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)

It is classicaly admitted that the intracranial internal carotid artery after a first intracavernous segment, becomes intra-dural by perforating or passing through the dura. Since 1949, the first of us has refuted this conception as well as that of the artery floating in the venious blood of the cavernous sinus and has described to so-called cavernous sinus as a latero-seller extradural space into which the artery has but neighbourhood relationship with a venous plexus. During embryonic development the internal carotid artery is englobed by the dura which differentiates around the cerebral vessels. At a later stage, owing to the adhesion of the dural leaf to the intracranial periosteum, the internal carotid artery becomes closely attached to the bone at the level of the base of the anterior clinoid process. This explains that tumors developping in the sellar and parasellar region may compress or obstruct the carotid artery at this level causing neurologic symptoms of ischemic origin. Three similar cases are reported, a glioma of the optic nerve, an adenoma of the hypophysis and meningioma of the sphenoidal wing.
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PMID:[Compression and obstruction of the internal carotid artery by sellar and parasellar tumors]. 75 14

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.
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PMID:[Familial occurrence of pituitary adenoma (author's transl)]. 94 79

Brain scintigrams with 8-10 mci of pertechnetate were studied refering to surgical, histological and other neuroradiological findings in 91 cases with diagnosis or suspect of basal midline lesions. Anterior view of 45 cases was stored in high speed magnetic tape, displayed on CRT of our data processing system and studied of the ratio of average count for regions of interest, 2 cm x 2 cm in size, placed on the areas of lesion, the sagittal sinus and the normal brain hemispheres. In 18 pituitary adenomas, excluding acromegaly and other intrasellar lesions, 89% of cases with surgical indication for optic nerve symptoms were reported as abnormal scintigrams. In 20 craniopharyngiomas, 11 positive cases consisted mainly of solid, recurrent or thick cystic tumors. Five of 6 ectopic pinealomas and all 6 parasellar or medial sphenoidal ridge meningiomas showed positive uptake. Average counts of the regions of interest placed on tumor areas were 169.4% of normal hemispheric areas in 9 pituitary adenomas, 192.5% in 3 solid craniopharyngiomas, 192.3% in 6 meningiomas and 193.3% in ectopic pinealomas. The difference in the average ratio of the lesion count to the normal hemispheric count was statistically significant between cystic craniopharyngioma and adenoma, ectopic pinealoma, meningioma, glioma and solid craniopharyngioma, and between adenoma and acromegaly with p less than 0.005, and between solid craniopharyngioma and acromegaly, and between glioma and acromegaly with p less than 0.025. In the ratio of the lesion count to the sagittal sinus count, on the other hand, the difference of the average ratio was significant with p less than 0.005, only between cystic craniopharyngioma and ectopic pinealoma, and between cystic and solid craniopharyngioma. These facts suggested that the sagittal sinus count was unsuitable to be the standard count of an anterior scintigram to compare with basal midline count. The routine Polaroid scintigram with Tc99m pertechnetate proved their useful clinical diagnostic value for various basal midline lesions, the size of which indicated the surgical procedures. The digital analysis of anterior scintigrams supported the clinical value of the routine brain scintigram in the detection of these lesions. The ratio of the average count of the basal midline lesion to the normal brain area on the anterior scintigram presents more useful clinical information than the ratio of the lesion to the sagittal sinus count. Brain scintigram is found to be very helpful for the differential diagnosis between solid and cystic sellar tumors which is very important for the decision of surgical indications, and is not always possible by any other conventional neuroradiological procedures.
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PMID:[Clinical evaluation of brain scintigrams for basal midline lesions (author's transl)]. 124 Jun 13

A case of anaplastic astrocytoma associated with pituitary adenoma is reported. The patient was a 33-year-old male, who was admitted with complaints of sensory aphasia, slight left motor paresis, and visual field defects. Neurological examination disclosed sensory and motor aphasia, Gerstmann's syndrome, slight left motor paresis, right homonymous hemianopsia, and bilateral choked discs. Computed tomography revealed a low density mass lesion with slight enhancement in the left temporal region and a ring-like enhanced mass lesion in the suprasellar region. In MRI, both the left temporal and the suprasellar lesions are depicted as low signal intensity areas in T1 weighted imaging, but as high signal intensity areas in T2 weighted imaging. Craniotomy was performed and both tumors were almost totally removed. The tumor in the left temporal region was diagnosed as anaplastic astrocytoma and the other in the suprasellar region was diagnosed as chromophobe adenoma. Multiple primary intracranial tumors of different cell types are rare. About a hundred cases can be found in medical literature. More than two thirds of them are cases of glioma associated with meningioma, but other combinations of tumors are extremely rare. We now report this case of astrocytoma associated with pituitary adenoma. In the literature, there are only 5 cases of similar combination. It is believed that astrocytoma and pituitary adenoma are histologically different. In three of five reported cases, the tumors were in close proximity to each other, but it is doubtful that their close proximity was related to the fact that they developed concurrently.
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PMID:[A case of anaplastic astrocytoma associated with pituitary adenoma]. 322 1

A surgical case of prolactinoma associated with craniopharyngioma is reported. A 47-year-old man was admitted to some neurosurgical clinic on October 12, 1982, because of visual disturbance, general fatigue and impotence. Laboratory study revealed hyperprolactinemia (360 ng/ml) and slight enlargement of sella turcica indicated the pituitary adenoma. Transsphenoidal surgery was performed to remove the tumor on November 20, 1982. Histopathological examination revealed chromophobe adenoma, and prolactin was stained in the tumor cells by means of immunoperoxidase staining. Though the clinical symptoms had been improved after surgery, visual disturbance became worse about one month later. At that time empty sella syndrome was suspected and the second operation (interhemispheric approach) was performed on January 21, 1983. No pathological changes were observed at all. On July 13, 1983, he was transferred to our clinic, because his visual acuity was deteriorating. At this time we reviewed the previous CT scan and noticed a suprasellar mass. It was supposed that the lesion had been overlooked and was the cause of the visual disturbance. On August 1, 1983, a bifrontal craniotomy was performed and the suprasellar tumor was removed. Pathological examination of the tumor revealed craniopharyngioma. So it was supposed that pituitary adenoma and craniopharyngioma had been coexisting since onset. Except for cases with von Recklinghausen's disease, multiple primary intracranial tumors of different cell types are relatively rare. A review of literature revealed 94 cases until 1986. The most frequent combination of multiple tumors was meningioma and glioma. But we could not find any case of pituitary adenoma associated with craniopharyngioma in the literature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of prolactinoma associated with craniopharyngioma]. 344 1

Pathological examination was carried out on 16 male Sprague-Dawley rats received single i. v. injection of 60 mg/kg of streptozotocin (SZ) at 5 weeks of age and maintained for 22 months. Insulinoma (63%), renal adenoma (50%), hepatocellular tumor (69%), cholangioma (31%) and Leydig cell tumor (56%) were found in a high incidence, and therefore occurrence of these tumors was considered to be attributable to the treatment with SZ. In addition to these tumors, though in a low incidence, various such tumors as leukemia, reticulum cell sarcoma, mammary tumor and glioma were also found.
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PMID:Neoplastic lesions in streptozotocin-treated rats. 622 53

Total sialic acid (TSA) and lipid-bound sialic acid (LSA) were determined in the cerebrospinal fluid (CSF) from 63 patients with various neurological diseases. Of these, 27 had brain tumors: 20 had glioma, and 7 pituitary adenoma. TSA levels were significantly increased in the CSF of 18 of the 20 glioma patients (p less than 0.001), while in the adenoma patients were indistinguishable from the controls; with a 90 and 0% test sensitivity respectively. Conversely, the LSA concentrations were significantly elevated, both, in the glioma and pituitary adenoma patients (p less than 0.001), with a 68 and 100% test sensitivity respectively. These preliminary data suggest that measurement of TSA and LSA in the CSF should prove useful for the diagnosis of brain tumors and, perhaps, in the follow-up of patients undergoing treatment for brain tumors.
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PMID:Total and lipid-bound sialic acid in the cerebrospinal fluid of patients with brain tumors. 648 35

Schwannoma-derived growth factor (SDGF) is a member of the epidermal growth factor (EGF) family, having mitogenic activity on rat astrocytes, fibroblasts and Schwann cells. The SDGF gene is significantly expressed in the newborn rat lung and in the adult rat sciatic nerve. However, except for one rat schwannoma cell line, from which SDGF and its cDNA were isolated, nothing is known about SDGF expression in established tumor cell lines. We examined the expression level of the SDGF gene in a variety of rat tumor cell lines by Northern blotting and found that it was increased in 11 of 25 established lines. The most abundant SDGF mRNA, which was about 50-fold higher than in the newborn rat lung, was expressed in rat liver adenoma dRLa74 cells. In rat glioma cell lines, such as C6, 9L and T9, and in the rat hepatoma dRLh84 and H411E cells, the SDGF expression level was about 10-fold higher than in the newborn rat lung. In 8 of 13 cell lines expressing SDGF mRNA, the EGF receptor (EGFR) gene, the product of which is regarded as a functional receptor of SDGF, was co-expressed. In addition, transfected gene-dependent anti-sense SDGF RNA expression under the control of the human metallothionein promoter significantly suppressed the in vitro growth as well as in vivo tumorigenicity of 9L glioma cells. Our results suggest that SDGF acts as an autocrine growth factor in the development and growth of rat tumors such as gliomas.
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PMID:Increased expression of schwannoma-derived growth factor (SDGF) mRNA in rat tumor cells: involvement of SDGF in the growth promotion of rat gliomas. 862 Dec 57

The present study was undertaken to explore the role of the Protein Kinase C (PKC) signal transduction system in growth regulation of pituitary adenomas. Primary tumor cultures were plated from fresh surgical tumor specimens. The PKC inhibitors Staurosporine and Tamoxifen were added at varying dosages to the cell cultures. Measurements of cell proliferation were performed by [3H]-thymidine uptake and the [3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H tetrazolium bromide] (MTT) assay. After a 48 h treatment period, both [3H]-thymidine uptake and absorbance on the MTT assay decreased in a dose-related manner in both the staurosporine and tamoxifen-treated cultures (IC50 of 10 nM and 30 microM respectively). Direct measurement of PKC activity using an in vitro assay revealed very high activity (range of 1465-5708 pmol/min/mg protein; within the range previously published for malignant glioma specimens) in 12 frozen specimens of pituitary adenomas (9 nonfunctional adenomas, 1 prolactinoma, 1 gonadotrophin-secreting and 1 corticotroph-secreting adenoma). In contrast, PKC activity measured in normal adenohypophysis was comparatively very low. These data indicate that pituitary adenoma cells display high PKC activity and are sensitive to growth inhibition by PKC inhibitors. These data suggest a role for the PKC system in regulating pituitary tumor growth, which may have implications for future therapy of these tumors.
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PMID:Protein kinase C and growth regulation of pituitary adenomas. 873 88

MRI is a sensitive tool for the investigation of pituitary microadenomas but cannot be used as a screening investigation. To establish a strategy for the use of MRI in patients with hyperprolactinaemia we investigated 74 women with serum prolactin levels above 52 ng/ml for the presence of microadenomas. We examined 55 premenopausal and 19 postmenopausal women, using a 1.5 T unit. We used T1-weighted spin-echo sequences, with coronal and sagittal images before and after intravenous gadolinium. We found microadenomas in 38 patients (51.3%), macroadenomas in 6 (8.1%) and an infundibular glioma in 1;29 patients had a normal pituitary gland (39.2%). The size of the adenomas was related to the prolactin level, and the mean level in patients with MRI evidence of adenomas was higher than in patients without microadenomas (155.72 +/- 131.01 ng/ml versus 110.14 +/- 80.86 ng/ml). The probability of the presence of an adenoma increased with rising serum prolactin levels. We suggest MRI in patients with prolactin levels more than 100 ng/ml. In patients on oestrogen therapy MRI should be performed with only slightly elevated prolactin levels. Evidence of a microadenoma should be considered in planning further therapy, especially concerning the use of hormone replacement therapy or of bromocriptine.
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PMID:MRI of microadenomas in patients with hyperprolactinaemia. 895 98


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