Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cells of two human glioma lines (UC-35AG, UC-58EG), a human medulloblastoma line (UC-51MB), two rat glioma lines C6, RG2), and a rat schwannoma line (Lew-MS) were injected i.v. into male nude mice (BALB/c nu/nu). Each animal was injected with 10(6) viable cells of a particular line; for each line there was a group of eight to nine animals. The mice developed disseminated (metastatic) tumors from all lines. The incidence of mice developing metastatic tumors was different for the various lines: 2/8 for the UC-34AG, 7/9 for the UC-58EG, 1/8 for the UC-51MB, 7/8 for the C6 line, 8/8 for the RG2 and 1/9 for the Lew-MS line. The shortest survival of the mice with tumors was observed with C6 (all died on days 10-14 post injection), and with RG2 (all died from day 32 to day 39 following injection). With the remaining lines, all mice survived until they were killed on day 40 after injection. Most frequently the tumors developed in the lung. Other organs, e.g., kidney or liver, were sometimes also involved, but usually to a considerably lesser degree than the lung. Metastases never developed in the CNS. It was observed that tumors of certain glioma lines tended to grow in the lung in characteristic patterns and involved or spared other organs.
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PMID:Disseminated (metastatic) tumors in nude mice produced by intravenous injection of cells of human and nonhuman neurogenic tumor lines. 646 77

The hormone sensitivity of some tumors seems to be mediated by the presence of specific receptor proteins, and a correlation seems to exist between the amount of receptor molecules and the behavior of the tumor evolution. Epidemiological data suggest a relation between the steroid sexual hormones and the development of some tumors of the central nervous system (CNS). The authors determine the amount of receptors specific to 17-beta-estradiol and progesterone in several cases of meningioma, glioma, neurinoma and intracerebral metastases. 17-beta-estradiol receptors were always detected, although in very variable amount (3 to 74 fm/mg protein). Progesterone receptors were found in all the studied CNS in women, and only in a few male gliomas, in amounts varying between 3 and 17 fm/mg protein. The significance of hormone receptors in the CNS tumors need further studies to know if they can be applied to prognosis and suggest the assay of a complementary endocrine therapy of CNS tumors.
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PMID:[Specific receptors for sex hormones in tumors of the central nervous system]. 654 9

A number of neural and nonneural tumor cell lines of rat and human origin were assayed for neuron-specific enolase (NSE) by radioimmunoassay. Most neural tumor cell lines had appreciably higher levels of NSE than did the nonneural tumor cell lines, the highest levels being found in two anaplastic rat glioma lines ( F98 and T24). These two lines contained more than twice the amount of NSE found in a rat pheochromocytoma line (PC12) and in neuroblastoma lines derived from rats ( B35 and B50 ) or humans (IMR-32 and SHSY - 5Y ). Several of the rat glioma and schwannoma lines were inoculated intracerebrally into syngeneic rats. In the resulting tumors, NSE was demonstrable by immunohistochemistry only in those from the F98 and T24 cell lines. A number of ethylnitrosourea-induced rat tumors were also examined immunohistochemically for NSE: NSE was demonstrated in three anaplastic gliomas; three astrocytomas; and two mixed gliomas. Reactive astrocytes were also positive. Fibroadenomas of apocrine and mammary glands in rats were weakly positive, but other extraneural tumors tested were negative. Since normal neuronal elements, axonal swellings, and amine precursor uptake and decarboxylation cells are strongly positive for NSE, whereas glia and most other normal cells are negative, we hypothesize that the elevated metabolic demands imposed on neoplastic and reactive glial cells and on some extraneural tumors necessitate the opening up of metabolic pathways that are normally operative only in neurons and neuroendocrine cells, therefore resulting in the synthesis of the more stable neuron-specific form of enolase.
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PMID:Immunoradiometric and immunohistochemical demonstration of neuron-specific enolase in experimental rat gliomas. 672 96

In a prospective study the effect of dexamethasone treatment on tumor volume and contrast enhancement was evaluated by computed tomography (CT) in 15 patients with intracranial lesions. Histological diagnoses were confirmed in 13 patients who had undergone surgical intervention. A CT study of the head, with and without contrast medium, was performed prior to the dexamethasone treatment and at various intervals during the treatment for 8-19 days. The volume, attenuation, and contrast enhancement of the tumor were measured and related to the time after the start of the treatment. In six meningiomas there was no change in the volume and enhancement of the tumors. Out of four gliomas, there was an increase in volume of two tumors, whereas the other two cases showed a decrease in the tumor volume. In one glioma a distinct decrease in enhancement was observed. In three cases of metastasis a decrease in enhancement and tumor volume was noted. An acoustic neurinoma and an unverified lesion, considered radiologically to be a glioma, also showed a decrease in tumor volume and contrast enhancement. In tumors that responded to the treatment, a decrease both in volume of the tumor and peritumoral brain edema as well as a decrease in contrast enhancement of the tumor were observed.
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PMID:Effect of dexamethasone treatment on volume and contrast enhancement of intracranial neoplasms. 683 63

Known and unknown host factors determine the individual susceptibility to carcinogenic agents. Such factors may interact with either the phase of transformation (initiation) or with the phase of proliferation (promotion). Some of these factors have been recognized as potential determinants of the degree of susceptibility or resistance to cancer. Transformation may be impeded by a low rate of absorption of carcinogenic agents (barrier effect), by the availability of deactivating enzymes operative at several steps of the metabolism of carcinogenic agents, and by a high repair capability of DNA damage. Proliferation of transformed cells may be impeded or prevented by immune defense mechanisms and by maturation factors such as nerve growth factor (NGF), glia maturation factor, fibroblast growth factor, and others. NGF has already been shown to be capable of maturing anaplastic glioma cells (clone F98) and reducing their rate of growth. Rats treated with NGF following implantation of anaplastic glioma cells had a significantly decreased tumor growth rate and increased survival time. NGF administration to pregnant rats preceding exposure to ethylnitrosourea (ENU) (50 mg/kg, 21st day of gestation) or to offspring transplacentally exposed to ENU resulted in reduction of neurinoma development. The importance of NGF as a suppressing agent of neoplastic proliferation and as a prospective tumor therapeutic needs further exploration.
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PMID:Potential factors in carcinogenesis and tumor regression. 685 28

The effect of ACNU on the in vitro viability of a methylnitrosourea-induced gliosarcoma (T9) and two ethylnitrosourea-induced brain tumors, TR-481 (a malignant neurinoma) and EB-679 (a glioma) was studied. T9 was highly sensitive to ACNU, demonstrating loss of cells following a 3 hour exposure time to 5 microgram/ml; TR-481 was sensitive to 40 microgram/ml of ACNU and EB-679 was highly resistant to 40 microgram/ml of ACNU. The in vitro sensitivity of the tumor cell lines to ACNU is: T 9 greater than TR-481 greater than EB-679. This data indicates that variability of response to both concentration and exposure time of ACNU of malignant brain tumor cells must be taken into consideration in planning in vitro and/or in vivo treatment of experimental brain tumors.
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PMID:In vitro sensitivity of nitrosourea-induced neurogenic tumors to ACNU. 695 45

Twelve malignant neurogenic rat cell lines induced by the carcinogen ethylnitrosourea (EtNU) have been investigated for invasiveness in an in vitro three-dimensional culture system. The histological pattern of invasiveness into embryonic chick heart fragments has been compared to the morphology in subcutaneous and intracerebral solid tumours as well as to other phenotypic properties of the cells. In all the cell lines invasiveness was seen both in vivo and in vitro. The site of in vivo transplantation seemed to influence the tumour-host tissue interface, since intracerebral tumours were more sharply delimited than subcutaneous tumours and primary EtNU-induced CNS tumours. The histological patterns in vivo (glioma versus neurinoma-like) were in most cases similar to invasive growth in vitro. The pattern of invasiveness did not correlate to other phenotypic properties of the cells (e.g. ploidy, doubling time, latency for tumour formation and surface microarchitecture). A rat fibroblastic cell line, RE-E was non-tumourigenic in rats and non-invasive in culture, but formed small subcutaneous tumours in nude mice.
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PMID:Invasive pattern and phenotypic properties of malignant neurogenic rats cells in vivo and in vitro. 711 99

The tumorigenicity of neonatally administered N-ethyl-N-nitrosourea (ENU) was studied in four different inbred strain rats, that is Wistar/Furth (WF), Long-Evans (LE), F1 of Wistar/Furth and Long-Evans (F1) and Fischer 344 (F344) rats. All strains developed tumors of the nervous system with high incidence (97-100%) during 6 months of observation. The incidence of tumor of the central nervous system, including the brain (82-88%) and the spinal cord (53-76%), was high in all strains, but that of the peripheral nervous system, including the cranial nerve (21-89%) and the spinal root (13-93%), differed by strain. The peripheral nervous system of WF and F344 rats had a low susceptibility to the tumorigenic effect of ENU, but that of LE rats had a high susceptibility. Many brain tumors were induced in the temporal and frontal cortex and subcortex in all strains of rats. Spinal cord tumors were observed at all levels of the white matter of the spinal cord without any predilection site. Spinal root tumors were located in lumbosacral plexuses in WF and F344 rats, but in LE and F1 rats cervical and thoracic root tumors were also observed. Histological examination revealed that most of the brain and spinal cord tumors were oligodendroglioma, but in F344 rats about half of the brain tumors were mixed glioma. Epidermoid cysts of the lumbar spinal cord were observed only in F344 rats. Tumors of the peripheral nervous system were so-called anaplastic schwannoma.
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PMID:Strain differences of tumorigenic effect of neonatally administered N-ethyl-N-nitrosourea in rats. 711 58

Penicillin-free-Picibanil was injected into the brain of Wistar/Fibiger strain rat to investigate the histological changes. Its effect on the growth of rat schwannoma inoculated in the brain was also examined histologically. Picibanil caused the most prominent but focal lymphoreticular cell reaction around the injected site in the brain 24 to 48 hours after injection. The cells infiltrating from the blood vessels were neutrophils, monocytes, lymphocyte-like cells, histiocyte-like cells and unidentified cells. This lympho-reticular cell reaction gradually subsided in the next 4 to 5 days. Neutrophils and monocytes (macrophages)stayed till the later phase. Two weeks later, the lesion was minimal with only mild glial changes. Picibanil was however, considered to exert at the site of injection neurotoxic and glia-toxic activity at a concentration of 0.1 KE/10 microliters. The rat schwannoma (T1) cells, when inoculated without any treatment, showed vivid growth in the brain and no lympho-reticular cell reaction was observed. When the T1 tumor cells, suspended in the Picibanil solution, were inoculated into the brain, no lymph-reticular cell reaction was observed 7 and 14 days after inoculation. However, when the rat was pretreated with Picibanil into the brain 7 days before inoculation, only a mild lymphoreticular cell reaction was observed around the T1 cells till 7 days after inoculation. Accordingly, Picibanil was considered to induce nonspecific immunological in the rat brain even around the glioma.
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PMID:[Intracerebral picibanil injection in the rat neurogenic tumor--its histopathological changes]. 712 28

The presence of natural anti-tumor antibodies (NAA) against fibrosarcoma- and glioma cells was revealed in the normal sera of 10 different strains of rats. By means of a direct cytotoxicity test using guinea-pig complement and an absorption tests, NAA in inbred WKA/Hok rats were observed to be cytotoxically reactive to all investigated syngeneic and allogeneic fibrosarcoma lines and one glioma line, but not to hepatoma, lymphoma, leukemia, and neurinoma lines. Moreover, NAA reactivity to fibrosarcoma cells was significantly absorbed with brain, lung, kidney, skin homogenates, and cultured normal fibroblasts of syngeneic rats, but not with liver homogenates, thymus, spleen, lymph node and red blood cells. NAA were identified as being predominantly IgM and were stables at 56 degree C for 30 min. With the exception of one strain, there were no strain or sex differences in NAA levels among any of the investigated strains of rats. The level of NAA correlated with the in vivo anti-tumor response: when NAA-reactive fibrosarcoma or glioma cells were implanted into syngeneic WKA/Hok rats, groups of rats with high NAA levels suppressed tumor growth and survived longer than groups of rats with low NAA levels, while there was no difference in length of survival days in NAA non-reactive hepatoma or lymphoma cells. When 3-methylcholanthrene was inoculated into these two groups of rats, the tumor incidence in the groups of rats with high NAA level was significantly suppressed as compared to the group of rats with low NAA level. We discuss the mechanism of the induction of NAA in relation to the anti-tumor immunity.
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PMID:[Cytotoxic natural anti-tumor antibodies against fibrosarcoma and glioma cells in rats (author's transl)]. 731 60


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