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)

Extracranial metastases arising from primary brain tumors are very unusual. We report a case of glioblastoma with intra-thoracic spread characterized by mediastinal lymph nodes metastasis and bronchial, lung parenchyma and pleura carcinomatous lymphangitis. Pathologic findings are consistent with non-differentiated cell proliferation but Glial Fibrillary Acidic Protein immunodetection can be helpful to relate such a non-differentiated cell proliferation to its glial origin. The mechanisms of extra-cerebral spread are discussed according to autopsic findings and to the data reported in the literature.
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PMID:[Pulmonary metastases of glioblastoma]. 856 81

Metastasis of intracranial glioblastomas have been described for the first time more than fifty years ago. They are exceptional and seem to develop clinically in less than 2% of cases. In fact, microscopic metastasis (necropsic series) of such glioblastomas are much more frequent: from 6% for supratentorial glioblastomas to 60% in infratentorial ones; but patients usually die before clinical symptoms appear. The authors report on an intraspinal metastasis which appeared clinically four years after the removal of a frontal glioblastoma. The metastasis was subdural, T3. Preoperative radiological data (CT-scan, MRI) evoked a meningioma, while surgical findings favoured the diagnosis of neurinoma. The diagnosis of glioblastoma metastasis was suggested by intra-operative pathological findings, and confirmed a few days later on smears and stains studies.
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PMID:[Secondary intraspinal localizations of glioblastoma. Apropos of a case]. 857 58

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

Numerous established human tumor lines co-express platelet-derived growth factor (PDGF) and cognate receptors, suggesting that an autocrine and/or paracrine growth mechanism may be a causal or contributing mechanism to their transformed phenotype. Indeed, it is known that a PDGF-autocrine system is functional in several established tumor lines, especially in human gliomas, and a model for a functional paracrine mechanism has been established in a human melanoma line. However, at least 168 human cell lines representing 26 different human tumor types have been reported to continuously express PDGF-A and/or -B chains, and 55 of these also express PDGF receptors. For the majority of these cases, the significance of co-expression and the relative roles of autocrine and paracrine mechanisms in transformation remains unclear. Here, we show that human glioblastoma T98G cells co-express PDGF-B/c-sis and moderate levels of the cognate beta-type PDGF receptor (PR-beta) but are not tumorigenic in athymic mice. In contrast, human breast carcinoma MCF-7 cells do not express PR-beta and are tumorigenic. Clonal lines of each cell type with greatly increased secretion of p16w(T98Gsis and MCF-7sis cells) were characterized. T98Gsis cells are 85% tumorigenic and occasionally develop pulmonary metastases, showing that endogenous PR-beta can mediate complete transformation upon sufficient stimulation. In contrast, MCF-7sis cells exhibit some growth slowing in vitro and an exactly proportional decrease in tumor growth rate. We conclude that a PDGF-autocrine, and not a paracrine, mechanism best accounts for the acquired tumorigenicity of T98Gsis cells, thereby emphasizing the potential significance of expression of even moderate levels of PR-beta by human tumor cells.
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PMID:Growth factor PDGF-B/v-sis confers a tumorigenic phenotype to human tumor cells bearing PDGF receptors but not to cells devoid of receptors: evidence for an autocrine, but not a paracrine, mechanism. 864 31

A 50 y.o. male presented with a right parietal tumor which was a glioblastoma on stereotactic biopsy. He was treated by radiation and steroids, with clinical improvement. Four months later, he presented with a left preauricular mass and cervical lymphadenopathy. CT scan showed destruction of the left mastoid and filling of the left tympanic cavity. One month later, he suffered progressive dyspnea. Chest X ray showed a mediastinal mass on the right side and numerous bilateral interstitial opacities in the lungs. A bronchial biopsy was inconclusive. His general condition worsened, and he died. Postmortem showed continuous neoplastic infiltration of the left part of the base of skull, extending into the neck. Numerous metastases were present in mediastinal lymph nodes, lung parenchyma, pleura and pleural aspect of the diaphragm. There were no subdiaphragmatic metastases. Neuropathological examination confirmed a poorly differentiated highly malignant glioblastoma with severe necrosis involving the internal part of the parietal lobe extending to the dura mater of the convexity and falx cerebri with invasion of the superior longitudinal sinus which was entirely occluded. The biopsy scar was not infiltrated. Visceral tumors were morphologically identical to the brain tumor. They were strongly GFAP positive and cytokeratin negative. Extraneural metastases of glioblastoma in the absence of surgery are uncommon in adults. Involvement of the dura mater and/or superior longitudinal sinus is an almost constant feature. In our case, this may have led to invasion of the base of skull and secondary regional, lymphatic, and hematogenous spread.
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PMID:[Extracerebral metastases of a glioblastoma, in the absence of surgery]. 872 51

Extracranial metastasis of cerebral glioblastoma is rarely seen. Craniotomy and diversionary shunt are widely accepted causes of dissemination. Prognosis is poor but new therapeutic modalities may improve the survival and lessen the patient's symptoms. It is also important to diagnose extracranial metastasis because of possible response to treatment and fine-needle aspiration cytology can then be helpful. Two cases of extracranial metastases of glioblastoma multiforme diagnosed by fine-needle aspiration cytology are reported and a review of the literature is presented.
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PMID:Extracranial metastasis of glioblastoma multiforme diagnosed by fine-needle aspiration: a report of two cases and a review of the literature. 940 15

Increased levels of human cysteine proteases have been implicated in the progression of tumors from the premalignant to the malignant state. The physiological activities of these proteases are regulated by their interactions with specific inhibitors. To our knowledge there have been no previous reports about the cysteine protease inhibitors (CPIs) in human brain tumors. In the study reported here, we determined CPI activity during glioma progression and compared that with normal human brain tissue. We also determined CPI activities in meningioma and glioblastoma cell lines in vitro. This activity was significantly higher in normal brain tissue and low-grade glioma than in anaplastic astrocytoma and glioblastoma. CPI activity was significantly higher in benign and atypical meningioma cell extracts in comparison with those from malignant meningiomas and with those from glioblastoma cell lines. After several passages, one benign meningioma cell line showed reduced levels of CPI and increased levels of cathepsin. Our results suggest that decreases in the activities of CPI may contribute to the malignant properties of brain tumors.
Clin Exp Metastasis 1996 Sep
PMID:Expression of cysteine protease inhibitors in human gliomas and meningiomas. 887 8

Primary brain tumors lack the metastatic behavior that is in part believed to be promoted by the extracellular matrix (ECM) components of the basement membrane. This study was intended to examine the influence of the ECM components present in the basement membrane that may act as natural barriers to tumor cell invasion. We examined the effect of type I and type IV collagens, fibronectin, laminin, and hyaluronic acid on the migration and invasion of four established glioblastoma cell lines, SNB19, U251, UWR1, and UWR2. Lower concentrations of all the ECM components induced the migration and invasion of all the cell lines. However, in the case of SNB19, laminin inhibited both migration and invasion in a concentration-dependent manner. We have also examined the influence of individual ECM components on the migration of cells from a spheroid to a monolayer on ECM component-coated coverslips. Consistent with the invasion studies using the modified Boyden chamber assays, lower concentrations of ECM components induced the migration of cells from spheroids to monolayer. Again, laminin inhibited the migration of cells from SNB19 spheroids. These results indicate that ECM components induce the invasion of glioma cells, apart from components like laminin, which may act as natural inhibitors.
Clin Exp Metastasis 1996 Sep
PMID:Role of extracellular matrix proteins in regulation of human glioma cell invasion in vitro. 887 10

Over the last several decades in Europe and 15 years in North America, numerous centers have used stereotactic high-activity brachytherapy for patients with malignant brain tumors. A number of nonrandomized series have contributed information regarding the efficacy compared to historical controls for patients with de novo and recurrent malignant gliomas and metastases. Two randomized studies for patients with de novo malignant astrocytoma and glioblastoma are nearing completion. Based on the author's personal experience with 115 patients and the reported literature, we conclude that brachytherapy is appropriate for a minority of patients with malignant brain tumors, that reoperation is frequently required, and complications of therapy can be significant. However, a proportion of highly selected patients benefit significantly from this therapy.
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PMID:Stereotactic high-activity brachytherapy for malignant intra-axial brain tumors. Status report as of March, 1995. 891 48

Extraneural metastases from glioblastoma multiforme are rare. Spread to the extracranial head and neck may be evident on routine follow-up images of the original lesion. We present two cases, one with documented metastatic adenopathy in the head and neck from glioblastoma and the other with probable metastatic disease in a lymph node in which biopsy was not performed, and discuss probable mechanisms of extraneural extension of this tumor.
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PMID:Lymph node metastases from glioblastoma multiforme. 893 81


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