's disease. A and B locus antigen frequencies were compared for the entire group of patients, for 51 patients studied in a prospective manner and for 62 patients surviving with Hodgkin's disease for more than 5 years. MLC typing (HLA-D) was performed in 51 unselected Caucasian patients using 6 differend HLA-D homozygous test cells which define 3 HLA-D specificity groups (DW2, DW3, and DW4). HLA-AW33 was found in 0.0% of patients and in 5.9% of random Caucasian blood donors at the Sloan--Kettering Institute (X2 equals 7.04, p less than 0.01). HLA-A1 was found to be increased to 35.8% in the entire patient group (N = 137) as compared to 25.4% in 855 random North American Caucasians (X2 = 5.97, p less than 0.02). There was no significant deviation of any A or B locus antigen in relation to sex, histology, age of patient, or duration of survival (newly diagnosed vs 5-year survivors). No significant deviation for either of the 3 common HLA-D determinants (DW2, DW3, or DW4) was observed.
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PMID:HLA and MLC typing in patients with Hodgkin's disease. 14 67

Two sisters who developed nodular sclerosis Hodgkin's disease (H.D., N.S.) within 3 months of their 25th birthdays were HLA and MLC identical. All family members possessed the HLA-B7 antigen. The propositi, a third HLA/MLC identical sister, and the mother, shared the maternal B7 and lacked Dw2. The father and a fourth sibling with the paternal B7 were heterozygous for Dw2. In six unrelated patients with H.D., N.S., the presence of B7 and Dw2 correlated precisely. In 69 consecutive patients with H.D., N.S., the frequencies of 23 HLA antigens did not differ significantly from the frequencies in 245 control subjects.
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PMID:Familial Hodgkin's disease and the major histocompatibility complex. 14 65

Lymphocytes from patients with primary and secondary immunodeficiency disease were tested for capacity to produce LMIF after mitogen and antigen stimulation as well as for ability to stimulate and respond in unidirectional MLC-LMIF assay. Different patterns of immune abnormality in vitro were detectable when Con A and Candida albicans antigen were used. In addition, significant abnormalities in LMIF responding and stimulatory capacity were demonstrated in patients with Hodgkin's disease. LMIF production after stimulation with different agents allows for a better characterization of cellular defects in immunodeficiency disease.
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PMID:Leukocyte migration inhibitory factor (LMIF) profile in primary and secondary immunodeficiency disease. 79 76

Neoplastic cells obtained from the pleural effusion of a patient with Hodgkin's disease have been maintained in culture since 1978. These tumor cells have been shown to have the cytologic features, cytochemical staining, and cell surface markers of Reed-Sternberg cells. In this study we demonstrate that the cell line termed L428 is a potent stimulator of the primary human mixed lymphocyte reaction. Significant proliferation occurred when mononuclear leukocytes obtained from normal donors were stimulated with radiated L428 cells at responder:stimulator ratios varying from 200:1 to 20:1. Proliferative responses occurred between days 3 and 6 of the cultures with maximal proliferation on day 5. Under optimal culture conditions, mean net proliferative response of 14 normal donors was 51,000 +/- 10,600 dpm. The mixed lymphocyte response was totally blocked by concentrations of monoclonal anti-Ia antibody that had no effect on concanavalin A-induced proliferation. However, the mixed lymphocyte response was not blocked by an anti-K562 cell monoclonal antibody of the same immunoglobulin subclass that binds to the L428 cells. Antigen processing by responder monocytes or Ia-positive cells was not required for the MLC. When responder T cells from two normals were depleted of Ia-bearing cells and monocytes, the mixed lymphocyte reaction between the two normals was eliminated, yet the stimulation of each normal by the L428 cells was not reduced. The cells that proliferated in response to stimulation by the L428 cells were T cells, primarily of the helper subset. No IL 1 activity could be detected in concentrated supernatants of L428 cultures after stimulation of L428 cells by mitogens, phorbol esters, or muramyl dipeptide, or in the MLC. All of these cultures contain fetal calf serum. However, the L428 cells are capable of producing IL 1, because IL 1 was detected when the L428 cells were stimulated with LPS in the absence of fetal calf serum. These neoplastic cells, obtained from Hodgkin's disease, have many similarities to the murine as well as human dendritic cells.
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PMID:Neoplastic cells obtained from Hodgkin's disease are potent stimulators of human primary mixed lymphocyte cultures. 622 13

The effect of sera from patients with Hodgkin's disease (HD) on monocyte dependent ConA and MLC-activation of normal lymphocytes to DNA synthesis was studied. Lymphocyte stimulation was greatly enhanced in the presence of monocytes at a monocyte : lymphocyte ratio of less than or equal to 8 : 1. Higher ratios were usually suppressive. Some HD sera suppressed monocyte mediated enhancement of ConA and MLC-stimulation efficiently. The degree of inhibition by the individual HD serum remained similar in the absence of monocytes and at various monocyte : lymphocyte ratios. Pretreatment of monocytes or lymphocytes with HD serum had no effect. Inhibition was only noted when serum was present during the whole culture period. It is concluded that HD sera do not hamper the activity of monocytes to augment lymphocyte growth. The effect may be explained by direct effects of serum factors on lymphocytes.
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PMID:Suppression of monocyte dependent lymphocyte stimulation by sera from patients with Hodgkin's disease. 646 67

Mantle field radiotherapy for Hodgkin's disease is complicated by significant dose gradient (up to 10-20%) across the large fields required. Many different strategies of tissue compensation have been investigated, including custom physical compensators to provide better dose distributions. We present a method using dynamic multileaf collimator (dMLC) fluence modulation to simultaneously shape the treatment field and give homogeneous dose at depth throughout the classic mantle field. Five patients were treated for early-stage Hodgkin's disease with a conventional anterior-posterior-posterior-anterior (AP-PA) mantle field. The patients were planned using the Varian Eclipse treatment planning system, version 6.1.3, and treated on a Varian 2300CD. An AP-PA dynamic MLC beam-shaped and dose-compensated plan was created for each, and compared with the conventional blocked plan. Nine dose points were calculated at midplane in each plan. Chamber measurements were taken to confirm accurate dMLC delivery of the planned doses. The mean dose per fraction, relative to a central axis dose of 1.8 Gy, was increased in the conventional plans compared with the dMLC plans in the right (R) neck, left (L) neck, R supraclavicular, L supraclavicular, and L axillary points. The mediastinum tended to be underdosed relative to central axis, with the mid-mediastinal and lower mediastinal points showing improved coverage with the dMLC plans. Measurements showed excellent agreement between planned doses and delivered doses, with less than 2% in-field variation. Dynamic MLC fluence modulation was used to effectively deliver a mantle field that is both shape- and electronically-dose-compensated with sliding window MLC. Homogeneity was significantly improved throughout the treatment field, and measurements confirmed accurate dose delivery using this technique.
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PMID:Mantle fields in the era of dynamic multileaf collimation: field shaping and electronic tissue compensation. 1690 47