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 case of multicentric glioblastoma with the clinical and histopathological findings is presented in which three lesions are located above and below the tnetorium. Multicentric glioblastomas are those which have no macroscopic or microscopic connection.
J Neurol 1979 Sep
PMID:A case of glioblastoma with multiple centers above and below the tentorium. 9 72

A culture line of mouse glioblastoma cells changed morphologically to differentiated astrocyte-like cells when cultured in medium with dibutyryl cyclic adenosine monophosphate and theophylline. Morphological alteration occurred within only 5 hr when 3 mM dibutyryl cyclic adenosine monophosphate and 1 mM theophylline were used, and in 1 day when 1 mM theophylline were used. Cells showing this morphological change reverted completely to immature cells when they were transferred to medium without these two chemicals. Addition of 1 or 3 mM dibutyryl cyclic guanosine monophosphate with 1 mM theophylline to the medium also induced development of cytoplasmic processes from these cells and the cells became stellate, although the cytoplasmic processes were not as long or as numerous as those induced by dibutyryl cyclic adenosine monophosphate, and the altered cells could not be referred to as differentiated glia cells. Sodium butyrate induced morphological alterations similar to those induced by dibutyryl cyclic guanosine monophosphate, but fewer cells showed these alterations. Addition of cyclic adenosine monophosphate or cyclic guanosine monophosphate in the presence of theophylline or addition of theophylline alone did not induce morphological changes of the cells.
Cancer Res 1975 Sep
PMID:Morphological differentiation of cultured mouse glioblastoma cells induced by dibutyryl cyclic adenosine monophosphate. 16 61

Autologous leukocytes (10(7) to 10(9)), obtained with the Haemonetic's Leukaphoresis apparatus, were inoculated directly into recurrent glioblastoma tumors via indwelling catheters or by direct intratumoral injection through existing craniotomy openings. The rational use for autologous leukocyte (lymphocyte) infusions was based on in vitro autologous lymphocyte cytotoxicity to glioblastoma cells in the absence of serum inhibitory factors. Seven of 17 patients treated had life expectancy under 1 month; all patients had received definitive surgery, and all but two received radiation, nitrosourea chemotherapy and/or dexamethasone, and showed evidence of clinically recurrent disease. Following autologous leukocyte infusion (lymphocyte/granulocyte ratio 1:1), eight patients sustained clinical improvement and were alive up to 17 months later. No neurotoxicity ascribable to the procedure has been observed. One patient, who was comatose at the time of single leukocyte infusion, returned to full activity and lived for 17 months without an increase in tumor mass by brain scan. These results suggest that infusions of autologous leukocytes (lymphocyte-monocytes) directly into glioblastoma may be a viable additional treatment for glioblastoma and certainly warrants further evaluation.
Cancer 1977 Sep
PMID:Immunotherapy with autologous white cell infusions ("lymphocytes") in the treatment of recurrrent glioblastoma multiforme: a preliminary report. 19 84

A case of coincidental glioblastoma and meningioma in which the first manifestation were focal convulsive fits is reported. As the association of intracranial tumors is infrequent, their clinical ways of presentation and the theories on their origin are discussed, as well as the importance of the preoperative diagnosis for the surgical planning and prognosis.
Arq Neuropsiquiatr 1978 Sep
PMID:[Concomitant meningioma and glioblastoma. Report of a case]. 21 Jul 46

The first two instances of mixed sarcoma-glioblastoma with a history of therapeutic irradiation to the head are reported, both occurring within one year of radiation therapy (for pituitary adenoma and residual meningioma). Two novel variants of mixed sarcomas of brain with extreme tumor metaplasia (fibromyxoosteochondrosarcoma and fibrochondroosteosarcoma-glioblastoma multiforme) are documented, and some of the problems concerning the origin of brain tumors with mixed population are discussed.
Ann Neurol 1978 Sep
PMID:Mixed intracranial sarcomas: rare forms and a new association with previous radiation therapy. 21 26

Four term infants were found by computerized cerebral tomography (CT) to have intraventricular hemorrhage. All were male infants who had experienced substantial intrapartum complications. One infant had subtle clinical signs at 2 days of age; the others had major neurologic findings including seizures and ophthalmoplegia that occurred at 1, 4, and 6 weeks of age, respectively. Three infants in whom the hemorrhages were indistinguishable by CT from those described in preterm infants now have arrested hydrocephalus and normal development. The fourth infant was found to have a large glioblastoma at the site of origin of his initial hemorrhage. These cases emphasize the need to consider this diagnosis in neonates born at term who have abnormal neurologic signs.
Am J Dis Child 1979 Sep
PMID:Intraventricular hemorrhage in the neonate born at term. 47 46

The familial occurrence of brain tumors are exceedingly rare except in cases with phacomatosis. We encountered pituitary adenomas in two sisters of a family, so far presenting no evidence of multiple endocrine adenomatosis (MEA). Case 1, K. O. a 26-year-old woman was admitted to our Hospital on September 10, 1970 with visual acuity and field disturbance, irregular menstruation and acromegaly. Neurological examination: Her visual acuity was Vd 0.6 and Vs 0.3, visual field was bitemporal hemianopsia, and ther was papilledema bilaterally. She had left exophthalmos and left abducens palsy. Roentgenogram of the skull, brain scanning, cerebral angiogram, pneumoencephalogram suggested the presence of a pituitary tumor. On Sep. 17, 1970, through a left frontotemporal craniotomy the tumor was removed subtotally. The pathological diagnosis was pituitary adenoma (chromophobe). Case 2, M. T. a 31-year-old woman, sister of case 1, was admitted to the Hospital on September 19, 1973, with mild headache, left visual field disturbance and amenorrhea. She had a child, and a past history of pulmonary tbc. Neurological examination: Her visual acuity was Vd 1.2 and Vs 0.03, and visual field of the right eye was temporal lower quandrant anopsia. There was optic nerve atrophy in the left eye. Plain X-ray craniogram, brain scanning, cerebral angiogram and pheumoencephalogram suggested the presence of a pituitary tumor. On Sep. 28, 1973, a right frontal craniotomy was performed. The tumor tissue with capsule was removed subtotally. The pathological diagnosis was pituitary adenoma (mixed type). In the literatures about familial brain tumors with histological diagnosis, glioma and glioblastoma are common, meningioma is relatively rare. Pituitary adenoma with no evidence of MEA is exceedingly rare. The two sisters presented in this paper, have no evidence of hyperparathyroidism, pancreas adenoma and peptic ulcer. So, we consider, at present, these cases should not be field in MEA.
 ...
PMID:[Familial occurrence of pituitary adenoma (author's transl)]. 94 79

Eighteen patients with Cushing's disease were treated with reserpine and pituitary irradiation. Complete remission was obtained in 9 out of 18 patients after reserpine treatment of 1-2 mg per day for a mean period of 20.4 months, and pituitary irradiation with a mean of 5,865 rads. In another 9 patients, reserpine 0.8-2 mg per day for a mean period of 22.5 months, and pituitary irradiation with a mean of 6,650 rads, were employed. Of these 9 patients, an additional subtotal adrenalectomy was carried out in 6 patients who are now in complete remission. Because of severe psychic symptoms resulted from the original disease in 2 of the remaining 3 patients, subtotal adrenalectomy was performed first and pituitary irradiation and reserpine treatment followed. Remission was eventually obtained in these 2 cases. One patient refused the operation, and thus had little clinical remission. All of the 17 cases in remission were followed up for periods of 6 months to 10 yr. During this time, only one case which had responded to reserpine and pituitary irradiation relapsed, but regained remission following resumption of therapy. Another died of cerebral glioblastoma 4 yr after remission of the disease. It was noteworthy that endocrinologic data including: plasma levels of ACTH and 11-OHCS, suppressibility by dexamethasone, responses of plasma GH to arginine and to insulin loads, and diurnal rhythm of plasma 11-OHCS were nearly normal in a considerable number of the cases in remission. Effectiveness of the combined therapy with reserpine and pituitary irradiation for treating Cushing's disease may support a working hypothesis that reserpine acts through some as yet unknown mechanism to correct a presumed central nervous disorder, while suitable pituitary irradiation probably corrects the pituitary dysfunction directly.
J Clin Endocrinol Metab 1975 Sep
PMID:Treatment of Cushing's disease with reserpine and pituitary irradiation. 115 59

Recent cloning studies confirm the presence of two subtypes of bombesin (Bn) receptors. In contrast to the gastrin-releasing peptide (GRP)-preferring subtype, which has been widely studied, nothing is known about the cellular mechanisms of the neuromedin B (NMB)-preferring subtype, which occurs widely in the central nervous system and gastrointestinal tissues, partially because of the lack of a cell line with functional receptors. In the present study we have investigated Bn receptors on the rat glioblastoma cell line C-6, reported to contain mRNA of the NMB receptor subtype. Binding of 125I-[D-Tyr0]NMB to these cells was time- and temperature-dependent, saturable, reversible, and only inhibited by Bn receptor agonists or antagonists. For Bn receptor agonists the relative potencies were: NMB (1.7 nM) approximately equal to litorin (3 nM) greater than ranatensin (8 nM) greater than Bn (19 nM) greater than neuromedin C (NMC) (210 nM) greater than GRP (500 nM). These relative affinities were almost identical to those for the NMB receptor subtype on rat oesophageal tissue and for Balb 3T3 cells stably transfected with the NMB receptor subtype. These potencies differed from those for the GRP receptor subtype on rat pancreatic acini [Bn approximately equal to litorin (4 nM) greater than ranatensin, NMC, GRP (15-20 nM) much greater than NMB (351 nM)]. The relative potencies of four different classes of Bn receptor antagonists were compared. Results from C-6 tumour cells agreed closely with those for binding to the NMB receptor subtype on rat oesophageal tissue and in Balb 3T3 cells stably transfected with this receptor, and differed markedly from those for binding to the GRP receptor subtype on rat pancreatic acini. Four Bn receptor antagonists had a higher affinity for the GRP subtype ([D-Phe6]Bn-(6-13)ethyl ester (500 x), [D-Phe6][psi 13-14,Cpa14]Bn- (6-14) (70 x) (where psi 13-14 refers to the replacement of the -CONH- peptide bond between Leu13 and Met14 by -CH2NH2) [psi 13-14,Leu14]Bn, [D-Phe6]Bn-(6-13) propylamide (30 x)] and two had a higher affinity for the NMB subtype on C-6 cells and transfected cells ([D-Pro4,D-Trp7,9,10] substance P-(4-11) (9 x) and [Tyr4,D-Phe12]Bn (18 x)]. In C-6 tumour cells, Bn receptor agonists caused an increase in cytosolic Ca2+ and the generation of inositol phosphates. For both responses, NMB was more than 50-fold more potent than GRP. Neither NMB nor GRP increased cyclic AMP. These results demonstrate that the rat glioblastoma cell line C-6 possesses functional NMB-preferring Bn receptors, and agonist occupation activates phospholipase C, thus increasing cytosolic Ca2+ and inositol phosphate formation. Because the interaction of Bn-related peptides with C-6 cell receptors is identical with that reported in other tissues containing the mRNA for the NMB subtype, this cell line should prove useful in exploring further the cellular basis of action of the peptides that interact with this receptor in the central nervous system and various other tissues.
Biochem J 1992 Sep 01
PMID:Activation of neuromedin B-preferring bombesin receptors on rat glioblastoma C-6 cells increases cellular Ca2+ and phosphoinositides. 132 46

Exogenously administered tumor necrosis factor-alpha (TNF-alpha) elicits several symptoms of generalized infections such as fever, increased sleep, and anorexia. The aim of the present work was to localize these effects of TNF-alpha to specific amino acid sequences of the parent molecule by characterizing the in vivo and in vitro activities of several synthetic TNF-alpha fragments. Intracerebroventricular injection of TNF-alpha elicited dose-dependent fevers and increases in non-rapid-eye-movement sleep (NREMS) in rabbits. Four fragments also promoted NREMS and five elicited monophasic fevers. All of the somnogenic fragments share the amino acid sequence 31-36. In rats, TNF-alpha and one of the fragments [TNF-alpha-(69-100)] suppressed 12-h food intake. Furthermore, TNF-alpha increased the expression of the intercellular adhesion molecule-1 and enhanced interferon-gamma-induced HLA-DR expression in human glioblastoma cell line. In contrast, none of the fragments possessed these in vitro activities. Our in vivo results support the concept that there are biologically active regions in the TNF-alpha molecule.
Am J Physiol 1992 Sep
PMID:Somnogenic, pyrogenic, and anorectic activities of tumor necrosis factor-alpha and TNF-alpha fragments. 135 84


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