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)

In the current retrospective study, the authors investigated the prognostic significance of total serum cholesterol values at the time of diagnosis in patients with Hodgkin's disease (n = 179). Cholesterol values were significantly lower in these patients than in age- and sex-matched controls. Subgroups with advanced stages (P less than or equal to 0.01), poor response to therapy (P = 0.04), and relapse after complete response (P = 0.026) (but not with bulky disease) had lower cholesterol values. By univariate analysis (cut-point value, 140 mg/dl), the 5-year survival rate was 2.5 times higher in patients with normal cholesterol values than in hypocholesterolemic patients (P less than 0.00009). Hypocholesterolemia was retained as an adverse, independent prognostic factor by multivariate Cox regression analysis. The authors concluded that total serum cholesterol values at the time of diagnosis may be a parameter with unrecognized significance in Hodgkin's disease.
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PMID:The prognostic significance of total serum cholesterol in patients with Hodgkin's disease. 173 71

CD30, a lymphoid activation marker, is shed into the cell environment after endoproteolytic cleavage of its ectodomain. Soluble (s)CD30 is able to suppress the Th1-type immune response. Because high serum levels of sCD30 and cholesterol-lowering drugs seem to be beneficial in some Th1-type autoimmune diseases, we focused on a link between CD30 shedding and the amount of cellular cholesterol. Cholesterol depletion of human Hodgkin lymphoma- and non-Hodgkin lymphoma-derived cell lines by methyl-beta-cyclodextrin led to a down-regulation of membrane-bound CD30 and increased release of sCD30. Additionally, the cholesterol-interfering drugs lovastatin, cholesterol oxidase, and filipin increased CD30 shedding. Both the down-regulation of membrane-anchored CD30 and the release of sCD30 were dependent on metalloproteinases. Using specific inhibitors, we detected TNF-alpha converting enzyme (TACE) as the leading enzyme responsible for cholesterol-dependent CD30 shedding. A Triton X-100-based method for lipid raft isolation revealed that CD30 was partially present in lipid rafts, whereas TACE was localized in the nonraft fractions. Disintegration of lipid rafts by cholesterol depletion might therefore lead to dynamic interactions of CD30 with TACE, resulting in enhanced shedding of CD30. Our results suggest a possible role of cholesterol-dependent shedding of CD30 in the pathogenesis of immune diseases.
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PMID:Depletion of cellular cholesterol and lipid rafts increases shedding of CD30. 1503 47

After radiotherapy treatment, there is an increased incidence of localized atherosclerosis in patients with Hodgkin's disease, breast cancer, and head and neck cancer. Here, we established a mouse model to study the development and progression of radiation-induced atherosclerosis and to compare the phenotype of these lesions with age-related atherosclerosis. Atherosclerosis-prone ApoE-/- mice fed a regular chow diet received single radiation doses of 14 Gy or sham treatments (0 Gy) to the neck, including both carotid arteries. At 22, 28, and 34 weeks after irradiation, blood samples were taken, and the arterial tree was removed for histological examination. Cholesterol levels in irradiated mice were not significantly different from age-matched controls, and markers of systemic inflammation (soluble intercellular adhesion molecule-1, soluble vascular cell adhesion molecule-1, and C-reactive protein) were not elevated. The lesions in irradiated arteries were macrophage rich, with a remarkable influx of inflammatory cells, predominantly granulocytes. Intraplaque hemorrhage and erythrocyte-containing macrophages were seen only in lesions of irradiated arteries. Based on these data, we propose that irradiation accelerates the development of macrophage-rich, inflammatory atherosclerotic lesions prone to intraplaque hemorrhage.
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PMID:Ionizing radiation accelerates the development of atherosclerotic lesions in ApoE-/- mice and predisposes to an inflammatory plaque phenotype prone to hemorrhage. 1643 78