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)

Transplanted lines of seven F-344 (Fischer) rat malignant gliomas induced transplacentally with ethylnitrosourea (ENU) were surveyed by in vivo immunoprotection assays for the presence of tumour rejection antigens. These gliomas were representative of commonplace histological types of human primary brain tumours and were analyzed in early transplantation passages. The classical tumour ligation method of immunizing animals was attempted with five glioma lines, but was found unusable in four of these because of a high incidence of local tumour recurrences and distant metastases. In most experiments the animals were immunized by repeated inoculations of heavily-irradiated tumour cells. Two gliomas, a glioblastoma multiforms and a mixed astrocytoma-ependymoma, demonstrated weak but statistically significant tumour rejection responses. Immunization with three other tumours, a mixed oligodendroglioma-astrocytoma and two glioblastomas multiforme, led to enhanced outgrowth of the challenge cell inocula. Neither a rejection nor an enhancement response was observed in assays of the remaining two neoplasms, a glioblastoma multiforme and a mixed astrocytoma-oligodendroglioma. Immunization with a 3-methylcholanthrene-induced urinary bladder carcinoma line, used as a control in assays of six gliomas, had no effect on the outgrowth of transplanted glioma cells. These results suggest that ENU-induced malignant rat gliomas do not uniformly elicit strong tumour-rejection responses in vivo.
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PMID:A survey of ethylnitrosourea-induced rat gliomas for the presence of tumour rejection antigens expressed in vivo. 723 38

Among the 54946 post-mortem examinations carried out by the Pathological Institute of the Medical Academy of Erfurt in the years 1953 to 1976 with a total of 1491 DNS-tumours (2.7%), the temporal lobe was involved in the following 10 types of tumours: glioblastoma, ependymoma, oligodendroglioma, plexus papilloma, tumour-like gliosis, sarcoma, angioma and angioblastoma, epidermoid tumour, teratoma. Only tumours that had formed in the cerebral tissue proper were evaluated, so that meningiomas and other tumours of the meninges or tumours of the meninges in the middle cranial fossa were left out of consideration. In a total of 949 cases of the above mentioned 10 tumours types, the temporal lobe was involved in 327 (34.5%) cases; these were mainly astrocytomas and glioblastomas (86.5%). Only 63 of the 327 tumours (19.3%) were exclusively located in the temporal lobe. The age peak of the occurrence of temporal lobe tumours was in the 6th decennium. The male showed with 55.4 per cent a slightly greater incidence. CLinically, the left-sided temporal lobe tumours with 79 per cent of the observations were found more frequently than the right-sided ones (67%). Accordingly, left-sided tumours were operated on more frequently (49%) than tumours on the right-hand side (40%).
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PMID:[Localization of brain tumors in autopsy. Part I: Tumors of the temporal lobe]. 734 Mar 11

Granulocyte-colony-stimulating factor (G-CSF) is a hematopoietic cytokine that regulates the differentiation of myeloid progenitors and the function of mature neutrophils. It is produced in vitro by monocytes/macrophages, mesothelial cells, fibroblasts and endothelial cells after appropriate induction by inflammatory mediators like IL-1 and TNF. Normal as well as tumorous glial cells can also be induced to produce CSFs in vitro. However, little is yet known about the in vivo expression of G-CSF as a mediator in inflammation and malignancy within the human central nervous system. The aim of the present study was to investigate by immunostaining the expression of the G-CSF protein within non-tumorous and tumorous glial tissues, and primitive neuroectodermal tumors. Using the murine monoclonal anti-G-CSF TM 82/60 antibody, we found high G-CSF expression in astrocytoma WHO grades I and II and reactive brain tissue, low expression in astrocytoma WHO grade III, and none in glioblastoma, oligodendroglioma WHO grades II and III, and medulloblastoma. In consecutive sections of the tissue samples, G-CSF protein was localized in GFAP-positive glial cells, but not in macrophages/microglial cells, which expressed HLA-DR, detected by the antibody CR3/43. Computer-assisted microdensitometric evaluation of the intensity of immunostaining for G-CSF and statistic analysis of the data revealed significant differences between the diagnostic entities studied (p < 0.0001). We conclude that in vivo expression of G-CSF is a characteristic of reactive as well as tumorous astrocytes, with the latter losing this feature at higher degrees of dedifferentiation.
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PMID:Immunolocalization of granulocyte-colony-stimulating factor in human glial and primitive neuroectodermal tumors. 751 14

The Turcot syndrome (TS) is a rare, probably autosomal recessive, disorder characterized by development of primary neuroepithelial tumors of the central nervous system (CNS) and numerous adenomatous colorectal polyps. To examine the possible involvement of mutations of the APC gene, which is responsible for familial adenomatous polyposis (FAP), in Turcot syndrome, we examined DNAs from TS patients for alterations in this gene by means of ribonuclease protection analysis. Germ-line APC mutations were detected in each of three unrelated cases of TS, and additional (somatic) mutations were observed in colonic adenomas that had developed in one of these patients. However, no somatic mutations in APC were found among 91 neuroepithelial tumors (medulloblastoma, glioblastoma, astrocytoma, and oligodendroglioma), whether sporadic or associated with TS. These results suggest that the APC gene is associated with pathogenesis of one feature of TS, but that at least one other gene is responsible for the genesis of neuroepithelial tumors in the CNS.
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PMID:Germ-line and somatic mutations of the APC gene in patients with Turcot syndrome and analysis of APC mutations in brain tumors. 751 58

Non-glial intermediate filament (IMF) proteins, as well as glial fibrillary acidic protein (GFAP) and vimentin, were studied by immunohistochemistry in 24 gliomas including low grade astrocytoma, pleomorphic xanthoastrocytoma, anaplastic astrocytoma, glioblastoma, oligodendroglioma, ependymoma and ependymoblastoma, which were fixed in ethanol and embedded in paraffin. Cytoskeletal elements isolated from two glioblastomas were examined with immunoblot analysis. All tumors had GFAP-positive neoplastic cells and vimentin was also found in all the tumors except one oligodendroglioma. Twenty-three gliomas were immunostained with anti-desmin polyclonal antibody (DM-P), but anti-desmin monoclonal antibody reacted to only one glioblastoma. DM-P might crossreact with GFAP and vimentin. Cytokeratin expression was investigated with six antibodies. Twenty gliomas (83%) were positive for the antibody against epidermal keratin (CK-SE), however positive immunoreactivity varied from 58 to 8% with other cytokeratin antibodies. With the Western blot method, CK-SE had protein bands at 53 and 60-66 kDa. Neurofilament was expressed in one pleomorphic xanthoastrocytoma, one anaplastic astrocytoma, one glioblastoma and one ependymoblastoma. Expression of nonglial IMF proteins were observed in 21 tumors (88%), and coexpression of 4 or 5 classes of IMF proteins in 3 tumors (13%). We conclude that, in addition to GFAP and vimentin, gliomas express several types of non-glial IMF proteins.
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PMID:Expression of non-glial intermediate filament proteins in gliomas. 751 71

In 1955, Collins made the observation that tumor recurrence in children with Wilms' tumor was correlated with the child's age plus 9 months. This concept of a period of risk for recurrence was later applied to a variety of tumors in children and became known as Collins' Law (CL). The law has been a successful predictor of survival for some children with neural tumors within the central nervous system and a poor predictor for others. We tested Collins' concept of a period of risk for recurrence and extended it to survival for 14 childhood neural tumors described in the Childhood Brain Tumor Consortium (CBTC) database. The CBTC data describe clinical, surgical, and histological details (over a 49-year period in 10 institutions) from 3921 patients under the age of 21 years at the time of their first surgical procedure for a brain tumor. CL was considered to be a good predictor of survival if fewer than 10% of patients who die survive beyond the expiration of the period of risk for that child. We found that CL applied to tumors such as anaplastic astrocytoma, glioblastoma, pineoblastoma, medulloblastoma or "primitive neuroectodermal tumor," teratoma, and germinoma, as well as ependymoma, papilloma, and tumors that could not be classified; it had no predictive value in craniopharyngioma, oligodendroglioma, or plain, fibrillary, pilocytic, or protoplasmic astrocytoma. We had sufficient follow-up data to determine adherence to CL when the child's age at diagnosis was less than 8 years; it is likely that CL applies to older children with these tumors, but we did not have the data to show this unequivocally.
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PMID:The applicability of Collins' Law to childhood brain tumors and its usefulness as a predictor of survival. 764 86

Clinical presentation, diagnosis, surgical technique and results of 25 cases of intramedullary tumours in patients under 16 years of age are analyzed. Pre-operative spinal deformity was present in 9 patients. Surgery was performed in all. After multilaminectomy with preservation of the intervertebral joints, total removal of the lesion was achieved in 11 patients and subtotal removal in 14 others. After surgery, external immobilization lasting an average period of 5 years was instituted in all patients. Postoperative radiation therapy was performed in 11 cases (5 "high grade" astrocytomas, 5 ependymomas, 1 glioblastoma). There were 11 recurrences: 4 of which (2 ependymomas and 2 "low grade" astrocytomas) were treated surgically, 7 (5 "high grade" astrocytomas, 1 glioblastoma, 1 oligodendroglioma) with palliative radiation treatment. Six patients eventually developed postlaminectomy spinal deformities as diagnosed roentgenographically 6 to 50 months postoperatively. Of the 16 patients still alive, 7 did not present relevant neurological deficit, 1 presented a monoparesis, while the other 8 presented invalidating deficits. Surgical treatment did not differ from that employed in the intramedullary tumours in the adult: radical resection is indeed the optimal therapeutic origin. The risk of radiation therapy are greater in children: it is crucial to limit radiation therapy to only some histotypes. The incidence of spinal column deformity after multilevel laminectomy is greater in young patients. It is advisable to implement prevention of spinal deformities by postoperative external immobilization and constant follow-up so as to detect early changes of spinal stability.
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PMID:Management of intramedullary tumours in children. 767 40

A series of 43 human gliomas, consisting of 30 glioblastomas, 7 anaplastic astrocytomas, 3 low grade astrocytomas, 2 ependymomas, and 1 oligodendroglioma, was studied for amplification of the epidermal growth factor receptor (EGFR) and mouse double minute 2 (MDM2) genes. DNA extracted from formalin-fixed, paraffin-embedded tissue sections was analyzed by differential PCR and the results were compared with slot blot examination of DNA extracted from frozen tissue from the same neoplasms. Twelve glioblastomas (40%) showed amplification of the EGFR gene, and overexpression of EGFR was evident in each of these tumors as indicated by the immunoperoxidase technique. Two of the tumors with EGFR gene amplification also revealed amplification of the MDM2 gene, while one additional glioblastoma revealed MDM2 amplification only. A 100% concordance in the detection of amplification was observed between differential PCR and slot blot analysis; consequently, these results indicate that differential PCR using DNA extracted from archival tissue sections is a reliable method of demonstrating gene amplifications in glial tumors.
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PMID:Reliability of differential PCR for the detection of EGFR and MDM2 gene amplification in DNA extracted from FFPE glioma tissue. 781 80

The history of brain tumor cultures is old. Established cell lines of brain tumors have increased in recent years, but reports concerning the results of these cultures are few. The results of cultures of gliomas (103 cases of astrocytoma, 9 of ependymoma, 2 of oligodendroglioma and others) obtained from 117 patients treated at our department between 1979 and 1993 were evaluated. The morphological characteristic of these glioma cells were studied, and their cellular kinetics were investigated by flow cytometry. Except for 5 cases, all tumors grew on the flask in the primary cultures, indicating that gliomas were readily cultured. Differences in morphological characteristics and cellular kinetics were not observed in cultures which had been maintained for more than 6 months in astrocytomas of grades II, III, and IV. Cells lines were successively established in 3 cases of glioblastoma and 2 of ependymoma. The results of FCM revealed that those cells which grew well on cultures had high proliferative indices.
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PMID:Long-term passage results of glioma cells and their cell kinetics. 787

To determine whether human brains contain deiodinating pathways, we studied the activity of T4 5-monodeiodinase (5-D) in 20 human brain tumors obtained intraoperatively, including astrocytoma (10), meningioma (4), oligodendroglioma (2), glioblastoma (2), medulloblastoma (1), and malignant lymphoma (1). Mitochondrial-microsomal fractions prepared from these tumor tissues were used as the source of T4 5-D. Each sample was incubated with 32.2 nmol/L T4 and 30 mmol/L dithiothreitol at 37 C for 90 min. T4 5-D activity was measured by the production of rT3 from T4 with a RIA. T4 5-D activity was found in 6 of 10 astrocytomas, 2 oligodendrogliomas, 1 of 2 glioblastomas, and 1 malignant lymphoma. This activity depended on protein concentration, incubation time, incubation temperature, and pH of the incubation mixture. It was also heat labile. T4 5-D was not inhibited by 1 mmol/L propylthiouracil, but was inhibited by iopanoic acid and aurothioglucose in a dose-dependent manner. The apparent Km and maximum velocity for T4 5-D at 30 mmol/L dithiothreitol were 106.6 nmol/L and 22.7 pmol/mg protein.h, respectively. These data suggest that human gliomas (and probably malignant lymphomas) contain T4 5-D activity, which is similar to type III enzyme activity in the rat. T4 5-D may regulate the intracellular concentration of thyroid hormone in gliomas.
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PMID:Thyroxine 5-deiodinase in human brain tumors. 807 12


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