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)

Patients with herpesvirus infections were given intravenous injections of 10-20 mg of adenine arabinoside (ara-A)/kg per day. When given the higher dosage, some patients with chronic hematologic conditions showed mild to moderate additional depressions in the level of hemoglobin. The number of neutrophils and platelets did not decrease, even when numbers were low at the onset of treatment with ara-A. Two patients with Hodgkin's disease who received 20 mg of ara-A/kg per day developed a transient motor aphasia resembling akinetic mutism. With the regimens of ara-A used and challenge inocula of approximately 50 plaque-forming units of virus, the minimal inhibitory concentrations of ara-A and hypoxanthine arabinoside for herpesviruses are usually not achieved in serum but may be attained in body fluids (urine and vesicular fluid). Antiviral activity in vesicular fluids is likely to involve a combination of ara-A, hypoxanthine arabinoside, and interferon.
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PMID:Microbiologic assays and neurological toxicity during use of adenine arabinoside in humans. 18 99

Most humans in the United States have been infected with BK virus (BKV), a human papovavirus. Because BKV has oncogenic properties, we have investigated whether it may be a cause of human cancer. Basic principles of tumor virology imply that BKV-induced tumors should contain BKV DNA sequences. Therefore, we assayed (by molecular hybridization) DNA from human tumors and malignant cell lines for BKV DNA, using BKV [(32)P]DNA as probe. The BKV [(32)P]DNA was labeled in vitro (nick translation) to specific activities of 1 to 2 x 10(8) cpm/mug. The BKV DNA used to prepare our probes had the properties expected of authentic BKV genomes, including density of superhelical DNA, sedimentation velocity in alkaline and neutral sucrose gradients, production of one fragment by endonuclease EcoRI cleavage and four fragments by endonuclease Hin II + III cleavage and reassociation properties. From these studies we conclude that our BKV probes hybridized well, and represented bona fide BKV DNA. Using three different BKV [(32)P]DNA probes, i.e., from three distinct plaque isolates, we have analyzed DNA from BKV-transformed cells, normal human tissues, and a large number of human tumors. All human DNAs (cell lines, normal tissues, tumors) hybridized 5% with BKV DNA. Hybridization analysis of BKV-transformed hamster cell DNA indicated 5-6 copies of at least 88% of the BKV genome per cell. No BKV DNA sequences were detected (above the normal 5% hybridization to all human DNAs) in the following normal human tissues: 10 kidney (BKV is usually isolated from urine), 3 spleen, 13 lung, 23 colon, 2 rectum, 1 ileum, and 1 skin. No BKV-specific DNA was found in 166 tumors, including 5 carcinomas (Ca) of stomach, 3 Ca small intestine, 26 Ca colon, 9 Ca rectum, 31 Ca lung, 9 adenocarcinomas and 5 oat cell carcinomas of lung, 17 melanomas, 5 Ca prostate, 4 Ca bladder, 6 Wilms tumors, 4 hypernephromas, 15 Ca kidney, 7 brain tumors, 5 Hodgkin lymphomas, 10 lymphomas (immunosuppressed patients have a high incidence of lymphomas), 2 reticulum cell sarcomas (spleen), and 3 skin tumors. We have also analyzed 7 human malignant cell lines (melanoma, lung, rhabdomyosarcoma, and glioblastomas), including several clones of a lung melanoma line; no BKV DNA sequences were detected. Because our probes could detect one copy of BKV DNA if only 10% of the cells were tumor cells, our results are very strong evidence that the tumors we analyzed did not have a BKV etiology. The tumors we tested represent about 50% of all cancers in the United States; there is no evidence that BKV is involved in the etiology of these types of tumors.
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PMID:Analysis of human tumors and human malignant cell lines for BK virus-specific DNA sequences. 20 40

51 patients suffering from Hodgkin's disease or non-Hodgkin's lymphoma participated in this double-blind, cross-over study in which 2 antiseptic mouthwashes were tested for their effects on various periodontal index scores and salivary microbial counts. All patients were receiving combination cytostatic treatment based on methotrexate and doxorubicin. The patients (49 +/- 14 years old, 28 men, 23 women) were allotted at random to 2 groups. One rinsed with a 0.12% chlorhexidine gluconate (CHX) solution, the other with a 0.025% amine-stannous fluoride (AmF + SnF) solution 2x daily for 2 weeks. Both groups then continued rinsing with a 0.05% sodium fluoride (F) solution for 2 weeks, before switching over to AmF + SnF or CHX, respectively. All solutions had been prepared in such a way that they had the same colour and taste. Visible plaque index and gingival bleeding index scores were significantly reduced after periods of rinsing with CHX solution (P less than 0.001) and AmF + SnF solution (P less than 0.05). Microbiological cultivations of saliva specimens revealed significant reductions in mutans streptococci immediately after commencing rinsing, while lactobacilli and yeast counts were not affected.
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PMID:Effect of antiseptic mouthwashes on some clinical and microbiological findings in the mouths of lymphoma patients receiving cytostatic drugs. 179 55

We investigated 31 cases of cutaneous malignant lymphoma diagnosed by skin biopsy during about 11 years at the University of Tsukuba Hospital. The specific eruption was occurred in 17.7% of all malignant lymphomas at the hospital. The skin was primarily affected in 5.8% of all malignant lymphomas including Hodgkin disease, and in 6.9% excluding Hodgkin disease. We divided 31 cases into 3 groups; Group A is the primary cutaneous lymphoma, and Group B and C are the secondary cutaneous lymphoma. The skin lesions of Group B share the major part. On the other hand, that of Group C is minimal and transient. The differences between group A/B and group C were the high frequency of epidermotropism. The T cell dominance, the widespread eruption and the variety of the eruptions for one case in Group A/B. Group A differed from group B/C by the specific plaque, and from Group B by the high frequency of Pautrier's microabscess. B cell lymphomas did not show dermal-epidermotropism as well as epidermotropism.
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PMID:[The study on the specific eruptions of malignant lymphoma. I. Clinical, pathological and immunopathological characters]. 237 Jul 4

A young man who presented with cervical Kikuchi's histiocytic necrotizing lymphadenitis later developed a cutaneous plaque lesion. Histologic study of the cutaneous lesion revealed dermal patchy infiltrates composed of large lymphoreticular cells and scattered cells resembling Hodgkin or Reed-Sternberg cells. This condition was initially mistaken for a large-cell lymphoma. But it was later discovered that the dermal cellular infiltrates were similar to that of the involved lymph node. Many of the large cells in the infiltrates were found to be histiocytes. Immunohistochemical study revealed that the cells resembling Hodgkin or Reed-Sternberg cells were activated fibroblasts. The presence of foamy histiocytes and the absence of neutrophils in the skin lesions were also similar to the involved lymph node. Cutaneous Kikuchi's disease may be mistaken for cutaneous lymphoma. Cutaneous involvement by Kikuchi's disease may also denote a worse clinical course.
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PMID:Cutaneous manifestation of Kikuchi's histiocytic necrotizing lymphadenitis. 192 46

Complete responses lasting from 4 to 14 years were documented in 65 of 331 (20%) patients with cutaneous T cell lymphoma treated with topical mechlorethamine (HN2) between 1968 and 1982. Such long-lasting remissions occurred most often, but not invariably, in patients with patch or plaque phase mycosis fungoides without palpable lymphadenopathy (stage Ia or Ib). The likelihood of a continuous remission was enhanced by initiation of treatment before an unequivocal pathologic diagnosis. Despite the long-lasting responses in these patients, however, relapses have been documented in 11 (17%) of these patients, and all relapses occurred within 8 years of discontinuing maintenance topical chemotherapy. Thus, in our experience, a continuous remission lasting 8 or more years provides evidence that cutaneous T cell lymphoma can be eradicated by aggressive topical chemotherapy. This circumstance was observed in 35 patients, representing a cure rate of at least 11% overall. In addition, when compared with the general population of the United States, patients who received topical HN2 were at an 8.6-fold and a 1.8-fold increased risk for the development of squamous cell carcinoma and enhanced for Hodgkin's disease and colon cancer but not for systemic cancers known to be induced by systemic administration of alkylating drugs. These results compare favorably with experiences with topical HN2 chemotherapy at other centers but raise questions about the risks associated with long-term administration for maintenance of remissions.
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PMID:Long-term efficacy, curative potential, and carcinogenicity of topical mechlorethamine chemotherapy in cutaneous T cell lymphoma. 253 48

Thirty patients, 13 female and 17 male, have been followed from 3 months to 22 years (mean, 81 months; median, 63 months) and special studies have been performed on a proportion of these in order to try to predict malignant evolution. Age at onset was from 20 to 70 years (mean, 43 years; median, 42 years). Duration of disease was from 1 to 30 years (mean, 119 months; median 161 months). Seven patients also had parapsoriasis en plaque or plaque-stage mycosis fungoides at the time of diagnosis and one patient had erythroderma. None of the 22 uncomplicated lymphomatoid papulosis patients developed malignant cutaneous lymphoma during the period of observation, while the remaining 8 patients who had concurrent parapsoriasis en plaque, mycosis fungoides, or erythroderma did not deteriorate further. Single-cell deoxyribonucleic acid (DNA) measurements on the dermal infiltrate were done in 13 patients and were abnormal in 7 patients. Two of these had greatly abnormal DNA histograms and at the same time an abnormal clinical presentation with multiple nodules and tumors. The remaining five patients had DNA histograms that indicated a potential for malignancy. Monoclonal antibody studies were performed on skin biopsy specimens of 10 patients. The dermal infiltrate was dominated by T-helper lymphocytes and some Hodgkin and Reed-Sternberg cells could be detected by the antibodies Ki-1, Ki-24, and Ki-27. Human T-lymphotropic virus type I (HTLV-I) antibodies were found in 3 of 18 patients examined. Treatment with psoralens plus ultraviolet A (PUVA) was effective (partial or complete remission) in six patients but they relapsed at cessation of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lymphomatoid papulosis. A follow-up study of 30 patients. 288 56

Alzheimer's disease is one of several brain disorders under the broad category of dementia. It is a gradually debilitating illness with no known cure. The first symptom is usually a slowly increasing memory loss, beginning between 40 and 65 years of age. As the disease progresses, the brain begins to deteriorate more rapidly, until it literally stops functioning. Of great concern is the projection that the number of people who will have Alzheimer's disease will double by the year 2030 because of the rising elderly population. Treating this population will escalate from the current estimate in excess of $2.5 billion to more than $6 billion. Speculation toward the increasing costs in money and workforce has led to an accelerated program in search of a cure or at least a symptomatic therapy for this condition. One of the most promising research leads is the striking connection between Alzheimer's disease and Down's syndrome and certain cancers: --Virtually 100% of patients with Down's syndrome who survive past age 35 show the same mental deterioration and identical brain changes seen in patients with Alzheimer's disease, including the presence of plaque and neurofibrillary tangles.--The presence of a high percentage of Down's syndrome among relatives of patients with Alzheimer's disease. --A high incidence of certain types of syndrome and among relatives of people who have Alzheimer's disease, such as leukemia, lymphomas, Hodgkin's disease, and immune system disorders. The key to the intercorrections between Alzheimer's disease and Down's syndrome seems to be a genetic component related to chromosome 21.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alzheimer's disease: an emerging affliction of the aging population. 293 67

The authors describe two patients with clinically and histopathologically documented advanced (tumor) stage mycosis fungoides. In each case the large, pleomorphic neoplastic cells lacked the monoclonal antibody-defined cell surface antigens commonly associated with immature and mature T-cells, i.e., T11, Leu-1, T3, T4, T6, T8, and T10, but expressed various T-cell-associated activation antigens, such as HLA-DR, Tac, and T21. Leu-M1, a monocyte-associated antigen, was not expressed by the small, cerebriform neoplastic cells in the plaque stage lesions of either patient. However, Leu-M1 was expressed by most of the large, pleomorphic neoplastic cells present in the nodular lesions of both patients. The pattern of Leu-M1 antigen expression was identical to that previously reported in the Reed-Sternberg cells of Hodgkin's disease. Identification of these two patients suggests using caution in the interpretation of the results of immunophenotypic analysis of cutaneous lymphoid neoplasms and that Leu-M1 should not be used as a diagnostic indicator of Hodgkin's disease or a histiocytic-derived neoplasm. These studies also suggest that Leu-M1 may be preferentially expressed on a subpopulation of activated, rapidly proliferating, and/or dedifferentiated neoplastic T-cells that proliferate in the advanced (tumor) stages of mycosis fungoides.
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PMID:Leu-M1 antigen expression in advanced (tumor) stage mycosis fungoides. 308 80

A patient with a 14-year history of lymphomatoid papulosis developed localized subcutaneous lymphoma with morphologic features of Hodgkin's disease at the age of 46 years. The lymphoma was clinically atypical in that it remained localized in the subcutis for 10 years before involvement of lymph nodes occurred. A review of the literature indicates that patients with lymphomatoid papulosis, especially those with plaque or nodular lesions in addition to papular lesions, are given to develop malignant lymphomas of various histologic types.
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PMID:Hodgkin's disease complicating lymphomatoid papulosis. 391 4


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