Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A human monoclonal antibody (CLN-IgG) was produced from a human-human hybridoma derived from lymphocytes of a patient with cervical carcinoma. The reactivities of this antibody with various human glioma tissues and cultured glioma cells and the characterization of the antigen recognized by CLN-IgG on malignant glioma cells were analyzed and reported. CLN-IgG reacted with various human glioma cells and glioma tissues, especially glioblastoma, but did not react with normal brain tissues or fetal brain tissues. A large amount of antigen recognized by CLN-IgG was expressed on cell membranes of undifferentiated glioma cells and of glioma cells at the G2/M tumor growth phase in cycling cells. Antigen recognized by CLN-IgG was detected in only one of seven samples of cyst fluid, and was not detected in 27 serum samples or 18 samples of cerebrospinal fluid from glioma patients. CLN-IgG exhibited antibody-dependent cell cytotoxicity against U-25 1 MG glioma cells and primary cultured cells of glioblastomas and anaplastic astrocytomas. These data suggest that the antigen recognized by CLN-IgG might be related to cell proliferation in malignant gliomas. Thus, CLN-IgG might be useful for immunotherapy or immunoimaging of malignant gliomas.
J Neurosurg 1990 Dec
PMID:Antigen related to cell proliferation in malignant gliomas recognized by a human monoclonal antibody. 223 Sep 72

Recent studies have shown a survival benefit for patients with recurrent glioblastomas treated with stereotactic brachytherapy. On the basis of these encouraging results, we began a prospective study in 1987 to evaluate the use of brachytherapy in patients with newly diagnosed glioblastoma. Patients were considered eligible for this study if they met the following criteria: Karnofsky performance status 70% or greater; tumor size not greater than 5 cm in any dimension; a radiographically well delineated, supratentorial lesion not involving the ependymal surfaces; and pathologically confirmed glioblastoma. We treated 35 such patients between 1987 and 1990 with stereotactic brachytherapy as part of their initial therapy. The treatment protocol involved surgery, partial brain external-beam radiotherapy (59.4 Gy in 33 fractions), and stereotactic brachytherapy with temporary high-activity iodine 125 sources giving an additional 50 Gy to the tumor bed. Chemotherapy was not used in the initial management of these 35 patients. To compare our results with those obtained in a matched control group, we identified 40 patients with glioblastoma treated with surgery and external radiotherapy, with or without chemotherapy, between 1977 and 1986 at our institution. These patients had clinical and radiographic characteristics that would have made them eligible for the brachytherapy protocol. Survival rates at 1 and 2 years after diagnosis were 87% and 57%, respectively, for patients receiving brachytherapy versus 40% and 12.5%, respectively, for the controls (P less than .001). We conclude that stereotactic brachytherapy improves the survival of patients with glioblastoma when it can be incorporated into the initial treatment approach. Unfortunately, only about one in four patients with glioblastoma are suitable candidates for brachytherapy at the time of initial presentation.
J Natl Cancer Inst 1990 Dec 19
PMID:Results of stereotactic brachytherapy used in the initial management of patients with glioblastoma. 225 Mar 12

The interferon (IFN)-induced enzyme 2',5'-oligoadenylate (2-5A) synthetase has been implicated in the development of antiviral activity in human and animal cells. However, its role in IFN-mediated growth inhibition remains unclear. To elucidate the function of 2-5A synthetase, we have stably introduced a human 2-5A synthetase cDNA into a human glioblastoma cell line (T98G). Constitutive expression of the cDNA in these cells is associated with increased levels of resistance to infection by encephalomyocarditis virus. One transfected subclone, which expresses elevated levels of 2-5A synthetase enzyme activity, also shows a reduced rate of cellular proliferation.
J Interferon Res 1989 Dec
PMID:Constitutive expression of a 2',5'-oligoadenylate synthetase cDNA results in increased antiviral activity and growth suppression. 248 99

Human glioblastoma A-7 (GB A-7) cells can apparently recover from potentially lethal X-irradiation. The authors, using a colony-forming assay, studied the influence of pretreatment with 1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) on the effectiveness of X-irradiation against GB A-7 cells grown in monolayers and as multicellular spheroids. Pre-exposure to ACNU inhibited the recovery of irradiated GB A-7 cells. In monolayer cells, the combination treatment was most effective when ACNU was applied 2 to 8 hours prior to irradiation, and the larger the X-ray dose, the more potent the effect. ACNU pretreatment was more effective against large spheroids (enhancement ratio 1.86) than against small ones (1.34). Large spheroids showed necrosis, whereas small ones did not. Isobolographic analysis disclosed that the effect of combining X-irradiation and ACNU is within an additive envelope at the surviving fraction of 10(-2), while supra-additive at the surviving fraction of 10(-3). These results suggest that the potency of X-irradiation is augmented by ACNU pretreatment through an interactive mechanism. Further, suppression of recovery from X-ray induced potentially lethal damage was influenced by the presence of necrosis.
Neurol Med Chir (Tokyo) 1989 Dec
PMID:[Enhancement of the effect of X-irradiation against cultured human glioblastoma cells by pretreatment with ACNU]. 248 84

Loss of constitutional heterozygosity for specific chromosomal loci, when found consistently in a particular tumor type, suggests that a recessive oncogene important in the genesis of that tumor may be present within the involved chromosomal loci. DNA markers that detect restriction fragment length polymorphisms are powerful tools that have been used to detect loss of chromosomal loci in a growing number of human malignancies. The human brain tumor astrocytoma is usually malignant and virtually incurable. Two types of malignant astrocytomas are recognized histopathologically:anaplastic astrocytoma and glioblastoma multiforme. We carried out a restriction fragment length polymorphism analysis of tumors from 15 patients with anaplastic astrocytoma and 20 patients with glioblastoma using polymorphic DNA markers for loci on chromosome 17. Loss of constitutional heterozygosity for loci on chromosome 17 was found in both anaplastic astrocytoma and glioblastoma patients with equal frequency (40% of cases). Our mapping data revealed a region of loss on chromosome 17p between physical loci p11.2 and pter that was common to both patient groups. Taken together with the previously reported finding of loss of heterozygosity for loci on chromosome 10 in glioblastoma, these results indicate that tumorigenesis in the astrocyte lineage may involve recessive oncogenes on two different chromosomes.
Cancer Res 1989 Dec 01
PMID:Loss of heterozygosity for loci on chromosome 17p in human malignant astrocytoma. 257 17

Expression of human LDL receptor mRNA and protein is induced in human glioblastoma-astrocytoma cells upon transfer into lipoprotein-deficient medium, a mode of induction likely to be physiological. The presence of cycloheximide (CHX) leads to up to 7.5-fold superinduction of LDL receptor mRNA within 4 hr and, upon removal of this inhibitor, to superinduction of LDL receptor protein as well. The extent of superinduction of LDL receptor mRNA reaches over 40-fold beyond the level expressed in medium containing regular serum. Despite its extensive superinduction, LDL receptor mRNA decays rapidly in the presence of CHX. Stabilization of LDL receptor mRNA is thus unlikely to account for the observed superinduction. These results show that normally the LDL receptor gene is expressed to only a small fraction of its full potential.
Biochem Biophys Res Commun 1989 Dec 15
PMID:Superinduction of the human gene encoding low density lipoprotein receptor. 259 46

The data on 645 patients with anaplastic neuroepithelial tumors subjected to radiotherapy, irradiation with radiosensitizers (metronidazole) and chemoradiotherapy are presented. Total-differential brain irradiation was applied: 10-40 Gy on the whole brain and 10-20 Gy on the tumor bed. Fractionation depended on tumor radiosensitivity. The median survival time for anaplastic astrocytoma was 50 +/- 5.6 mos., oligodendroglioblastoma - 42 +/- 7.4 mos., ependymoblastoma - 61 +/- 8.2 mos. and glioblastoma - 22 +/- 1.5 mos. High-dose dynamic fractionation proved to be most effective in cases of glioblastoma. The outcome of glioblastoma was modified neither by radiosensitizers nor by cytotoxic agents.
Med Radiol (Mosk) 1989 Dec
PMID:[Radiation and combined treatment of anaplastic neuroepithelial neoplasms]. 260 90

MR is generally known to be more sensitive but less specific than CT in the detection of brain lesions. In our opinion multiple echo sequences can markedly improve MR specificity in the diagnosis of tumors. We reviewed a series of 343 intracranial tumors studied with MR using multiple echo sequences and histologically verified. On the basis of the different signal patterns we divided brain tumors into 5 classes. Class 1: the signal intensity of the tumor increases progressively in T2 WI (100% of craniopharyngiomas, 21/21; 100% of epidermoid tumors, 12/12; 81% of astrocytomas (grades I to III), 64/79; 65% of neurinomas, 30/46). Class 2: the signal intensity of the lesion decreases progressively in T2 WI: A) the tumor has higher signal intensity than the parenchyma in all echoes (100% of medulloblastomas, 14/14; 53% of pituitary adenomas, 15/28); B) the tumor has the same signal intensity as the parenchyma in late echo acquisitions (100% of ependymal tumors, 12/12; 60% of meningiomas, 25/41). Class 3: the tumor has the same signal intensity as the parenchyma in all echoes (34% of meningiomas, 14/41). Class 4: glioblastoma model: one or more cysts of high signal intensity in T2 WI and slightly hyperintense nodules and/or rings and hyperintense peritumoral edema (73% of glioblastomas, 35/48; 72% of metastases, 18/25). Class 5: oligodendroglioma model: mixed hyper/hypointense pattern; cyst, calcifications and edema are very difficult to recognize within the lesion (95% of oligodendrogliomas, 18/19). The signal pattern was sometimes characteristic but never pathognomonic. Nevertheless, this classification proved to be an useful criterion to restrict the number of possible diagnoses. The study of T1 and T2 values seems to be less useful.
Radiol Med 1989 Dec
PMID:[Magnetic resonance in brain tumors: a classification based on signal behavior in multiple echo sequences]. 262 52

Tumour blood flow was estimated by fractional distribution of rubidium in two allografts (B16 melanoma and Lewis lung tumour) and two xenografts (Glioma 522, a human grade IV astrocytoma and Mel-mo, a human melanoma), in order to investigate the influence of certain tumour characteristics on tumour perfusion. In all four tumours perfusion decreased with increase in tumour weight. The rubidium extraction in Mel-mo was markedly lower than that of the other three tumours; this tumour was the most necrotic. Necrosis was patchy in Glioma 522 and Mel-mo, but predominantly central in B16 and Lewis lung tumour. However, all tumour nodules examined showed a similar pattern of rubidium extraction: high at the rim with a rapid fall towards the centre. It appeared that while overall blood flow may be related to the extent of necrosis, blood flow distribution within tumour nodules did not correlate closely its pattern.
Eur J Cancer Clin Oncol 1989 Dec
PMID:Blood flow distribution within transplantable tumours in the mouse. 263 52

The human ROS1 gene, which possibly encodes a growth factor receptor, was found to be expressed in human tumor cell lines. In a survey of 45 different human cell lines, we found ROS1 to be expressed in glioblastoma-derived cell lines at high levels and not to be expressed at all, or expressed at very low levels, in the remaining cell lines. The ROS1 gene was present in normal copy numbers in all cell lines that expressed the gene. However, in one particular glioblastoma line, we detected a potentially activating mutation at the ROS1 locus.
Proc Natl Acad Sci U S A 1987 Dec
PMID:Expression and rearrangement of the ROS1 gene in human glioblastoma cells. 282 75


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