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

The immunohistochemical distribution of alpha and beta subunits of S-100 protein (S-100 alpha, S-100 beta, respectively) in 138 cases of human brain tumors was investigated by the avidin-biotin immunoperoxidase method. Brain tumors can be divided into four groups: group 1 [S-100 alpha (+) and/or S-100 beta (+)]; astrocytoma, glioblastoma, ependymoma, subependymoma, oligodendroglioma, choroid plexus papilloma, gangliocytoma, meningioma, chordoma, malignant melanoma. Group 2 [S-100 alpha (+) and S-100 beta (-)]; pineoblastoma, pituitary adenoma, craniopharyngioma, rhabdomyosarcoma. Group 3 [S-100 alpha (-) and S-100 beta (+)]; acoustic Schwannoma. Group 4 [S-100 alpha (-) and S-100 beta (-)]; medulloblastoma malignant lymphoma, germinoma. The S-100 beta immunoreactivity pattern in brain tumors was similar to those obtained using conventional anti-S-100 protein sera. In the first group of brain tumors both the number of positively stained tumor cells and the staining intensity were generally greater for S-100 beta than for S-100 alpha with a few exceptions including one gemistocytic astrocytoma, one subependymoma, one malignant melanoma, and some cases of glioblastomas. As to the relationship between malignancy and S-100 protein in glioma, S-100 beta immunoreactivity decreased according to degree of malignancy, while that of S-100 alpha varied, suggesting a heterogeneity of tumor cells in glioblastomas. Immunostaining for S-100 alpha and S-100 beta might become a useful diagnostic procedure in brain tumors and may give us more detailed and precise data of S-100 protein in brain tumors.
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PMID:Immunohistochemical study on the distribution of alpha and beta subunits of S-100 protein in brain tumors. 188 40

Diffuse astrocytomas of the cerebrum, cerebellum, brain stem, and spinal cord are classified into three groups according to the degree of tumor anaplasia. These groups are the astrocytoma, anaplastic astrocytoma, and glioblastoma multiforme. Juvenile pilocytic astrocytomas have a better prognosis and are clinically and biologically distinct from the diffuse, fibrillary astrocytomas. The prognosis of astrocytomas depends not only on histologic characteristics, but also age of the patient, location of the tumor, and extent of surgical resection. The pattern of invasion into surrounding brain distinguishes gliomas from metastatic carcinomas and sarcomas. Topographic correlations have shown that malignant gliomas may invade the brain for distances of up to several centimeters from the enhancing rim seen on CT scan. However, the junction between glioblastoma and adjacent brain may also be fairly abrupt, with a peripheral margin of less than 1 mm. Recurrent glioblastomas are more widely invasive and often extend into areas that appear normal on CT scan. The optimal site for tumor biopsy corresponds to areas of contrast enhancement. Primitive neuroepithelial tumors are malignant neoplasms with a poor prognosis. They tend to recur locally and metastasize throughout the neuraxis via the CSF. It remains controversial whether these tumors should be classified as a single entity with the potential for differentiation along different cell lines, or whether the categories of neuroblastoma, spongioblastoma, ependymoblastoma, pineoblastoma, and medulloblastoma should be retained as specific entities. The medulloblastoma is the most common of these neoplasms, its clinicopathologic features are well characterized, and the current 5-year survivals of 50 to 60 per cent are better than for other "primitive" neoplasms. Glial fibrillary acidic protein is a specific marker for immature, reactive, and neoplastic astrocytes and ependymal cells. Although the absence of GFAP in a neoplasm does not exclude an astrocytic origin, the presence of GFAP indicates astrocytic or ependymal differentiation. This has important diagnostic applications. The expression of GFAP is used to distinguish astrocytic neoplasms from epithelial or mesenchymal tumors that may on occasion mimic a glioma. The detection of GFAP is also useful in the investigation of tumor histogenesis and differentiation both in vivo and in vitro. Although meningiomas exhibit a wide variety of histologic patterns, most tumors exhibit similar biologic and clinical behavior regardless of the histologic subtype.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pathologic analysis of primary brain tumors. 300 88

A monoclonal antibody termed "FR77" was obtained from a hybridoma clone established by fusion between P3x63Ag8.653 mouse myeloma cells and spleen cells of a Fischer F344 rat hyperimmune to syngeneic 9L/R3 glioma cells. Immunoperoxidase staining of various cultured cells showed that FR77 was reactive to both rat and human glioma cells, but was not reactive with other nonglioma cells. Immunohistochemical examination of paraffin-embedded or cryostat-frozen sections of various human tissues revealed that FR77 was strongly reactive with glioblastoma, grade III astrocytoma, and craniopharyngioma; partially reactive with intracerebral primitive neuroectodermal tumor, pineoblastoma, and desmoplastic medulloblastoma; and weakly reactive with low-grade astrocytoma. It was not reactive with other types of brain tumors and normal human tissues tested. The FR77-defined antigen was observed to be predominantly localized in the cytoplasm of antigen-bearing cells as suggested by the immunostaining pattern, but part of it was also expressed on the cell surface of glioma cells as demonstrated by a complement-mediated cytotoxic test. Fractionation of the antigenic component and periodic acid treatment of tumor tissue bearing the FR77-defined antigen indicated that the antigen is of a neutral glycolipid nature and that the antigenic determinant to FR77 is present on its sugar portion.
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PMID:Detection of human glioma-associated antigen by rat monoclonal antibody raised against syngeneic rat glioma cells. 376 Sep 59

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

The distribution of type VII collagen was examined in the normal human nervous system, in brain tumour biopsies and in glioma cell lines by immunohistochemistry and western blotting. In normal tissue, positivity was observed beneath choroid plexus epithelial cells and around pineal gland and pituitary gland cell nests, while other brain regions and peripheral nerves were negative. Expression was preserved in most related tumours (choroid plexus papilloma, pineoblastoma, pituitary adenoma). Scattered abnormal vessels showed neo-expression of type VII collagen in about half of the astrocytic and ependymal tumours. Glioma cells in situ were consistently negative for type VII collagen, whereas the glioblastoma cell lines were positive. Our results suggest that anchoring fibrils or at least epitopes of their major structural component are present in normal and pathological cerebral structures, indicating a unique distribution of type VII collagen in the nervous system.
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PMID:Expression of type VII collagen, the major anchoring fibril component, in normal and neoplastic human nervous system. 775 91

Cadherins are a family of glycoproteins that are associated with cell adhesion mechanisms. They are divided into subclasses. The E- and P-cadherins are regarded as the epithelial subtype. Their expression has been demonstrated in many different carcinoma types. Using immunomorphological techniques, we studied the expression of E-cadherin in a series of 145 human brain tumours with the monoclonal antibody 5H9. Western blot analysis was used to confirm the immunohistochemical data. The tumour types represented were astrocytoma WHO I (n = 7), astrocytoma WHO II (n = 6), astrocytoma WHO III (n = 14), glioblastoma WHO IV (n = 8), oligodendroglioma WHO II (n = 5), ependymoma WHO II (n = 5), choroid plexus papilloma WHO I (n = 5), pineoblastoma WHO IV (n = 5), medulloblastoma WHO IV (n = 5), neurinoma WHO I (n = 5), meningioma WHO I and WHO III (n = 75) and pituitary adenoma WHO I (n = 5). Only choroid plexus papillomas (5/5) and meningiomas showed E-cadherin expression. In benign meningiomas (n = 45; 100%), positive E-cadherin immunoreactivity was found regardless of the histomorphological subtype. E-Cadherin was also expressed in 21 WHO I meningiomas (100%) invading dura, bone, brain, and muscle. In contrast, E-cadherin was absent from the majority of morphologically malignant meningiomas (6/9, 66.6%). In addition, in recurrent meningiomas (n = 9), E-cadherin expression in the recurrent tumours was identical to that in the primary neoplasm except in cases with malignant progression, where the malignant recurrent tumour was E-cadherin negative. In 2 cases of metastasizing meningiomas, no E-cadherin immunoreactivity was found in the primary tumours or their metastases.
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PMID:E-Cadherin in human brain tumours: loss of immunoreactivity in malignant meningiomas. 950 62

The authors retrospectively reviewed 48 patients treated at Seoul National University Hospital (SNUH) between 1986 and 1995. There were 35 children and 13 adults, accounting for 10.1% of 345 pediatric and 0.68% of 1914 adult brain tumors in SNUH during the same period. The 48 cases consisted of 33 cases of germ cell tumor (69%, GCT); 6 of pineoblastoma (PB, 12.5%); 3 of pineocytoma (PC, 6.3%); 3 of anaplastic astrocytoma (6.3%); 1 of astrocytoma; 1 of glioblastoma; and 1 of ependymoma. The median age was 13 years (range 1-59) and the male-to-female ratio was 3.36:1. The most frequent presenting symptom was due to increased intracranial pressure (90%), followed by Parinaud syndrome or diplopia (50%). Patients with a benign tumor, such as teratoma (TE), astrocytoma, or ependymoma, underwent surgery by the occipital transtentorial approach (OTT) for attempted radical resection without adjuvant therapy, while patients with immature teratoma (imTE), PC, and anaplastic astrocytoma underwent regional radiotherapy (RT) after debulking via OTT. Seven patients with nongerminomatous malignant GCT (NG-MGCT) and 3 with germinoma (GE) underwent craniospinal radiation only, 6 with GE, a NG-MGCT, and 2 with GE+TE received craniospinal radiotherapy (CSRT) after debulking via OTT. Three patients with GE, 4 with NG-MGCT, and 3 with PB underwent radiochemotherapy after debulking via OTT. Forty-four patients were followed up after treatment. The median follow-up period was 36 months. All patients with GE were alive after RT at 36 months (median) of follow-up (range 7-70 months). All with GE+TE and TE were alive. Three patients with PC or astrocytoma were also alive with stable or no evidence of disease. In 1 of the 3 cases of imTE there was a recurrence. However, 4 patients with NG-MGCT died, all of whom had undergone CSRT only; 2 PB patients were alive (12, 19 months), 1 in a moribund status (36 months), and 2 were dead (6, 60 months). The overall mean survival time with pineal tumors was 66 months and the 3-year survival rate was 84% with minimal posttreatment complications. It is concluded that pineal region tumors have male and childhood predominances, and the most common tumor is GCT. The majority of pineal region tumors are malignant. Pineal region tumors can be approached safely and effectively and the surgical complications are mostly transient. Their prognosis is dependent on the pathologies and treatment modalities.
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PMID:Pineal tumors: experience with 48 cases over 10 years. 954 42

Ten children (6 girls and 4 boys) who completed a protocol in which their localized brain tumors were successfully treated without cranial irradiation were referred for neuropsychological assessment. At the time of testing, they were disease free without any neuroaxis dissemination or leptomeningeal disease. Tumor types included pineoblastoma, glioblastoma, ependymoma, PNET and medulloblastoma. They had a mean age of 5 years and 8 months (SD = 1.86; range = 2.1-8.9 years) and were an average of 37.8 months post bone marrow transplant (SD = 16.42; range = 14-58 months). Neuropsychological data from this study reveal that the mean scores for this nonradiated group of children were within the average range for the following domains: academic achievement tests of reading, spelling and mathematics, verbal and visual memory, visual-motor integration, social-emotional and behavioral functioning. Furthermore, this group of children were performing within the low average range of overall Intelligence, as well as both verbal IQ/verbal reasoning and performance IQ/abstract visual reasoning. On tasks of fine motor dexterity, this group was within the low average range when using their dominant hand; however, they performed within the borderline range when using their non-dominant hand. Of note, this group of children demonstrated significant deficits within the borderline to impaired ranges on language tasks of expressive picture naming and receptive picture vocabulary.
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PMID:Pilot neuropsychological findings from a treatment regimen consisting of intensive chemotherapy and bone marrow rescue for young children with newly diagnosed malignant brain tumors. 984 Mar 84

A Phase I trial of irinotecan was performed to determine the maximum tolerated dose (MTD), the dose-limiting toxicities (DLTs), and the incidence and severity of other toxicities in children with refractory solid tumors. Thirty-five children received 146 courses of irinotecan administered as a 60-min i.v. infusion, daily for 5 days, every 21 days, after premedication with dexamethasone and ondansetron. Doses ranged from 30 mg/m2 to 65 mg/m2. An MTD was defined in heavily pretreated and less-heavily pretreated (i.e., two prior chemotherapy regimens, no prior bone marrow transplantation, and no radiation to the spine, skull, ribs, or pelvic bones) patients. Myelosuppression was the primary DLT in heavily pretreated patients, and diarrhea was the DLT in less-heavily pretreated patients. The MTD in the heavily pretreated patient group was 39 mg/m2, and the MTD in the less-heavily pretreated patients was 50 mg/m2. Non-dose-limiting diarrhea that was well controlled and of brief duration was observed in approximately 75% of patients. A partial response was observed in one patient with neuroblastoma, and in one patient with hepatocellular carcinoma. Stable disease (4-20 cycles) was observed in seven patients with a variety of malignancies including neuroblastoma, pineoblastoma, glioblastoma, brainstem glioma, osteosarcoma, hepatoblastoma, and a central nervous system rhabdoid tumor. In conclusion, the recommended Phase II dose of irinotecan administered as a 60-min i.v. infusion daily for 5 days, every 21 days, is 39 mg/m2 in heavily treated and 50 mg/m2 in less-heavily treated children with solid tumors.
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PMID:A phase I study of irinotecan in pediatric patients: a pediatric oncology group study. 1120 14

Primitive neuroectodermal tumors (PNET) occur either in the central nervous system (CNS; central PNET, cPNET) or in the peripheral sites (peripheral PNET, pPNET). Recent molecular approaches have been defining a new concept of PNET, that is, the pPNET including Ewing's sarcoma (ES) which expresses MIC2 glycoprotein and shows the specific chimeric gene of EWS-FLI1. The expression of MIC2 and the genetic rearrangement of EWS-FLI1 are considered to be highly specific to the pPNET/ES. This study examined the expression of MIC2 and EWS-FLI1 gene by means of immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) on various small round cell tumors originating in the CNS or non-CNS organs. All peripheral PNET tested expressed MIC2 and were positive for EWS-FLI1 (11/11). In contrast, all cPNET and other blastic CNS tumors were negative for MIC2: medulloblastoma (0/3), cerebral PNET (0/2), spinal PNET (0/2), glioblastoma (0/2), retinoblastoma (0/3), and pineoblastoma (0/2). These MIC2-negative tumors were also negative for the chimeric gene product of EWS-FLI1. Interestingly, one PNET originating in the intracranial dura mater was positive for both MIC2 and EWS-FLI1 fusion gene. The results indicate that cPNET lacks any genetic or protein markers, except for a meningeal PNET which falls into the same phenotypic spectrum of pPNET.
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PMID:Alternative EWS-FLI1 fusion gene and MIC2 expression in peripheral and central primitive neuroectodermal tumors. 1130 41


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