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 patient presented with myelopathy due to intramedullary thoracic spinal cord glioblastoma 10 months after treatment for a supratentorial glioblastoma. There was no supratentorial recurrence, and no evidence of gross leptomeningeal dissemination documented by CSF cytology, complete myelography, and MRI imaging. Gross examination of the spinal cord and arachnoid at the time of exploratory thoracic spinal surgery was normal. However, histological review of thoracic arachnoid demonstrated microscopic deposits of glial fibrillary acidic protein (GFAP) positive tumour consistent with malignant astrocytoma. Intramedullary spinal cord metastasis of cerebral glioblastoma rarely occurs, but may develop in association with leptomeningeal tumour dissemination. As local control of primary tumours improves, distant metastasis is likely to become a more common clinical problem. Leptomeningeal gliomatosis may be very difficult to document, even when clinically suspected and GFAP staining of a biopsy of arachnoid tissue can play an important role in confirming the diagnosis. This information can be critical to establish prognosis and develop an appropriate treatment strategy.
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PMID:Supratentorial glioblastoma with spinal cord intramedullary metastasis. 838 62

A 43-year-old man died from the complications of astrocytoma metastasis. He first noticed symptoms of a lumbar disc prolapse in 1979. In 1987 a pilocytic astrocytoma (grade I) of the spinal cauda was removed. In 1989 a tumor recidivation at the same site was partially removed. Histology showed a grade II astrocytoma. Two months later the patient developed symptoms of increased intracerebral pressure. CSF cytology showed polymorphic giant tumor cells with hyperchromatic nuclei and a glioblastoma of the cerebral ventricles was diagnosed. The patient died from cardiovascular complications. The post-mortem investigation revealed an astrocytoma of the conus medullaris with an anaplastic ventral area (grade IV). This area was inaccessible to the biopsy. It is believed that tumor metastases from anaplastic parts spread along the spinal cord and brainstem and finally invaded the brain and cerebral ventricles.
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PMID:Ascending central nervous spreading of a spinal astrocytoma. 859 75

A primary histopathological feature of Alzheimer's disease is the accumulation of beta-amyloid (A beta) in the brain of afflicted individuals. However, A beta is produced continuously as a soluble protein in healthy individuals where it is detected in serum and CSF, suggesting the existence of cellular clearance mechanisms that normally prevent its accumulation and aggregation. Here, we demonstrate that A beta forms stable complexes with activated alpha2-macroglobulin (alpha2M*), a physiological ligand for the low-density lipoprotein receptor-related protein (LRP) that is abundantly expressed in the CNS. These alpha2M*/125I-A beta complexes are immunoreactive with both anti-A beta and anti-alpha2M IgG and are stable under various pH conditions, sodium dodecyl sulfate, reducing agents, and boiling. We demonstrate that alpha2M*/125I-A beta complexes can be degraded by glioblastoma cells and fibroblasts via LRP, because degradation is partially inhibited by receptor-associated protein (RAP), an antagonist of ligand interactions with LRP. In contrast, the degradation of free 125I-A beta is not inhibited by RAP and thus must be mediated via an LRP-independent pathway. These results suggest that LRP can function as a clearance receptor for A beta via a physiological ligand.
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PMID:Alpha2-macroglobulin complexes with and mediates the endocytosis of beta-amyloid peptide via cell surface low-density lipoprotein receptor-related protein. 934 34

Retrospective analysis of case records of 9793 patients with brain tumors operated on at the Burdenko Neurosurgical Institute from 1985 to 1992 was done. 323 patients (3.2%) had postoperative CNS infectious complications with deaths registered in 46 cases. Cholesteatomas and choriopapillomas had the highest complication rates: 12% of all cases and 11.4%, respectively. Variable incidence was observed in the glial tumors group: from 3% in glioblastoma patients to 4.7% in oligodendroglioma patients. Concurrent infections, surgical approaches via parabasal sinuses and CSF leakage at the operation site were considered as risk factors for postoperative CNS infectious complications.
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PMID:[Craniocerebral suppurative-inflammatory complications in nervous system cancer patients in the postoperative period]. 958 45

The clinicopathological features of two cases of gliomatosis cerebri associated with secondary glioblastoma formation are reported. In both cases, glial cells were diffusely distributed in the supra- and infratentorial regions and underlying brain structures were preserved from the onset. In spite of such diffuse distribution of neoplastic glial cells, similar to that observed in low-grade astrocytoma, in both cases the tumor underwent complete remission after radiotherapy. However, the tumor recurred as a localized glioblastoma in both cases, 37 months (case 1) and 7 months (case 2) after the radiotherapy. In both cases, recurrence was accompanied by prominent dissemination of CSF. The recurrent tumors were radiation resistant, and the patients' conditions deteriorated rapidly after recurrence. The present two cases demonstrated that gliomatosis cerebri, classified among brain tumors of unknown origin by the World Health Organization, may transform into highly proliferative circumscribed tumors, in spite of their good response to radiotherapy. Examination of pathological features and their correlation with MRI findings may allow us to better understand the response to radiotherapy and the process of recurrence.
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PMID:Gliomatosis cerebri with secondary glioblastoma formation: report of two cases. 1032 49

Granulocyte colony-stimulating factor (G-CSF) and granulocyte macrophage colony-stimulating factor (GM-CSF) and/or their receptors are increasingly detected in solid human tumors, although little is known about their function in tumor growth and invasion. We analyzed RNA and protein expression of both factors and their receptors in 22 human gliomas (WHO grade II, III, and IV) and derived cell cultures. G-CSF, GM-CSF, and/or their receptors were expressed in all tumors and derived cell cultures, but coexpression of both factors and receptors was almost exclusively found in grade IV glioblastomas and thus correlated with advanced tumor stage. The functional significance of G-CSF and GM-CSF as regulators for glioma cells was demonstrated by 1) stimulation of proliferation and migration in tumor cells expressing one or both receptors by the corresponding factor; 2) inhibition of growth and migration of glioma cells expressing G-CSF, GM-CSF, and their receptors by neutralizing antibodies to both factors. These results indicate a significant role for both factors in the autocrine regulation of growth and migration in late-stage malignant gliomas and suggest a shift from paracrine to autocrine regulation with tumor progression. The implication of G-CSF and GM-CSF in glioblastoma growth regulation could make these factors further prognostic indicators and raises questions concerning their use in cancer therapy.
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PMID:Autocrine growth regulation by granulocyte colony-stimulating factor and granulocyte macrophage colony-stimulating factor in human gliomas with tumor progression. 1055 Mar 13

We investigated the ability of Fischer rat T9 glioblastoma cells transduced with cDNA genes for the secreted (s) or membrane-associated (m) isoform of M-CSF to elicit an antitumor response when implanted into syngeneic animals. Intracranial (i.c.) implantation of 1 x 10(5) T9 cells expressing mM-CSF (T9/mM-CSF) resulted in 80% tumor rejection. Electron microscopy of the T9/mM-CSF tumor site, 2-4 days postimplantation, showed marked infiltration by macrophages, many of which were in physical contact with the T9/mM-CSF cells. Animals that rejected T9/mM-CSF cells were resistant to i.c. rechallenge with T9 cells, but not syngeneic MadB106 breast adenocarcinoma cells, suggesting that T9-specific immunity can be generated within the brain via the endogenous APCs. Intracranial injection of parental T9, vector control (T9/LXSN), or T9 cells secreting M-CSF (T9/sM-CSF) was 100% fatal. Subcutaneous injection of 1 x 10(7) T9/sM-CSF, T9/LXSN, or parental T9 cells resulted in progressive tumors. In contrast, T9/mM-CSF cells injected s.c. were destroyed in 7-10 days and animals developed systemic immunity to parental T9 cells. Passive transfer of CD3+ T cells from the spleens of immune rats into naive recipients transferred T9 glioma-specific immunity. In vitro, splenocytes from T9/mM-CSF-immunized rats specifically proliferated in response to various syngeneic glioma stimulator cells. However, only marginal T cell-mediated cytotoxicity was observed by these splenocytes in a CTL assay against T9 target cells, regardless of restimulation with T9 cells. Subcutaneous immunization with viable T9/mM-CSF cells was effective in eradicating i.c. T9 tumors.
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PMID:Development of systemic immunity to glioblastoma multiforme using tumor cells genetically engineered to express the membrane-associated isoform of macrophage colony-stimulating factor. 1055 82

Glioblastoma multiforme is one of the commonest primary malignant tumours of the brain with rare incidence of extracranial metastases. Systemic dissemination via the CSF or CSF diversionary shunt procedures is also rare. The reported 9-year-old child was a case of thalamic glioblastoma with hydrocephalus who underwent biventriculoperitoneal shunting before tumour decompression and radiotherapy. The child developed incapacitating ascites 8 months following surgical decompression and 9 months after the shunt diversion which was found to be caused by CSF dissemination of the glioblastoma via the ventriculoperitoneal shunt. The child ultimately succumbed to his disease.
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PMID:Thalamic glioblastoma with cerebrospinal fluid dissemination in the peritoneal cavity. 1068 78

Cadherins are Ca2+-dependent cell adhesion molecules that play an important role in tissue construction and morphogenesis in multicellular organisms. Because in recent years there have been reports of cadherin involvement in tumor metastasis, we conducted an immunostain for E-cadherin and N-cadherin monoclonal antibodies in paraffin-embedded surgical specimens of primary and recurrent lesions in 13 cases of glioblastoma and nine cases of anaplastic astrocytoma. No expression of E-cadherin was detected in the tumor cells. On the other hand, expression of N-cadherin was observed in malignant astrocytic tumor cells, but the N-cadherin positive rate tended to be less at the time of recurrence. Decreased expression of N-cadherin was detected at the time of recurrence in 11 of the 13 cases in the glioblastoma group. Cerebrospinal fluid (CSF ) dissemination and extracranial metastasis were observed in nine (81.8%) of these 11 patients. Therefore, we tried to analyze the clinical backgrounds and the N-cadherin positive rates by statistics. We concluded that decreased expression of N-cadherin at the time of recurrence correlates with dissemination in malignant astrocytic tumors.
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PMID:Expression of cadherin and CSF dissemination in malignant astrocytic tumors. 1080 86

We present three cases of glioblastoma with CSF dissemination that contrast-enhanced fluid-attenuated inversion recovery MRI was sensitive enough to detect compared with contrast-enhanced T1-weighted MRI. An autopsy was performed on one patient, and its histologic findings proved the existence of CSF dissemination.
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PMID:Contrast-enhanced fluid-attenuated inversion recovery MRI is useful to detect the CSF dissemination of glioblastoma. 1171 10


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