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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isoproterenol, corticotropin (ACTH), and triodothyronine immobilized on glass and Sepharose beads by diazotization procedures have been shown to interact with cultured tumor cells of "target tissue" origin. Cells used were rat glioma cells (C6), rat adrenal tumor cells (Y-1), and rat pituitary tumor cells (GH3). The rat glioma cells bound principally to immobilized isoproterenol, whereas the rat adrenal tumor cells bound to immobilized corticotropin, and rat pituitary tumor cells bound to immobilized triiodothyronine. Binding was inhibited by preincubation of the cells in soluble drug or hormone. With C6 cells there was a positive correlation between adenylate cyclase [ATP pyrophosphate-lyase (cyclizing, EC 4.6.1.1] stimulation and the degree of binding to the immobilized isoproterenol. Norepinephrine, bound through the ethanolamine side chain via an amide linkage, did not bind cells, demonstrating specific structural requirements for drug-cell interactions. HeLa cells were shown to bind tightly to diphtheria toxin coupled to Sepharose beads via an amide bond. This binding was inhibited by prior incubation of the Sepharose toxin with purified antitoxin. Toxin bound to Sepharose via an azo bond did not bind cells. These data suggest that the cell affinities are due to cell surface receptors interacting with the immobilized drugs and hormones, and that the observed affinities possibly reflect the relative receptor complement of these cells.
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PMID:Affinity isolation of cultured tumor cells by means of drugs and hormones covalently bound to glass and Sepharose beads. 18 May 34

Thirty-three patients with malignant glioma were randomly divided into two groups after extensive tumor resection. Those in group A received, every five to eight weeks, a course of chemotherapy consisting of intravenously administered carmustine, 80 mg/sq m/day for three days, and vincristine sulfate, 1.4mg/sq m on days 1 and 8. Patients in group B were treated identically and received radiation therapy (RT) as well, 4,500 rads whole brain plus 1,500 rads to the side of the tumor. The median survival time of group A was 30 weeks, while that of group B was 44.5 weeks, but the overall survival curves were not significantly different. The median survival times exceeded the 17 weeks reported elsewhere in comparable patients not receiving postoperative therapy. Estimates of the quality of survival suggested (1) the two groups were not comparable following randomization, possibly influencing the results; and (2) postoperative radiation and chemotherapy do not increase morbidity and offer a longer period than other treatments during which patients' conditions remain stable or improve.
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PMID:Treatment of malignant glioma. A controlled study of chemotherapy and irradiation. 18 Sep 38

A retrospective ethnic study was made of 16,311 cases of primary central nervous system (CNS) tumors seen at the Armed Forces Institute of Pathology (AFIP), Washington, D.C., from 1958 to 1970. Results showed a considerably higher Caucasian:Negro (C:N) case ratio (13.7:1) than the C:N population ratio (8.4:1), indicating a higher relative frequency of primary CNS tumors in American Caucasians as compared to American Negroes. The glioma was significantly more frequent in Caucasians than in Negroes (p less than 0.005). In contrast, Negroes had an excess of the pituitary adenoma as compared to Caucasians (P less than 0.01). The proportional frequencies of the meningioma and the nerve sheath tumor were also higher in Negroes than in Caucasians. When this pattern of the tumor distribution of American Negroes was compared to that of African Negroes (a composite African series), the preponderance of the pituitary adenoma and the meningioma and the relative paucity of the glioma in the Negro race as compared to Caucasians were again confirmed. The differences in the relative frequency and the tumor distribution between American Negroes and Caucasians and the considerable similarity of the tumor distribution between American and African Negroes emphasize the importance of genetic factors in the development of at least some primary CNS tumors.
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PMID:The ethnic distribution of primary central nervous system tumors: AFIP, 1958 to 1970. 18 96

Computerized tomography (CT) is known to be very helpful in demostrating the presence and extent of supratentorial gliomas, practically in combination with intravenous injection of contrast material. Certain specific density patterns were found to exist and enabled us to differentiate with confidence the low-grade gliomas from the glioblastomas. Overlapping did occur, however, as was to be expected, since histological proof was sometimes obtained by the needle biopsy with its inherent doubt as to true tumor representation. Future CT techniques such as sequential scanning after intravenous injection of contrast material may further increase the usefulness of CT scans in the diagnosis and therapeutic approach to the patient with a suspected glioma.
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PMID:Computerized tomography as a possible aid to histological grading of supratentorial gliomas. 19 55

One must know tumor cell kinetics in order to devise a rational drug regimen for gliomas. With tritiated thymidine, the Labelling Index of astrocytomas is less than 1 per 100; of glioblastomas from 5-10 per 100. The duration of S phase is fairly constant, ranging from 7 to 10 hours. Double radioautography reveals a cell cycle time of 2 to 3 days and a Growth Fraction of 10 to 30 per 100 in glioblastomas. Calculations based on volume of tumor at recurrence after a gross total resection, analysis of primer dependent D.N.A. polymerase (P.D.P.), and analysis of cells by Flow Microfluorometer, all confirm these approximate figures. Thus most of the cells of a glioma are not sensitive to a cell-cycle phase specific drug. Such an agent, if given, should be administered over a 2 to 3 day period, in order to affect as many cells as possible. The most important part of a drug regimen should be an agent which attacks non-proliferating as well as proliferating cells, such as an alkylating agent. The effects of various drugs and schedules can be examined by animal models with the technqiue of colony forming efficiency.
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PMID:Current status of population kinetics in gliomas. 19 96

A search of the records of 10 pediatric oncology centers revealed 102 children with more than one malignant neoplasm. In this group of 102 patients, all pediatric cancers were seen as initial lesions, but Wilms' tumor and retinoblastoma were over-represented and leukemia and brain tumors underrepresented. Survival variation as well as tumor susceptibility may be responsible for this disproportion. Osteosarcomas and chondrosarcomas were the most frequent second malignant neoplasms (SMN). Embryonal tumors were rare as SMN and adult-type tumors (carcinomas) appeared at earlier than expected ages, whether arising after irradiation or not related to that form of therapy. Radiation was associated with 69 SMN, genetic disease accounted for 27 SMN and both conditions were noted in 15 SMN. In the group of 21 patients for whom neither radiation nor a known genetic disorder could be implicated, there were three with colon carcinoma and glioma and five with leukemia or lymphoma and glioma. These combinations may reflect new tissue-specific hereditary cancer syndromes.
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PMID:Patterns of second malignant neoplasms in children. 19 10

We have recently reported that fetal BD IX-rat brain cells (FBC), transferred to long-term culture after a transplacental pulse of EtNU on the 18th day of gestation, undergo neoplastic transformation in vitro ("BT-cell lines"). Tumors developed upon s.c. reimplantation of BT-cells into baby BD IX-rats, appeared histologically as neurinoma-, glioma- or glioblastoma-like, and frequently as pleiomorphic neoplasms. In spite of a more atypic cellular morphology, these tumors grossly resembled the different types of neuroectodermal rat neoplasms induced by EtNU in vivo. Like the neoplastic cell culture lines derived from EtNU-induced, neuroectodermal BD IX-rat tumors ("V-cell lines"), the BT-lines contained multipolar glia-like cells, but also flat cells with fewer and shorter cytoplasmic processes, and occasionally giant cells. Both the V- and BT-lines showed different levels of aneuploidy. They contained multiple subpopulations of cells, as reflected, e.g., by plurimodal pulse-cytophotometric DNA distributions. All lines contained, to varying degrees, the nervous system-specific protein S-100, a "marker" not yet expressed in FBC. There was no indication of more than borderline neurotransmitter activity, suggesting that proliferating (precursor) cells of glial lineages may preferentially undergo malignant transformation after exposure to EtNU during this stage of brain development.
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PMID:Phenotypic properties of neoplastic cell lines developed from fetal rat brain cells in culture after exposure to ethylnitrosourea in vivo. 19 83

Twenty-nine primary intraspinal neoplasms in children observed between 1936 and 1975 in Connecticut are reviewed. Most of them were gliomas: 45 per cent astrocytoma, 24 per cent ependymal neoplasm, 10 per cent glioblastoma multiforme and 7 per cent glioma. Symptoms, physical findings and therapy are reviewed.
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PMID:Intraspinal neoplasms in children. 20 2

The variable effect of immunizations with cell-free tumor extract (TE) in a weakly antigenic (Morris hepatoma 3924a) and a highly antigenic (glioma 9L) inbred rat model system was described. Tumor enhancement was noted with the weakly antigenic tumor following either immunization with a low dose of TE admixed with Freund's adjuvant or immunization with high doses of TE. Enhancement was observed at four tumor cell challenge levels. Tumor enhancement with the highly antigenic tumor was found at only one level and was seen following immunization with intermediate doses of TE and a high tumor cell challenge. Tumor protection was only detected with the weakly antigenic tumor following immunizations with an intermediate dose of TE and challenge with a tumor cell dose 5-fold over threshold. This protection was tumor specific, as judged by an amputation and rechallenge experiment.
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PMID:Growth of transplanted rat tumors following administration of cell-free tumor antigens. 20 57

Experimental animal models resembling most human brain tumor types can be induced by exposure to oncogenic viruses or chemical carcinogens: Astrocytomas and glioblastoma multiforme can be produced experimentally by intracerebral injection of oncornaviruses, whereas medulloblastomas, choroid plexus papillomas, and ependymomas can be induced by the papovaviruses. Adenoviruses have been utilized to cause medulloepitheliomas, neuroblastomas, and retinoblastomas. All three groups of viruses can result in sarcoma production. Gliomas represent the primary tumor type induced in the brain by chemical carcinogens. These autochthonous tumor systems are reviewed, with emphasis on methods, tumor type, latency period, advantages, and disadvantages. In addition, recent investigations of molecular events involved in neoplastic transformation by chemical carcinogens are summarized.
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PMID:Chemical- and virus-induced brain tumors. 20 37


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