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)

Angiogenesis entails new vessel formation from preexisting vessels. It follows vasculogenesis during embryo development. In post-natal life, it occurs both in physiological conditions (wound repair and cyclically in the female genital system) and pathological conditions such as tumors. Several sequential steps are involved, including basement membrane degradation by proteolytic enzymes secreted by the endothelial cells, chemotaxis toward the stimulus and proliferation of these cells, canalization, branching and formation of vascular loops, stabilization and functional maturation of neovessels following perivascular apposition of pericytes and smooth muscle cells, and neosynthesis of basement membrane constituents. Tumor angiogenesis is regulated by several factors, mainly growth factors for the endothelial cells secreted by both the tumor and host inflammatory cells, and mobilized from extracellular matrix stores by proteases secreted by tumor cells. Regulatory factors also include the extracellular matrix components and endothelial cell integrins, hypoxia, oncogenes and tumor suppressor genes. Angiogenesis is mandatory to the process of tumor progression (growth, invasion and metastasis), since it conveys oxygen and metabolites, whereas endothelial cells secrete growth factors for tumor cells and a variety of proteinases which facilitate invasion and increase opportunities for tumor cells to enter the circulation. We present our results concerning the relationship between angiogenesis and progression in patients with melanoma, multiple myeloma, B-cell non-Hodgkin's lymphomas and mycosis fungoides. Lastly, it is becoming increasingly evident that agents interfering with blood vessel formation also interfere with tumor progression. These include antagonists of angiogenic growth factors, angiogenic receptors, endothelial cell integrins, and proteolytic enzymes, as well as non-specific toxic agents for vessels and low-dose chemotherapeutic agents. Their recent applications in preclinical models and in neoplastic patients are reviewed.
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PMID:[Angiogenesis and anti-angiogenesis in human neoplasms. Recent developments and the therapeutic prospects]. 1084 87

A new type of shape descriptor is proposed to describe the spatial orientation for non-covalent interactions. It is built from simple, anisotropic Gaussian contributions that are parameterised by 10 adjustable values. The descriptors have been used to fit propensity distributions derived from scatter data stored in the IsoStar database. This database holds composite pictures of possible interaction geometries between a common central group and various interacting moieties, as extracted from small-molecule crystal structures. These distributions can be related to probabilities for the occurrence of certain interaction geometries among different functional groups. A fitting procedure is described that generates the descriptors in a fully automated way. For this purpose, we apply a similarity index that is tailored to the problem, the Split Hodgkin Index. It accounts for the similarity in regions of either high or low propensity in a separate way. Although dependent on the division into these two subregions, the index is robust and performs better than the regular Hodgkin index. The reliability and coverage of the fitted descriptors was assessed using SuperStar. SuperStar usually operates on the raw IsoStar data to calculate propensity distributions, e.g., for a binding site in a protein. For our purpose we modified the code to have it operate on our descriptors instead. This resulted in a substantial reduction in calculation time (factor of five to eight) compared to the original implementation. A validation procedure was performed on a set of 130 protein-ligand complexes, using four representative interacting probes to map the properties of the various binding sites: ammonium nitrogen, alcohol oxygen, carbonyl oxygen, and methyl carbon. The predicted 'hot spots' for the binding of these probes were compared to the actual arrangement of ligand atoms in experimentally determined protein-ligand complexes. Results indicate that the version of SuperStar that applies to our descriptors is capable to predict the above-mentioned atom types in ligands correctly with success rates of 59% and 74%, respectively, for all ligand atoms (regardless of their solvent accessibility), and a subset of solvent-inaccessible ones. If not only exact atom-type matches are counted, but also those that identify ligand atoms of similar physicochemical properties, the prediction rates rise to 75% and 89%. These rates are close to those obtained by the original SuperStar method (being 67% and 82%, respectively, for the prediction of exact matching atom types, and 81% and 91% in the case of predicting similar atom types).
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PMID:Simple knowledge-based descriptors to predict protein-ligand interactions. methodology and validation. 1113 70

The authors report a case of Fournier's gangrene in a 54-year-old patient subjected 6 days earlier to chemotherapy for mediastinal Hodgkin's disease. The patient had fever and reported the onset of worsening pain and heat sensations in the inguinal, perineal and scrotal areas. Objectively, there was local oedema followed by the onset of crepitation. The patient had a very low white blood cell count (900/cu.mm). The Patient underwent emergency surgery with multiple, communicating incisions in the inguinal, perineal and scrotal areas, with the removal of necrotic tissue and daily washing with physiological solution and 12% H2O2. He also received antibiotic treatment with metronidazole and gentamicin and 5 cycles of high-pressure oxygen therapy, with disappearance of pain and fever and good local tissue repair.
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PMID:[Fournier's gangrene in a patient with Hodgkin's disease: a clinical case]. 1182 71

The response of tissue to ischemia (cessation of blood flow and deprivation of oxygen) includes swelling of the intracellular space, shrinkage of the extracellular space, and an increase in the extracellular potassium concentration. The responses of cardiac and brain tissue to ischemia are qualitatively different in that cardiac tissue shows a rise in extracellular potassium over several minutes from about 5 to 10-12 mM followed by a plateau, while brain tissue shows a similar initial rise followed by a very rapid increase in extracellular potassium to levels of 50-80 mM. During hypoxia the flow of blood (or perfusate) is maintained and, while there is a substantial efflux of potassium from cells, there is little accumulation of potassium in the interstitium. A mathematical model is proposed and studied to try to elucidate the mechanism(s) underlying the increase in extracellular potassium, and the different time courses seen in neural and cardiac tissue. The model involves a Hodgkin-Huxley-type description of transmembrane ion currents, allows for ion concentrations as well as volumes to change for both the intracellular and extracellular space, and includes coupling of damaged tissue to nearby healthy tissue. The model produces a response to ischemia much like that seen in neural tissue, and the mechanism underlying this response in the model is determined. The same mechanism is not present in cardiac ion models, and this may explain the qualitative difference in response shown in cardiac tissue.
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PMID:A mathematical study of volume shifts and ionic concentration changes during ischemia and hypoxia. 1245 53

Chromosomal translocations and somatic mutations occurring in the 5' noncoding region of the BCL6 gene, encoding a transcriptional repressor, are most frequent genetic abnormalities associated with non-Hodgkin B-cell lymphoma and result in deregulated expression of BCL6. However, the significance of deregulated expression of BCL6 in lymphomagenesis and its effect on clinical outcomes of lymphoma patients have remained elusive. In the present study, we established Daudi and Raji B-cell lymphoma cell lines that overexpress BCL6 or its mutant, BCL6-Ala333/343, in which serine residues required for degradation through the proteasome pathway in B-cell receptor-stimulated cells are mutated. BCL6 overexpression did not have any significant effect on cell proliferation, but significantly inhibited apoptosis caused by etoposide, which induced a proteasome-dependent degradation of BCL6. BCL6-Ala333/343 was not degraded after etoposide treatment and strongly inhibited apoptosis. In these lymphoma cell lines, etoposide increased the generation of reactive oxygen species (ROS) and reduced mitochondria membrane potential, both of which were inhibited by the antioxidant N-acetyl-L-cysteine (NAC). NAC also inhibited apoptosis. Furthermore, BCL6 overexpression was found to inhibit the increase in ROS levels and apoptosis in response to etoposide and other chemotherapeutic reagents. These results raise the possibility that deregulated expression of BCL6 may endow lymphoma cells with resistance to chemotherapeutic reagents, most likely by enhancing the antioxidant defense systems.
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PMID:BCL6 overexpression prevents increase in reactive oxygen species and inhibits apoptosis induced by chemotherapeutic reagents in B-cell lymphoma cells. 1288 2

The beneficial role of corticosteroid therapy for the treatment of methotrexate-induced pneumonia remains controversial. We report two cases of acute severe interstitial pneumonia induced by methotrexate in patients with non-Hodgkin lymphoma given a polychemotherapy protocol (M'BACOD). The first signs appeared on the eleventh day of the first cycle in patient one and on the tenth day of the third cycle in patient two. The causal implication of methotrexate was based on the history, the clinical and radiological presentation, and the negative tests in both patients: lymphocyte alveolitis with granulomatous lesions on the transbronchial biopsy in patient one and positive leukocyte migration test in the presence of methotrexate in patient two. Early acute respiratory failure required high flow rate oxygen therapy with positive expiratory pressure ventilatory assistance. The course was rapidly favorable both for blood gases and radiographic presentation without corticosteroids. These two cases illustrate that pulmonary disease can be cured without corticosteroids despite severe respiratory failure at onset. This provides a further argument on reservations about using corticosteroids for suspected methotrexate-induced pneumonia.
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PMID:["Spontaneous" resolution of two severe methotrexate-induced pneumonias]. 1470 26

Fetal tissue is the richest source of primordial stem cells and has several properties that make it particularly useful for transplantation. It is superior to adult (mature) tissue in certain respects. First, fetal cells are capable of proliferating faster and more often than mature, fully differentiated cells. This means that these donor cells are able to quickly reverse the lost function of the host. In addition, these fetal cells can often differentiate in response to the environmental cues around them. This is because of their location--they can grow, elongate, migrate, and establish functional connections with other cells around them in the host. It has been found that fetal tissue is not easily rejected by the recipient due to the low levels of histocompatibility antigens in the fetal tissue. At the same time, angiogenic and trophic factors are at high levels, enhancing their ability to grow once they are transplanted. Since early fetal hematopoietic tissue lacks lymphocytes, graft vs host reactions are minimized. Fetal cells tend to survive excision, dissection, and grafting better because they generally do not have long extensions or strong intercellular connections. Finally, fetal tissue can survive at lower oxygen levels than mature cells. This would make them more resistant to the ischemic conditions found during transplantation or in vitro situations. Studies on fetal cell/tissue transplant have been encouraging. Fetal tissue can be used in different indications, for instance, fetal liver transplants may be used in combating aplastic anemia, placental umbilical cord whole blood transfusion can serve as an emergency alternative to adult whole blood transfusion, fetal adrenal transplant has been tried in combating intractable pain in arthritis, and fetal thymic transplant in combating leucopenia in non-Hodgkin's lymhoma and other immunodeficiency conditions like DiGeorge Syndrome, only to name a few. Fetal brain tissue transplant has also been done in a heterotopic site and the proliferation of the tissue has been observed. Neurotransplantation with fetal tissue in Parkinsonism shows positive results in some globally accepted studies. There are futuristic potential uses of fetal tissue in bioengineering through coating/seedling of fetal tissue on implants, stents and other artificial surgical life-saving devices to improve their functioning, and it may also extend the life of these costly gadgets. By properly using pre-HLA fetal tissue seedling in orthopedic, thoracic and also neurosurgical appliances, there could be a reduction of long-term irritation sequelae of the implant and the host interphase, and thus, a better device, i.e., a more biofriendly interphase could be developed. This may help in the reduction of pseudomembrane formation, loss of patency and other resultant TH2 reactions of the host system.
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PMID:Fetal cell/tissue therapy in adult disease: a new horizon in regenerative medicine. 1549 Oct 58

It has been reported that patients with Hodgkin's disease (HD) show altered porphyrin metabolism, and suggested that the cause is the neoplastic process itself. If this is true, disease progression should be associated with higher levels of porphyrin excretion. The aim of this study was to evaluate urinary coproporphyrin levels in patients with Hodgkin's disease at different stages. As many of the patients received chemotherapy, another aim was to verify experimentally whether chemotherapeutic agents might increase porphyrin levels in rabbits. All of the patients had above-normal urinary coproporphyrin levels. On the other hand, rabbits receiving the porphyrin precursor 5-aminolevulinic acid (5-ALA), and also treated with doxorubicin, showed very high plasma porphyrin levels. The increased levels of urinary coproporphyrins seem to be due to the disease itself, since the patients in stages III and IV had higher excretion values, presumably due to biochemical heme synthesis lesions that lead to the availability of the porphyrin precursor, as well as coproporphyrin accumulation and excretion. The altered porphyrin synthesis may be attributable to the cytotoxic oxygen species generated in the presence of NADH and iron. As the patients also received extensive chemotherapy regimes, the altered porphyrin metabolism may be affected by antineoplastic treatment generating oxygen reactive radicals. The alterations in porphyrin metabolism induced by chemotherapeutic agents appear to be demonstrated in rabbits in which doxorubicin increases porphyrin synthesis after porphyrin precursor treatment.
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PMID:Increased urinary coproporphyrin excretion observed in patients with differently staged Hodgkin's disease treated with chemotherapy. 1566 80

All-trans-retinoic acid (ATRA) and its synthetic analog fenretinide (4HPR) are potent anticancer drugs. Only a few reports are available about the effects of retinoids on B lymphoma cells. In our study, non-Hodgkin lymphoma cells (HT58) were treated with ATRA and 4HPR. Both agents induced cell death time- and dose-dependently. Reactive oxygen species (ROS) production was elevated in 4HPR-treated cells, but not in ATRA-treated cells. The depolarization of the mitochondrial membrane occured earlier after ATRA than after 4HPR treament. Z-VAD-fmk, the general caspase inhibitor, decreased the DNA fragmentation in ATRA-treated cells, but simultaneously increased necrosis. However, z-VAD-fmk did not influence the DNA fragmentation in 4HPR-treated cells. Endonuclease G was released from the mitochondria during 4HPR treatment, which could be an inducer for caspase-independent DNA fragmentation. Our results suggest that natural (ATRA) and synthetic (4HPR) retinoids induce different apoptotic pathways in B lymphoma cells, which is particularly relevant for their potential use in leukemia treatment.
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PMID:Different ways to induce apoptosis by fenretinide and all-trans-retinoic acid in human B lymphoma cells. 1630 14

Pyothorax-associated lymphoma (PAL) is a non-Hodgkin lymphoma of exclusively B-cell phenotype developing in the pleural cavity of patients after more than 20-year history of pyothorax resulting from an artificial pneumothorax for the treatment of pulmonary tuberculosis or tuberculous pleuritis. The most common symptoms on admission are chest pain and fever. Serum neuron-specific enolase level suggesting a diagnosis of small cell lung cancer is occasionally elevated. Histologically PAL usually shows a diffuse proliferation of large cells of B-cell type (diffuse large B-cell lymphoma [DLBL]). In PAL cells, representative B-cell markers other than CD20 are frequently negative with aberrant expression of T-cell markers such as CD2. A gene expression profile of PAL is distinct from nodal DLBL in its higher expression level of interferon-inducible genes. PAL is strongly associated with Epstein-Barr virus (EBV) infection with expression of EBV latent genes such as EBNA-2, LMP-1, together with EBNA-1. Taken together, PAL is a distinct entity both in its clinicopathologic presentation as well as its gene expression profile. Use of an artificial pneumothorax, EBV infection, and cytokines and reactive oxygen species produced in longstanding pyothorax might be important factors for PAL development.
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PMID:Pyothorax-associated lymphoma: a lymphoma developing in chronic inflammation. 1633 Sep 29


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