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 5-year experiences of a center for pediatric oncology in a children's university hospital are reported. Currently (1-1-1975) 60 of 135 treated leukemic and 88 of 152 treated tumor patients are living. 1974, there were in the average 34 ambulatory complete blood counts per week, and in addition 263 bone marrow and 196 ambulatory lumbar punctures per year. The standardized routine of an outpatient visit is described. Advice for parents and family physicians are given. A standardized diagnostic approach for M. Hodgkin as a prototype is proposed, and a standardized therapy for Wilms' tumor. Of 24 thus treated children with Wilms' tumor 16 ("67 p.c.") survive, included 7 of 15 ("47 p.c.") with metastasized disease (observation time 21-71 months). Current treatment of 49 children with acute lymphoblastic leukemia resulted in continuous complete remission of 22 patients ("45 p.c.") (observation time 1-4 years), but 6 dead in complete remission due to infection. The need for specialized treatment centers with skilled persons is emphasized.
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PMID:[Standardized fight against cancer in childhood (author's transl)]. 17 43

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

Cancer chemotherapy was purely palliative until the early sixties. Tumor cures have been since obtained, first in malignant trophoblastoma and Burkitt's lymphoma, and more recently in Hodgkin's disease, diffuse histiocytic lymphoma, acute lymphocytic leukemia in children, Wilms's tumor and osteosarcoma. Preliminary data are suggestive of tumor cures in testicular teratomas and, possibly, in small cell carcinoma of the lung. Five patients with trophoblastoma, Hodgkin's disease, melanoma, chronic myelocytic leukemia and anaplastic carcinoma of the lung are briefly presented, all without evidence of tumor relapse 3 years or more after chemotherapy. Theoretical bases for improvement of the curative effect of cancer chemotherapy are discussed, including the development of new agents, and new pharmacological problems concerning drug interactions, complexes of drugs with macromolecules or immunoglobulins and liposomes are considered.
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PMID:[Curability of malignant neoplasms: value and limitations of chemotherapy]. 21 68

The sensitivity of 37 solid tumours of children was tested in vitro towards cytostatic agents by means of an autoradiographic short-term method. Sensitivity was measured as the magnitude of inhibition of 3 H-thymidine incorporation. The test was performed with the cytotoxic agents Cyclophosphamide, Trenimon, Bleomycin, Adriamycin, Daunomycin, Actinomycin D, and Cytosin-Arabinosid in 9 Wilms' tumours, 9 neuroblastomas, 7 non-Hodgkin-lymphomas, 5 osteogenic sarcomas, 3 soft tissue sarcomas, and 4 special tumours. None of the tumours is resistant to all cytotoxic substances. The tumours show a marked individual sensitivity pattern, and, with few exceptions, they are sensitive against 2 or more cytostatics. This behaviour is explained mainly by the usually high proliferative activity of dysontogenetic tumours, malignant lymphomas and various sarcomas. The possibilities and limits of the short-term methods for sensitivity-testing are discussed critically and in detail. For the evaluation of the results of in vitro testing and of in vivo effectiveness the close coreelations are not always taken into consideration between the type of cytostatic agent and effect on tumour metabolism, cytostatic agent and proliferation kinetics of the tumour as well as the effect of the cytostatics and the nucleic acid precursor used for the test. Despite the methodological limitations preclinical testing should be preferred in comparison with unselected chemotherapy.
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PMID:[Testing of solid tumors in childhood for sensitivity against cytostatic agents using an autoradiographic in vitro method (short-term method) (author's transl)]. 22 41

VM-26, a semisynthetic podophyllotoxin, was tested for antitumor activity and clinical toxicity in 181 children. The drug was administered iv at weekly intervals, beginning at a dose of 130 mg/2/week. The dose was increased, as tolerated, after 3 and 6 weeks to 150 and 180 mg/m2/week, respectively. The only major toxicity was hematologic, with neutropenia predominating. Anaphylaxis occurred in one patient. The drug demonstrated significant activity in acute lymphocytic leukemia (four responses among 15 patients) and neuroblastoma (ten responses among 31 patients). Objective responses were also noted in one patient each with acute myelogenous leukemia, Hodgkin's disease, histiocytic lymphoma, Wilms' tumor, Ewing's sarcoma, undifferentiated carcinoma, and sacrococcygeal sarcoma. Further trials of VM-26 in these childhood malignancies are warranted.
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PMID:Phase II study of VM-26 in acute leukemia, neuroblastoma, and other refractory childhood malignancies: a report from the Children's Cancer Study Group. 38 Aug 3

Vindesine is a new vinca alkaloid with broad-spectrum antineoplastic activity in experimental tumor models. Phase-I studies have shown that a weekly dosage regimen of 3--4 mg/m2 IV produces manageable toxicity, with leukopenia and peripheral neuropathy being dose-limiting. Two hundred seventy-five patients have been enlisted in Phase-II trials at the Memorial Sloan-Kettering Cancer Center. Major objective responses (complete and partial remissions) were seen in bronchogenic carcinomas, melanoma, testicular carcinoma, esophageal carcinoma, acute lymphocytic leukemia, malignant lymphoma (Hodgkin's and non-Hodgkin's) and Wilms' tumor. Patients with hematologic and germ cell neoplasms were treated on a daily administration schedule (1.0--1.3 mg/m2 IV for 5--7 days). Vindesine was well tolerated, with less than 5% of patients having a WBC nadir of less than 1000 cells/mm3 and with a platelet-sparing effect noted. Dose-related peripheral neuropathy occurred frequently and was generally mild to moderate in degree. Vindesine appears to be an active agent whose role will be further defined by completion of ongoing trials.
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PMID:Vindesine. A review of phase-II trials. 45 87

Supranormal temperatures inhibit selectively the growth of malignant cells more than that of normal cells. The autoradiographic determination of the 3H-thymidine-labelling-index (LI) in vitro is a suitable method for the examination of thermosensitivity of individual human tumours. 44 solid tumours of children (Wilms' tumours, neuroblastomas, osteogenic sarcomas, non-Hodgkin-Lymphomas and other tumours) were studied by the temperatures 37.5 and 42.5 degrees C/120 min, with this method. 90% of the histologically undifferentiated tumours showed a highly significant inhibition of the 3H-thymidine incorporation between 28.6 and 79.9% with an average of 51.1%. In 4 histologically mature tumours (carcinoma of the adrenal cortex, malignant hepatoblastoma, fibrosarcoma, hamartoblastoma) no significant decrease of the LI was present. The inhibition of incorporation with hyperthermia cannot be correlated with the primary magnitude of the LI with normothermia. In 1 neuroblastoma a 75% rise of the LI was found possibly due to exogenic caused thermotolerance. The individuality of the reaction towards heat may contribute to the biological characterization of tumours.
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PMID:The effect of hyperthermia 42.5 degrees C on the incorporation of 3H-thymidine into the DNA of solid tumours in childhood. 51 52

We have investigated whether Group B human adenoviruses (Ad) (Ad3, Ad7, Ad11, Ad14, Ad16, and Ad21), which are widespread in the human population and are tumorigenic in hamsters, may play a role in human cancer. Hybridization of Ad7-radiolabeled DNA with DNA's from an Ad7-induced primary hamster tumor and from two cell lines (5728 and Ad7 P-cell) established from Ad7-induced hamster tumors indicated multiple copies per cell of 17, 30 to 36, and 20%, respectively of the Ad7 genome. Thus, cells transformed by Group B Ads resemble cells transformed by Group C and Group A Ad's in that they retain multiple copies of a variable fraction of the viral genome. These model studies suggest that possible Group B Ad-induced human cancer cells should contain one or more copies of virus DNA per cell. Therefore, we assayed human cancer DNA's for Ad sequences, by highly sensitive "saturation-hybridization" reactions with Ad7 or Ad11 DNA (4 X 10(6) to 2.1 x 10(8) cpm/microgram). We concentrated on cancers of the respiratory and digestive systems, because these systems are the most common sites of infection by Group B Ad's. In 8 independent experiments, no Ad7 sequences were detected in DNA's from 16 normal lung tissues, 18 normal tissues of the digestive system, 34 cancers of the respiratory system, 19 cancers of the digestive system, 11 cancers of the urinary system, 5 cancers of the genital system, 3 cancers of the breast, and 6 Hodgkin's lymphomas. Reconstruction controls with added Ad7 DNA indicated that about 0.05 to 0.1 copy of Ad7 DNA per cell should be detected. Ad11 is strongly implicated as a cause of acute hemorrhagic cystitis. In two independent experiments, no Ad11 sequences were detected in DNA's from 9 carcinomas of bladder, 10 carcinomas of prostate, 24 carcinomas of kidney, 3 hypernephromas, 3 Wilms' tumors, or 2 normal kidneys. Reconstruction experiments indicated that the cancer DNA assays had a sensitivity of 0.05 to 0.1 copy of Ad11 DNA per cell. The DNA's of Group B Ad's are greater than 85% homologous by hybridization; thus, these results are applicable to all Group B serotypes. Our data provide evidence (but not formal proof) that none of the human cancers that we analyzed were induced by Group B Ad's. These tumors represent about 50% of the tumors that affect humans. The possible involvement of Group B Ad's in other less common forms of human cancers is under investigation in our laboratory.
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PMID:Analysis of human cancer DNA's for DNA sequence of human adenovirus serotypes 3, 7, 11, 14, 16, and 21 in group B1. 57 74

The etiology of Hodgkin's disease is complex, as is evident in studies suggesting the importance of horizontal transmission, occupational factors, racial and ethnic background, and familial, genetic factors, or both, including HL-A associations. The present study is of a remarkable kindred in which Hodgkin's disease was histologically verified in two sibships involving second-cousins related through maternal great-grandparents. Cancer of the lung, breast, endometrium, ovary, pancreas, and brain, as well as leukemia and Wilms' tumor, occurred in first and second-degree relatives of the Hodgkin's patients. HL-A haplotypes in patients with Hodgkin's disease in this family showed HL-AB5 or HL-ABW35, an association confirmed in other reports. The findings of associated malignant neoplasms in familial Hodgkin's disease, here and elsewhere in the literature, suggest that in the quest for etiology of Hodgkin's disease one must view the disorder eclectically, with a painstaking search for multiple etiologies, genetic and environmental.
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PMID:Familial Hodgkin's disease and associated cancer. A clinical-pathologic study. 99 Nov 17

A study on the prevalence of cancer at autopsy in Chilean children with special reference to leukaemia, was made. In a series of 15300 consecutive autopsies of Chileans, 70% of deceased patients had an autopsy. Of these 15300 cases (male:female ratio 1:0.92) 6431 were children (0-15 years of age); 90% of deceased children patients had an autopsy. The autopsy population of children and adults is a homogeneous ethnic group, and exhibits a low socioeconomic level. Data on the 6431 post-mortem examinations (1945-1966) came from the atuopsy records of five hospitals (four of them are teaching hospitals) in the city of Santiago. Each one of the leukaemia and solid tumour cases were diagnosed microscopically. In the children population, 54.92% were males and 45.08% were females. Of the 6431 autopsies, 142 exhibited cancer (2.21%), 2.43% being male cases and 1.93% being female cases. The autopsy cases showed a marked excess of boys (73.92%) and girls (69.77%) under 1 year of age. The prevalence of major morphological groups of cancer was as follows: leukaemias 50.70%, intracranial and other neural neoplasms 25.35%, malignant lymphomas, including Hodgkin's disease, 14.07%, and mixed malignant tumours (Wilms' tumour) 4.93%. 4.93%. Acute leukaemias (42.96%), medulloblastoma (7.65%), Hodgkin's disease (6.34%), Wilms' tumour (4.93%), and lymphosarcoma (4.93%) were the most prevalent types of cancer. Leukaemia cases had a corrected male:female ratio of 1:0.61. The prevalence of leukaemia in the atuopsy population was 1.12%.
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PMID:Malignant disease of infancy and childhood with special reference to leukaemia: a survey of 6431 autopsy cases. 126 15


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