Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Therapeutic options for the treatment of malignant brain tumors have been limited, in part, because of the presence of the blood-brain barrier. For this reason, the Sixth Annual Meeting of the Blood-Brain Barrier Disruption Consortium, the focus of which was the "Importance of Dose Intensity in Neuro-Oncology Clinical Trials," was convened in April 2000, at Government Camp, Mount Hood, Oregon. This meeting, which was supported by the National Cancer Institute, the National Institute of Neurological Disorders and Stroke, and the National Institute of Deafness and Other Communication Disorders, brought together clinicians and basic scientists from across the U.S. to discuss the role of dose intensity and enhanced chemotherapy delivery in the treatment of malignant brain tumors and to design multicenter clinical trials. Optimizing chemotherapy delivery to the CNS is crucial, particularly in view of recent progress identifying certain brain tumors as chemosensitive. The discovery that specific constellations of genetic alterations can predict which tumors are chemoresponsive, and can therefore more accurately predict prognosis, has important implications for delivery of intensive, effective chemotherapy regimens with acceptable toxicities. This report summarizes the discussions, future directions, and key questions regarding dose-intensive treatment of primary CNS lymphoma, CNS relapse of systemic non-Hodgkin's lymphoma, anaplastic oligodendroglioma, high-grade glioma, and metastatic cancer of the brain. The promising role of cytoenhancers and chemoprotectants as part of dose-intensive regimens for chemosensitive brain tumors and development of improved gene therapies for malignant gliomas are discussed.
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PMID:Importance of dose intensity in neuro-oncology clinical trials: summary report of the Sixth Annual Meeting of the Blood-Brain Barrier Disruption Consortium. 1130 17

OLIG2 is a recently identified transcription factor involved in the specification of cells in the oligodendroglial lineage. We investigated the expression of OLIG2 by in-situ hybridisation in 21 brain tumours: nine grade II and III oligodendrogliomas, three grade II oligoastrocytomas, and nine non-oligodendroglial tumours (four grade IV astrocytomas, two meningiomas, a dysembryoplastic neuroepithelial tumour, and two metastases). OLIG2-positive cells corresponding to neoplastic oligodendrocytes were present in all oligodendrogliomas and oligoastrocytomas. By contrast, OLIG2 expression was not detected in the non-oligodendroglial tumours. Thus, oligodendroglioma probably arise from oligodendrocyte precursor cells. OLIG2 should prove a useful marker for the diagnosis of oligodendroglial tumours.
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PMID:OLIG2 as a specific marker of oligodendroglial tumour cells. 1149 20

Extraneural metastases from primary intracranial tumours are extremely rare. We present a case of metastatic oligodendroglioma causing extradural spinal cord compression at the level of the sixth thoracic vertebrae resulting in paraplegia. We discuss the routes of tumour dissemination and possible reasons for the rarity of cases of metastatic oligodendroglioma.
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PMID:Extradural cord compression due to metastatic oligodendroglioma. 1216 Jan 43

Epileptic seizures are common in patients with cerebral metastases as well as in patients with primary brain tumors. In cancer patients without primary brain tumors or brain metastasis, epileptic seizures may occur due to metabolic or toxic causes, or due to infections. We performed a retrospective analysis from our neurooncological database concerning the occurrence of seizures in patients with primary brain tumors, patients with cerebral metastases and in cancer patients without brain tumors. Patients with low grade gliomas, such as astrocytoma WHO I + II (69%), oligodendroglioma WHO II (50%), and mixed glioma WHO II-III (56%) were more likely to have seizures than patients with anaplastic glioma WHO III (44%), glioblastoma WHO IV (48%) or meningeoma (45%). In patients with brain metastasis, melanoma (67%), cancer of the lung (29%), and gastrointestinal tumors (21%) were the primaries with the highest frequency of seizures. In cancer patients without brain metastases or primary brain tumors, seizures occurred in 4%. In conclusion, the occurrence of epileptic seizures in patients suffering from primary brain tumors, as well as in patients with cerebral metastases, varied within the tumor entity. Therefore, especially in brain tumors where a higher probability of epileptic seizures is expected, they should be taken into account in the care of cancer patients.
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PMID:[The frequency of seizures in patients with primary brain tumors or cerebral metastases. An evaluation from the Ludwig Boltzmann Institute of Neuro-Oncology and the Department of Neurology, Kaiser Franz Josef Hospital, Vienna]. 1252 23

Oligodendroglioma is a rare primary brain tumour. These tumours rarely metastasis extraneurally because of the absence of a lymphatic system, the presence of the blood-brain barrier and the patient's poor overall survival. Oligodendroglioma may spread via the cerebrospinal fluid or after surgical intervention. Metastasis to bone marrow is extremely rare. Oligodendroglioma is now considered a chemosensitive disease. If chemotherapy leads to prolonged survival, we may see more extraneural metastases in future.
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PMID:Bone marrow metastasis in anaplastic oligodendroglioma. 1280 Apr 73

Tissue Factor Pathway Inhibitor (TFPI) prevents further participation of Tissue Factor (TF) in the coagulation process by forming a stable quaternary complex of TF-FVIIa-FXa-TFPI. Recently, plasma TFPI level were found to be elevated in patients with malignant disease outside the brain. Therefore the aim of this study was to investigate the TFPI plasma level in patients with primary brain tumors and intracerebral metastases. From May 2000 to December 2001 the total tissue factor pathway inhibitor antigen (TFPI) was preoperatively determined in blood samples of 225 patients with primary or metastatic brain tumors. Tumor histology classified as benign (WHO grade I and II) and malignant (WHO grade III and IV, intracerebral metastases) was correlated to plasma TFPI-levels. Plasma TFPI was significantly higher in patients with malignant tumors including intracerebral metastasis compared to benign tumors (80.1 +/- 34.31 versus 64.3 +/- 25.8 ng ml-1 [p < 0.01; t-test]). To exclude the influence of primary systemic neoplasms with secondary brain metastasis on plasma TFPI-level a subgroup of patients with primary brain tumors (meningioma, astrocytoma, oligodendroglioma and glioblastoma) was separated. In this group TFPI-level was also significantly elevated in patients with malignant (n = 66) (78.6 +/- 29.9) compared to benign brain tumors (n = 127) (64.3 +/- 25.8 ng ml-1 [p < 0.01; t-test]). To the authors' knowledge this is the first study describing the correlation of increased plasma TFPI and malignancy in patient with brain tumors. Further studies are needed to clarify the pathogenic mechanism and the clinical relevance of this phenomenon.
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PMID:Increased levels of plasma tissue factor pathway inhibitor in patients with glioblastoma and intracerebral metastases. 1287 Feb 58

Metastatic involvement of the cerebro-spinal fluid (CSF) pathway in oligodendrogliomas is not uncommon; however, symptomatic involvement of the spinal cord is very rare: less of 10 cases have been published. To our knowledge, an intracranial oligodendroglioma presenting with symptoms of drop metastases in the cauda equina has never been reported. We report a case of 67-year-old woman who after 1 month of severe low back and legs pain developed symptoms of raised intracranial pressure. A spinal cord MRI showed multiple intradural nodular lesions at the level of the cauda equina, a MRI of the brain showed an intraventricular brain tumor. The histopathological diagnosis of both surgically treated lesions was anaplastic oligodendroglioma. The choices adopted in planning diagnostic and therapeutical procedures are discussed. The importance of the clinical and neuroradiological data in the diagnosis is stressed. Pathophysiology of the seeding of intracranial tumours via the cerebrospinal fluid is reviewed.
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PMID:Anaplastic oligodendroglioma presenting with drop metastases in the cauda equina. 1602 38

We report on a patient with oligodendroglioma metastatic to bone, presenting with pancytopenia and fever 10 years after initial tumor resection. Our review of the literature showed a total of 30 reported extraneural metastases, with only 19 of these being similar cases of bone metastases. These bony lesions have increased signal intensity in T2-weighted and low signal intensity on T1-weighted images, with intense homogeneous enhancement. However, on MR imaging, we were unable to find necrosis or compression deformity of the vertebrae, despite extensive metastatic disease.
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PMID:Oligodendroglioma metastatic to bone marrow. 1621 56

Primary brain tumours of a single histological type and metastatic brain tumours are well described in dogs in the current veterinary literature. However, the concurrent presence of a primary and secondary tumour in the brain of a dog has never, to the authors' knowledge, been previously reported. The clinical and pathological features of a nine-year-old, female boxer with an oligodendroglioma and metastases from a mammary gland adenocarcinoma occurring simultaneously in the brain are described in this case report. Information in the veterinary literature on multiple malignancies affecting the central nervous system is very limited; therefore, a discussion about comparative situations in human medicine has been included.
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PMID:Primary and secondary tumours occurring simultaneously in the brain of a dog. 1700 54

We report the first case of a 22-year-old man, with a previously neurosurgically treated intramedullary anaplastic oligodendroglioma (World Health Organization grade III), who developed 19 months later two histologically proven intracranial metastases. We support a hypothesis whereby the anaplastic parts of tumors have spread along the spinal cord and brainstem via the cerebrospinal fluid pathways, a process that could be promoted by surgical manipulation, although the relative contribution of the two factors remains speculative.
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PMID:Intracranial dissemination of primary spinal cord anaplastic oligodendroglioma. 1743 21


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