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)

Tumors are rare, but well-documented causes of precocious puberty in both sexes. The therapeutic and prognostic implications of a diagnosis of cancer require that the presence of a neoplastic process be ruled out in any case of precocious puberty. Granulosa-cell tumor of the ovary and Leydig-cell tumor of the testis are the most frequent gonadal tumors inducing precocious pseudopuberty in the two sexes. Adrenal tumors sustain a variety of endocrine syndromes, the most frequent one being virilization with or without hypercortisolism. Pure feminizing adrenal neoplasms have been described. For reasons not yet well understood, hypothalamochiasmatic glioma (beta-HCG) secreting tumors have almost never been described in association with female precocious puberty. Among these neoplasia, pineal germ-cell tumor inducing sexual maturation must be included. Hypothalamochiasmatic glioma and craniopharyngioma are the two cerebral tumors capable of inducing true precocious puberty. Even if equally distributed between both sexes, these tumors interfere with sexual maturation less frequently in girls than in boys. Hypothalamic hamartoma is considered a benign tumor, since it does represent a space-occupying mass. It more correctly could be called a malformation if its histologic characteristics are recalled. This cerebral lesion is now frequently described in children with true precocious puberty, probably because of improved diagnostic imaging methods.
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PMID:Oncologic causes of precocious puberty. 270 2

The authors present a case of an optic nerve hemangioblastoma in a young woman with von Hippel-Lindau disease. The initial diagnosis was made by incisional biopsy. Tumor growth led to progressive proptosis and loss of light perception. Excision was carried out by lateral orbitotomy. Clinically and radiographically, the tumor resembled an optic nerve meningioma or glioma. Review of the other known cases offers no information as to the potential spread of this benign tumor from the intraorbital optic nerve to the optic canal. Optic nerve hemangioblastoma must be considered in the differential diagnosis of optic nerve tumors in patients with or without von Hippel-Lindau disease.
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PMID:Hemangioblastoma of the optic nerve. Report of a case and review of literature. 305 Jun 87

Malignant transformation in tumors is characterized by changes in cell surface components such as glycolipids and glycoproteins and is determined by the sialic acid content of the glycoconjugates. Our purpose was to investigate whether or not a similar change occurred in the brain tumor cells during malignant transformation. Change in the electrical charge of the cell surface was studied by means of cell electrophoresis. Experimental cell lines of rat gliomas and fibroblasts were cultured and compared for electrical charge by cell electrophoresis. Four various grade gliomas and three meningiomas from human subjects were cultured and compared for electrical charge by cell electrophoresis. Free flow electrophoresis (Elphar Vap 5) was used because it characteristically does not interfere with the use of the cells for biochemical and biological studies following electrophoresis and because it also allows the possibility of subsequent cell culture. The rat glioma cells had lower electrical charges than the fibroblasts, and the human malignant brain tumor cells exhibited lower electrical charges than the benign tumor cells. These findings suggest a lower sialic acid content in malignant than in benign tumors and agree with theories which postulate a decrease in sialic acid content accompanying malignant transformation. This differentiation between benign and malignant tumors was made on the basis of the cell surface electrical charge and could be used for clinical diagnosis and treatment.
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PMID:[Electrokinetic property of brain tumor cells by the aid of free flow electrophoresis (author's transl)]. 709 70

We attempted to determine whether the plasma concentration of basic fibroblast growth factor (bFGF) was elevated in brain tumor patients. The plasma concentration of bFGF was measured in 55 brain tumor patients and 17 normal subjects by enzyme immunoassay. Upper limit of plasma bFGF in the normal subjects was 1.6 pg/ml. Elevated plasma bFGF levels were observed in 28 patients including 13 of 17 glioma patients, eight of 19 benign tumor patients, and seven of 19 malignant tumor patients. Twelve of 14 malignant glioma patients had elevated plasma bFGF levels. There was a good correlation (r = 0.42, p < 0.05) between the elevated plasma bFGF level and the tumor volume. Further studies are needed to determine whether the plasma bFGF level is a clinically useful diagnostic and prognostic marker for patients with brain tumors.
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PMID:Elevated plasma basic fibroblast growth factor in brain tumor patients. 900 14

The term nasal glioma has been used to describe a congenital benign tumor of the nasal region containing neural tissue. The nature of these lesions remains open to controversy, because of the different locations of the heterotopic neural tissue involved, the deficient development of the bony structures and the persistence or not of the structural relations with the central nervous system. More recent terms define these lesions as ectopic nervous tissue. A clinical, morphological, ultrastructural and immunohistochemical study is made of two cases of nasal glioma, one associated with agenesis of the corpus callosum. In this case, the mother had been treated with clomiphene. In such cases, morphological and immunohistochemical findings support that "nasal glioma" remain valid as a descriptive term defining a congenital benign tumor composed of heterotopic neural tissue within the nasal region and covered by skin, that may recur following incomplete surgical resection.
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PMID:Nasal glioma or nasal glial heterotopia? Morphological, immunohistochemical and ultrastructural study of two cases. 1200 54

To screen and evaluate protein biomarkers for the detection of gliomas (Astrocytoma grade I-IV) from healthy individuals and gliomas from brain benign tumors by using surface enhanced laser desorption/ionization time of flight mass spectrometry (SELDI-TOF-MS) coupled with an artificial neural network (ANN) algorithm. SELDI-TOF-MS protein fingerprinting of serum from 105 brain tumor patients and healthy individuals, included 28 patients with glioma (Astrocytoma I-IV), 37 patients with brain benign tumor, and 40 age-matched healthy individuals. Two thirds of the total samples of every compared pair as training set were used to set up discriminating patterns, and one third of total samples of every compared pair as test set were used to cross-validate; simultaneously, discriminate-cluster analysis derived SPSS 10.0 software was used to compare Astrocytoma grade I-II with grade III-IV ones. An accuracy of 95.7%, sensitivity of 88.9%, specificity of 100%, positive predictive value of 90% and negative predictive value of 100% were obtained in a blinded test set comparing gliomas patients with healthy individuals; an accuracy of 86.4%, sensitivity of 88.9%, specificity of 84.6%, positive predictive value of 90% and negative predictive value of 85.7% were obtained when patient's gliomas was compared with benign brain tumor. Total accuracy of 85.7%, accuracy of grade I-II Astrocytoma was 86.7%, accuracy of III-IV Astrocytoma was 84.6% were obtained when grade I-II Astrocytoma was compared with grade III-IV ones (discriminant analysis). SELDI-TOF-MS combined with bioinformatics tools, could greatly facilitate the discovery of better biomarkers. The high sensitivity and specificity achieved by the use of selected biomarkers showed great potential application for the discrimination of gliomas patients from healthy individuals and gliomas from brain benign tumors.
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PMID:Serum protein fingerprinting coupled with artificial neural network distinguishes glioma from healthy population or brain benign tumor. 1559 84

Nasal glioma is a rare benign tumor that usually occurs during infancy. We report a case of nasal glioma in a 6-month-old boy in which the histomorphologic features resembled those of an anaplastic astrocytoma.
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PMID:Nasal glioma (neuroglial heterotopia) mimicking an astrocytoma: case report. 1638 48

Neurofibromatosis-1 (NF1) is a common tumor predisposition syndrome in which affected individuals develop benign and malignant tumors. Previous studies from our laboratory and others have shown that benign tumor formation in Nf1 genetically engineered mice (GEM) requires a permissive tumor microenvironment. In the central nervous system, Nf1 loss in glia is insufficient for glioma formation unless coupled with Nf1 heterozygosity in the brain. Our subsequent studies identified Nf1+/- microglia as a critical cellular determinant of optic glioma growth in Nf1 GEM. Using NF1 as an experimental paradigm to further characterize the role of microglia in glioma growth, we first examined the properties of Nf1+/- microglia in vitro and in vivo. Nf1+/- microglia exhibit increased proliferation and motility and express elevated levels of genes associated with microglia activation. We further show that Nf1+/- microglia harbor high levels of activated c-Jun-NH(2)-kinase (JNK) without any significant changes in Akt, mitogen-activated protein kinase (MAPK), or p38-MAPK activity. In contrast, Nf1-/- astrocytes do not exhibit increased JNK activation. SP600125 inhibition of JNK activity in Nf1+/- microglia results in amelioration of the increased proliferation and motility phenotypes and reduces the levels of expression of activated microglia-associated transcripts. Moreover, SP600125 treatment of Nf1 optic glioma-bearing GEM results in reduced optic glioma proliferation in vivo. Collectively, these findings suggest that Nf1+/- microglia represent a good model system to study the role of specialized microglia in brain tumorigenesis and identify a unique Nf1 deregulated pathway for therapeutic studies aimed at abrogating microenvironmental signals that promote brain tumor growth.
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PMID:Increased c-Jun-NH2-kinase signaling in neurofibromatosis-1 heterozygous microglia drives microglia activation and promotes optic glioma proliferation. 1907 5

The authors report a case of glioma nasopalatine Multifoil in wallet, location-intra nasal and palatal left. The nasal glioma is a rare congenital malformation presenting as a nasal mass composed of neuroglial tissue heteropias resulting from an abnormality in embryonic development. It is a benign tumor that fits into the nosology of the masses of the midline. This abnormality arises primarily a diagnostic problem because often mistaken for a meningo-encephalocele or a nasal dermoid cyst. Localization nose and palate, an hourglass, is extremely rare if not exceptional; The computed tomography (CT) has enabled the accurate assessment of injury and has guided the choice of surgical technique. The resection was done successfully without recurrence. Histology examination of the surgical specimen confirmed the nature of astrocytic neuroglial tumor. The location of the tumor pedide palate to that of the left nostril is special and especially histological diagnosis of this congenital malformation.
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PMID:[Diagnostic and surgical approach to an hourglass-shaped nasopalatine glioma in an infant]. 2132 23

We present estimates of population-based 5-year relative survival for adult Europeans diagnosed with central nervous system tumors, by morphology (14 categories based on cell lineage and malignancy grade), sex, age at diagnosis and region (UK and Ireland, Northern, Central, Eastern and Southern Europe) for the most recent period with available data (2000-2002). Sources were 39 EUROCARE cancer registries with continuous data from 1996 to 2002. Survival time trends (1988 to 2002) were estimated from 24 cancer registries with continuous data from 1988. Overall 5-year relative survival was 85.0% for benign, 19.9% for malignant tumors. Benign tumor survival ranged from 90.6% (Northern Europe) to 77.4% (UK and Ireland); for malignant tumors the range was 25.1% (Northern Europe) to 15.6% (UK and Ireland). Survival decreased with age at diagnosis and was slightly better for women (malignant tumors only). For glial tumors, survival varied from 83.5% (ependymoma and choroid plexus) to 2.7% (glioblastoma); and for non-glioma tumors from 96.5% (neurinoma) to 44.9% (primitive neuroectoderm tumor/medulloblastoma). Survival differences between regions narrowed after adjustment for morphology and age, and were mainly attributable to differences in morphology mix; however UK and Ireland and Eastern Europe patients still had 40% and 30% higher excess risk of death, respectively, than Northern Europe patients (reference). Survival for benign tumors increased from 69.3% (1988-1990) to 77.1% (2000-2002); but survival for malignant tumors did not improve indicating no useful advances in treatment over the 14-year study period, notwithstanding major improvement in the diagnosis and treatment of other solid cancers.
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PMID:Survival of European patients with central nervous system tumors. 2180 73


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