Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 11 North American veterinary university hospitals and clinics, 248 animals were a confirmed diagnosis of nervous-tissue tumor were identified; 7 tumors were found in cattle, 28 in horses, 14 in cats, 199 in dogs, and none in other species. Tumors were divided for analysis into three categories-glial, meningeal, and peripheral nerve. In cattle and horses, all tumors involved peripheral nerves, the risk of which, in horses, reached a plateau at 4-6 years of age and remained constant thereafter. In cats, the tumors were equally distributed among the three tumor categories whereas, in dogs, twice as many glial tumors as meningeal and peripheral nerve tumors were found. The risk for glial tumors in dogs reached a peak at 10-14 years of age, for meningeal at 7-9 years, and for peripheral nerve at 2-3 and 7-9 years. Three canine breeds-English bulldog, boxer, and Boston terrier-had an excessive rish of glial tumors. Except for an excess of skin tumors in dogs with peripheral nerve tumors, there was no unusual occurrence with second primary neoplasms for any species. There was no detectable predisposition by sex for any of the categories of nervous-tissue tumors among any of the four species. The role of genetic abnormalities associated with nervous-tissue tumors and other etiologic factors (e.g., chronic hypoxia) may be clarified by further studies involving canine breeds of "bulldog" ancestry.
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PMID:Occurrence of nervous-tissue tumors in cattle, horses, cats and dogs. 16 49

In 17 years we have performed 6,505 neurosurgical procedures in the neurosurgical unit of the Salisbury Hospital Group. Only 62% were performed on Africanpatients and 38% on European patients, despite the fact that the African population exceeds the European population by 20 times. This is partly due to the tolerance of rural people towards disease and partly to a number of social factors. The European group has a greater percentage of elderly people than the African group and, although we could not estimate the incidence of tumors among the African group, we would expect their overall incidence per capita to be lower because malignant tumors tend to occur in older people. We do not suspect the existence of a genetic factor in tumor incidence. There were 205 primary intracranial neoplasms in Africans and 244 in Europeans. Histological study shows that 33% of all tumors were meningiomas in the African group compared to 19% in the European group. Gliomas comprised 61.3% of the European series and 48.8% of the African series but the distribution by Kernohan's grading of astrocytomas was the same in both groups. If age was a factor, Grades I and II should have predominated in the African group, but did not. The incidence for each tumor among our European patients followed the patterns reported in various European and USA series. Likewise the pattern emerging from our African series closely paralleled the reports of other workers in Africa. Acoustic neuromas appear to be rather rare among Africans. The average age of all adults with tumors was 15 years lower in the African group than in the European group. However, this is entirely related to the age structure of the population, and not to an earlier age of occurrence. The average ages of medulloblastoma cases were identical. In our European series the occurrence according to age was much the same as that reported by overseas workers. The sex incidence of tumors in the European group seems to be a fair reflection of the situation elsewhere; in the African group it is questionable because men go into the towns to work and leave their families in the country. There was no significant difference in the location of tumors in the two groups. Results of treatment were uniformly inferior in the African group, partly due to the lateness of arrival at the hospital so that the growth was already far advanced and also because many patients suffered poor health from concomitant disease.
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PMID:Primary cerebral neoplasia in Rhodesia. 16 60

Extracts of solid mouse tumors were examined for deoxycytidine kinase and deaminase activities. 1beta-D-Arabinofuranosylcytosine nucleotide was formed at a rate of 45 nmoles/hr by Glioma 26/57 and only 14 nmoles/hr by Ridgway osteogenic sarcoma. Deaminase activity was highest in Lewis lung (114 nmoles of 1-Beta-D-arabinofurano-syluridine formed per hr) and in CaD2 (104 nmoles of u-beta-D-arabinofuranosyluridine formed per hr). Deaminase activity in tumor extracts is sensitive to freezing, while deaminase activity in monkey serum is not. It was observed that kinase activity varies by as much as 50% in different cell lines of the same tumor. In the presence of tetrahydrouridine, kinase activity was significantly increased in most of the tumors studied.
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PMID:Kinase and deaminase activity in a variety of subcutaneous mouse tumors. 16 84

Six biochemically differentiated clonal lines have been established from a transplantable glioma (tg26) of the C57BL/6 inbred mouse strain. Antibodies have been previously raised against G26 tumor cells, which define a cell surface component(s), NS-1 (nervous system antigen-1), found exclusively in the nervous system. NS-1 concentrations approximate the levels of the original G26 tumor when the clonal lines are grown as clonal tumors in vivo, but are reduced when the cells are grown in vitro. NS-1 concentrations are further reduced in vitro upon incubation of the cells with 1 mM dibutyryl 3:5-cyclic AMP. H-2 histocompatibility antigen concentration, in contrast, is unaffected by dibutyryl cAMP. In addition to expressing NS-1, the neuroectodermal origin of these cell lines is further confirmed by their synthesis of the nervous system specific acidic protein S-100 and by the high specific activity of the enzyme 2:3-cyclic nucleotide 3-phosphohydrolase. In addition, they respond to catecholamines by the elevation of intracellular 3:5-cyclic AMP levels. Whereas expression of S-100 protein is high under in vitro conditions but negligible after one passage in vivo, 2:3-cyclic nucleotide 3-phosphohydrolase is not detectable in vitro but becomes detectable again in vivo. The two membrane-bound constituents, NS-1 and 2:3-cyclic nucleotide 3-phosphohydrolase, therefore seem to be subjected to different regulatory mechanisms from that of the soluble, intracellular S-100 protein.
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PMID:Biochemically differentiated mouse glial lines carrying a nervous system specific cell surface antigen (NS-1). 16 83

The use of conditioned medium (CM) obtained from monolayer cultures of human glioma cells induced colony formation from single glioma cells in culture. In contrast, no colonies were observed in cultures incubated with nonconditioned standard Eagle's basal medium. The number of colonies formed closely depended on the concentration of CM. The glioma CM not only stimulated colony formation but also induced the formation of fibrillary cell extensions. Culture conditions influencing the production of colony-stimulating factors included cell density and duration of culture medium contact with glioma cells. The colony-stimulating activity (CSA) was stable after freezing and thawing, but decreased 30-40% when CM was exposed to temperatures over 66 degrees C for 30 minutes. In addition, the CSA was filtratable (0.45 mu), dialyzable, and passable through an Amicon PM10 filter, which indicated a molecular weight less than 10,000. The use of CM provided an improved method for quantitative assays of neural tumor cells, based on their colony formation in culture.
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PMID:Quantitative cloning of malignant human glioma cells by conditioned medium. 17 66

X-ray and histological studies of 138 patients with tumors of subcortical nodes displayed signs of hypertension in 86.3% of the cases (119 cases). Calcified foci on the craniograms were found in 29 cases (21%) and in histological findings - in 48 cases (34.6%). Petrified foci in benign glial tumors were located between the tumor cells, perivascularly and in the tissue of the perifocal zone of the tumor. In malignant tumors the petrified foci were mainly in the area of necrosis, in microcysts and hemmorrhagical foci. According to the pattern of calcification on the x-ray it was impossible to determine the histological type of the tumor or the degree of malignancy. The volume of calcification on the craniograms do not correspond to the volume and configuration of the intracranial tumor.
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PMID:[An x-ray and histologic study of calcifications of tumors of the subcortical ganglia of the brain]. 17 47

The brains of 396 old albino rats of the breed Wistar-AF/Han-EMD were examined for spontaneous tumors of the CNS and the following tumors were diagnosed: 1 oligodendroglioma, 1 astrocytoma, 1 mixed glioma, 1 pleomorphic glioma, and 19 meningiomas. Thus the CNS tumor rate was 5.8%. In addition 6 micromeningiomas were found. Knowledge of the spontaneous tumor rate including the tumor incidence in the CNS of the animal strains used for these examinations is a necessary condition for the evaluation of the results of cancerogenicity tests. CNS tumors deserve particular attention because during recent years it was found that certain chemical compounds like for instance N-methyl-N-nitrosourea induce organ-specific tumors in the brain of rats. It is recommended, therefore, to always include the central nervous system in the autopsy and histologic examination of animals from cancerogenicity trials. For cerebral autopsy transversal sections through the different cerebral regions and histologic examination of transversal section surfaces of all tumors and suspected tumor areas are suggested.
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PMID:The incidence of spontaneous tumors of the central nervous system of Wistar rats. 17 67

Sixty-five patients with malignant brain tumors were treated with a combination of BCNU (100 mg/m2 qd X 1) and procarbazine (100 mg/m2 qd X 14); the cycle was repeated in 1 month and then on a 6-week schedule with procarbazine being given for 21 days. Forty-five patients had malignant gliomas (glioblastoma multiforme, anaplastic astrocytoma, malignant glioma, or gemistocytic astrocytoma) and were evaluated as a group. All patients had either shown evidence of tumor regrowth after previous surgery and/or radiotherapy, or had deep unbiopsied tumors presumed to be malignant gliomas. Of these 45 patients, 13 of 45 (30%) were judged to be unequivocal responders and an additional eight of 45 (17%) were designated as probable responders. The median duration of clinical response was 34 weeks for responders and 20 weeks for probable responders. The combination of BCNU and procarbazine, therefore, was somewhat inferior to a previous combination of procarbazine, CCNU, and vincristine.
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PMID:BCNU (NSC-409962) and procarbazine (NSC-77213) treatment for malignant brain tumors. 17 10

In tissue culture experiments, cells derived from glioma 26, a transplantable tumor of C57B1/6 mice, were sensitive to both floxuridine (5-fluorodeoxyuridine) and 5-fluorodeoxyuridine-5'-(5-iodo-3-indolyl)phosphate, an enzyme-mediated drug activated by 5'-nucleotide phosphodiesterase. When these compounds were tested on the tumor in animals at a level of 5 mg/kg for 5 days, tumor growth was inhibited approximately 20% by both compounds. When higher levels of 5-fluorodeoxyuridine, 100 mg/kg four times weekly throughout the lifespan of the mouse, were given, the tumor, although inhibited at first, developed resistance and continued to grow until it killed the animal. Phosphodiesterase levels in the tumor rose as the tumor grew. On the other hand, thymidine kinase levels dropped as anticipated from the known 5-fluorodeoxyuridine-resistant hepatoma tissue culture data. This enzyme pattern was maintained in transplantable mouse glioma lines established from the resistant tumors. One of these lines, tested at a level of 5 mg/kg for 5 days, showed no response to 5-fluorodeoxyuridine but was still sensitive to 5-fluorodeoxyuridine-5'-(5-iodo-3-indolyl) phosphate. These experiments, therefore, offer a model system and a rationale for the design and study of more compounds that could be activated by the enzyme phosphodiesterase. Such compounds might be used alternatively when resistance to 5-fluorodeoxyuridine develops, a common clinical experience in the use of this anticancer drug.
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PMID:5'-nucleotide phosphodiesterase activity of floxuridine-resistant mouse glioma. 17 49

A controlled, prospective, randomized study evaluated the use of mithramycin in the treatment of anaplastic glioma compared to a similar group of patients receiving best conventional care. From a total of 116 patients in the study, 96 were within the valid study group. All patients were operated on, had histological confirmation of anaplastic glioma, and received radiotherapy at the discretion of the principal investigator. Fifty-two patients received mithramycin at a dose of 25 mug/kg/day for 21 days, while 44 patients were in the control group. There was no significant difference in the median survival from time of randomization in those receiving mithramycin (21 weeks) as compared to those not receiving mithramycin (26 weeks). There was no significant difference between the two groups in relation to age distribution, sex, location, diagnosis, tumor characteristics, signs or symptoms, or radiotherapy received. Duration of symptoms correlates positively with survival and was also significantly longer in the control group than in the treated group. This, however, did not account for the failure of mithramycin to be found an effective agent. Although the study was not designed to evaluate the efficacy of radiotherapy, patients who were so treated had a significant improvement in survival. The toxic complications of mithramycin included gastrointestinal symptoms, dermatological involvement, anemia, and liver dysfunction, indicating the need for close supervision.
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PMID:Evaluation of mithramycin in the treatment of anaplastic gliomas. 17 38


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