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 55 year old female with a history of three different malignancies including a cerebral glioblastoma developed two bone metastases (in the spine and iliac crest). Histologic and immunohistochemical studies of biopsy specimens demonstrated the presence of glial fibrillary acidic protein, establishing that the bone tumors were metastases from the glioblastoma. Specific features of these rare metastases are discussed.
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PMID:[Osteo-medullary metastases from cerebral glioblastoma]. 805 31

This report describes a case of a cerebral glioblastoma with multiple metastases appeared two years after craniotomy and revealed by a diffuse vertebral involvement with a lumbo-sciatic pain. The experimental and clinical data from the literature about distant localizations of glioblastoma give the arguments for the rarity and the pathogenic modes of the natural course. The distant localizations of cerebral glioblastoma, identified by immunohistochemical staining for glial fibrillary acidic protein, occurred in young patients, late in the follow-up which the duration is longer than those of classical glioblastomas; their occurrence hasten the disease course. Two distinct oncological entities might be identified: metastases, using blood or lymphatic pathways, commonly from a supra-tentorial primary tumor, are facilitated by surgical treatment; their exclusive extraneural sites are usually symptomatic; grafts, by seeding via cerebrospinal fluid pathways, are spontaneous or facilitated by tumoral removal and are disseminated along the neuraxis; they occur frequently and are usually asymptomatic; when shunts induce them, it gives rise to symptomatic peritoneal seeding; they seem to concern poor invading primary glioblastomas. The extraneural (metastasis) or neuraxial (graft) sites and the ways of occurrence (spontaneous, or facilitated by craniotomy or induced by surgical shunts) allow to classify the distant localizations of glioblastoma in six pathogenic types.
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PMID:[Secondary localizations of cerebral glioblastoma. Pathogenic and anatomoclinical focus apropos of a case of multiple bone metastases disclosed by vertebral involvement]. 806 90

Nervous system-specific transcription factors that bind to the octameric deoxyribonucleic acid sequence motif ATGCAAAT (or ATTTGCAT) are known as N-Oct proteins. Neurons and glia contain the ubiquitous Oct-1 protein and four polypeptide complexes termed N-Oct-2, N-Oct-3, N-Oct-4, and N-Oct-5. Previously, we showed that N-Oct proteins are differentially expressed by human neuroblastoma and glioblastoma cell lines in vitro. We have now extended this work to freshly isolated human primary and metastatic brain tumors. Contrary to brain tumor cell lines, of the five astrocytomas and three glioblastomas analyzed, all but two tumors displayed the complete N-Oct protein profile, irrespective of histopathological tumor grade. Two astrocytomas were negative for N-Oct-4. Ten of 13 ependymomas exhibited N-Oct-2, N-Oct-3, and N-Oct-4 but lacked the N-Oct-5 complex. In contrast, brain metastases of two patients with extracerebral carcinomas contained only Oct-1, and cerebral metastases from two cases of B cell lymphomas showed Oct-1 and Oct-2 complexes, the characteristic Oct protein pattern of B lymphocytes. Thus, metastatic carcinoma and lymphoma expressed a non-nervous system phenotype of Oct proteins.
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PMID:Primary brain tumors differ in their expression of octamer deoxyribonucleic acid-binding transcription factors from long-term cultured glioma cell lines. 812 49

More than 80% of malignant gliomas have been reported to recur locally after conventional chemoradiation therapy. This regional pattern of recurrence has encouraged the introduction of new treatments for local tumors. Since 1987 interstitial brachytherapy using Iridium-192 seeds has been carried out in our department for malignant brain tumors. The present study was designed to evaluate the patterns of recurrence following interstitial brachytherapy and to assess how this recurrence differs from that observed in patients treated by conventional means. Ten patients who satisfied the following criteria were selected among 41 patients treated with brachytherapy. The criteria were; 1) histologically diagnosed to be malignant glioma (astrocytoma grade III or glioblastoma), 2) followed up with MRI every month after the brachytherapy, 3) follow-up period was more than 6 months, and 4) the time of recurrence was confirmed. The patients were classified into 3 groups according to the patterns of tumor recurrence as follows; 1. Local recurrence group: The tumor recurred near the pretreatment tumor site. 2. Necrotomy group: Reoperation was performed because of neurological deterioration and radiographic evidence of increasing mass effect with surrounding edema. Neurological symptoms were unchanged or improving during the 6 months after the reoperation. 3. CSF seeding group: Primary tumor was well controlled, but seeding via cerebrospinal fluid was recognized on MRI. Local recurrence occurred in three patients, necrotomy was carried out in three patients, and CSF metastases were defined by both MRI and clinical symptoms in four patients. Median radiation does was 33 Gy in the local recurrence group, 57.6 Gy in the necrotomy group, and 43.2Gy in the CSF seeding group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Patterns of recurrence in malignant gliomas after brachytherapy]. 816 95

EGFR is a member of the tyrosine kinase family of cell surface receptors with a wide range of expression throughout development and in a variety of different cell types. The receptor can transmit signals to cells: i) upon interaction with ligands such as EGF, TGF alpha, amphiregulin or heparin binding EGF, ii) upon truncation or mutation of extracellular and/or intracellular domains, iii) upon amplification of a basal receptor activity (in the absence of ligand) through cooperation with other cellular signaling pathways or nuclear events (e.g. expression of v-erbA). The activated EGFR can exert pleiotropic functions on cells, depending on their tissue origin and state of differentiation. Under certain conditions it can also contribute to neoplasia and development of metastases. Such conditions can exist upon aberrant receptor/ligand expression and activation (e.g. in the wrong cell; at the wrong time; in the wrong amounts). Aberrant signalling can also occur through constitutive EGFR activation. Oncogenic potential of EGFR has been demonstrated in a wide range of experimental animals. EGFR is also implicated in human cancer, where it may contribute both to the initiation (glioblastoma) and progression (epithelial tumors) of the disease. EGFR may influence key steps in the processes of tumor invasion and dissemination. Involvement of EGFR in tumor spread may indicate a potential use of this receptor as a target for antimetastatic therapy.
Cancer Metastasis Rev 1993 Sep
PMID:EGF receptor in neoplasia and metastasis. 828 12

3 1/2 years after two operations and radiation therapy of a biparietally, parasagittaly localised grade III oligoastrocytoma, a 34-year-old patient developed symptoms of the spinal cord. By performing magnetic resonance tomography and laminectomy, multiple metastases of the anaplastic part of the primary tumour could be identified. Spinal seedings of a tumour of this grading are even rarer than those sporadically reported on corresponding complications of a multiform glioblastoma. Risk factors for the development of such a complication are youth of the patient, primary site of the tumour near the midline and anaplastic parts of the tumour in adults. If such a constellation exists, one should definitely consider the possibility of a spinal seeding in a grade III glioma, especially because in these younger patients thus would be of greater relevance for therapy than in patients with multiform glioblastoma.
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PMID:[Spinal seeding metastasis of a WHO grade III oligo-astrocytoma]. 830 97

Primary intracranial tumours develop in 420 adult Norwegians each year. Of these tumours, gliomas are the most frequent, followed by meningiomas, pituitary adenomas and acoustic neurinomas. Glioblastomas represent more than 50% of the gliomas. Less than 10% of the patients with glioblastoma survive for two years, despite aggressive therapy (surgery, radiotherapy and chemotherapy). The prognosis for low grade gliomas is much better. In the case of meningiomas, 95% of the tumours are benign. The primary treatment for meningiomas is surgery. If surgery is impossible, radiosurgery should be considered. Pituitary adenomas are often hormone-secreting (e.g. prolactin, growth hormone, adrenocorticotrophic hormone). Many prolactinomas are treated with bromocriptine alone. The rest of the pituitary adenomas are treated by microsurgery and radiotherapy. The prognosis for patients with pituitary adenomas is good. Acoustic neurinomas, which in most cases are benign, are treated by microsurgery or radiosurgery. Postoperative morbidity due to cochlear nerve and facial nerve dysfunction is a problem. Brain metastases are far more frequent than primary intracranial tumours. Solitary metastases in patients with stable systemic disease should be treated by surgery or radiosurgery.
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PMID:[Intracranial tumors in adults (over 15 years)]. 833 22

Matrix metalloproteinases play an important regulatory role in tissue morphogenesis, cell differentiation and motility, and tumor cell invasiveness. We have recently demonstrated elevated activity of the 92 kDa type IV collagenase (MMP-9) in human glioblastoma and in the present study examine the relative amounts of MMP-9 protein and mRNA in human gliomas and as well as the distribution of MMP-9 in human glioma tumors in vivo. Using an enzyme-linked immunosorbent assay for the quantitative determination of MMP-9 protein, we found that levels were significantly higher in malignant astrocytomas, especially in glioblastoma multiforme, than in normal brain tissues and low-grade gliomas. In addition, the amount of MMP-9 mRNA, as determined by northern blot analysis was higher in anaplastic astrocytomas and glioblastoma multiforme than in normal brain tissue and low-grade gliomas. Immunocytochemical staining for MMP-9 showed strong cytoplasmic immunoreactivity in the tumor cells and the proliferating endothelial cells of glioblastoma multiforme and anaplastic astrocytomas. The staining intensity was lowe in low-grade astrocytomas, and was undetectable or very low in normal brain astrocytes. The results indicate that expression of MMP-9 is dramatically upregulated in highly malignant gliomas and correlates with the highly malignant progression of human gliomas in vivo, and support a role for the MMP-9 in facilitating the invasiveness seen in malignant gliomas in vivo.
Clin Exp Metastasis 1996 Jan
PMID:Expression and localization of 92 kDa type IV collagenase/gelatinase B (MMP-9) in human gliomas. 852 11

Recent studies suggest that cysteine proteinase cathepsin L is involved in the process of tumor invasion and metastasis. We examined cathepsin L activity in brain tumor tissue samples by an enzymatic assay, and cathepsin L protein content by enzyme-linked immunoadsorbent assays and Western blotting to determine whether increased levels of cathepsin L correlate with the progression of human gliomas. Native and acid-activatable cathepsin L activities were highest in glioblastomas followed by anaplastic astrocytomas and were lowest in low-grade gliomas and normal brain tissues. Significantly higher amounts of an M(r) 29,000 cathepsin L were present in glioblastomas and anaplastic astrocytomas than in normal brain tissues and low-grade glioma tissue extracts. Using specific antibodies to cathepsin L, we also studied its cellular distribution by immunohistochemical procedures. Higher diffuse cathepsin L immunoreactivity was found in glioblastomas than in low-grade gliomas and normal brain tissue samples. Finally, the addition of cathepsin L antibody inhibits the invasion of glioblastoma cell lines through Matrigel invasion assay. These results suggest the expression of cathepsin L is dramatically upregulated in malignant gliomas and correlates with the malignant progression of human gliomas in vivo.
Clin Exp Metastasis 1996 Jan
PMID:Expression and immunohistochemical localization of cathepsin L during the progression of human gliomas. 852 13

Autocrine stimulation by platelet-derived growth factor-B (PDGF-B)-like factors has been widely implicated as an important mechanism in the cause and/or maintenance of a variety of human tumors. However, normal human cells appear to be resistant to transformation by PDGF-B-like molecules, and a direct demonstration of the tumor-promoting or tumor-maintaining property of a PDGF-B autocrine system is lacking. T98G human glioblastoma cells are nontumorigenic in athymic mice. We show that these cells express predominantly PDGF-beta type receptors and continuously secrete small amount of PDGF-B/c-sis. Addition of suramin or specific anti-PDGF-B/v-sis antibody inhibits proliferation in culture. Conversely, multiple clonal lines that stably overexpress PDGF-B/v-sis (T98Gsis cells) exhibit a striking 200-250% increased proliferation rate and an enhanced colony-forming frequency in soft agar. Clonal lines with stable expression of PDGF-B/v-sis (T98Gsis cells) reliably (80%) develop tumors in 4-6 weeks, whereas the empty-vector control cells are nontumorigenic. Moreover, in some cases, T98Gsis cells disseminate to form bilateral and multifocal pulmonary metastases. The results show that T98G cells contain functional PDGF receptors that, upon sufficient stimulation, can cause greatly increased mitogenic response, which may account for the development of the malignant phenotype. Metastatic tumor formation in athymic mice by PDGF stimulation has not been reported previously. The mechanism may depend on preexisting changes such as the lost p53 function of these cells. T98Gsis cells provide a model of growth factor-dependent tumorigenesis and metastases, which may be helpful in elucidating these relationships.
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PMID:Platelet-derived growth factor-B/v-sis confers a tumorigenic and metastatic phenotype to human T98G glioblastoma cells. 854 81


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