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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microvascular proliferation, a hallmark of malignant brain tumors, represents an attractive target of anticancer research, especially because of the quiescent nonproliferative endothelium of the normal brain. Cerebral neoplasms sequester copper, a trace metal that modulates angiogenesis. Using a rabbit brain tumor model, normocupremic animals developed large vascularized VX2 carcinomas. By contrast, small, circumscribed, relatively avascular tumors were found in the brains of rabbits copper-depleted by diet and penicillamine treatment (CDPT). The CDPT rabbits showed a significant decrease in serum copper, copper staining of tumor cell nuclei, microvascular density, the tumor volume, endothelial cell turnover, and an increase in the vascular permeability (breakdown of the blood-brain barrier), as well as peritumoral brain edema. In non-tumor-bearing animals, CDPT did not alter the vascular permeability or the brain water content. CDPT also inhibited the intracerebral growth of the 9L gliosarcoma in F-344 rats, with a similar increase of the peritumoral vascular permeability and the brain water content. CDPT failed to inhibit tumor growth and the vascularization of the VX2 carcinoma in the thigh muscle or the metastases to the lung, findings that may reflect regional differences in the responsiveness of the endothelium, the distribution of copper, or the activity of cuproenzymes. Metabolic and pharmacologic withdrawal of copper suppresses intracerebral tumor angiogenesis; angiosuppression is a novel biologic response modifier for the in situ control of tumor growth in the brain.
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PMID:Inhibition of angiogenesis and tumor growth in the brain. Suppression of endothelial cell turnover by penicillamine and the depletion of copper, an angiogenic cofactor. 170 Jun 17

In 121 proven cases of intracranial metastases, lung cancer was as high as 48 per cent. Multiple lesions were noted (67.8%) in almost every type of organ source. Brain parenchyma (80.3%), predominantly supratentorium was the major site of metastases. The minority was observed in leptomeninge, cranial bone and subgaleal tissue. Subarachnoid seeding tumors along CSF pathways spread mainly from pineal neoplasms; a few cases from lung and choriocarcinoma. Extensive brain edema occurred in metastases from almost every type of primary organ source. Calcification exhibited 5.8 per cent and their origins were lung and breast. Bleeding tumors were noted in 10.7 per cent mainly from choriocarcinoma, a few from lung and GI. Hyperdense tumors occurred in 86.8 per cent on noncontrast scans. Almost all tumors (95.2%) showed contrast enhancement, predominantly ring-shaped lesions. Their organ sources were GI, lung and breast. A few patterns of enhancement were homogeneous and heterogeneous. Non-enhanced lesion were noted in 4.8 per cent mainly due to the high density of calcium and blood inside the tumors. Apart from seeding, calcified and bleeding tumors, the CT findings were not specific for various types of metastases.
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PMID:CT findings of brain metastases. 279 20

Metastatic brain tumors from colorectal cancers are relatively rate. In previous reports, the incidence, ranged from 1.9 to 3.5 percent of all metastatic brain tumors. We reported 2 cases of metastatic brain tumors from colorectal cancers. Metastasis to the lung and liver were not found in 2 cases at the time of the diagnosis of the single brain metastasis. The CEA levels in the serum were highly elevated in these 2 cases. On a contrast-enhanced CT scan, tumors were equally demonstrated as high density and cystic, with a ring-like mass with surrounding brain edema. Brain metastases of colorectal cancer were discussed with a review of the literature.
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PMID:[Brain metastases of colorectal cancer--a case report]. 356 Apr 51

Results of surgical treatment in 85 cases with metastatic brain tumors are reviewed. The lung was the most frequent site of primary lesion and the following sites were GI tract and the breast. Adequate treatment consisted of total removal of tumor, irradiation and/or chemotherapy were carried out in 51 cases. The remaining 34 cases had an unsuccessful treatment because of their poor physical condition. Mean survival time after adequate treatment was 8.75 months in the former group and 3.06 months in the latter group. Of 51 patients (86.3%) in the former group, 44 showed improvement of the neurological signs after treatment. In the latter group, only 14 patients (41.2%) revealed neurological improvement. Total removal of tumor was carried out in 55 of 85 cases. The one-month operative mortality for all patients was 19.2%. Postoperative one-year survival rate was 12.5% in 16 cases with multiple metastases and in 36 cases with single metastasis was 25.6%. Follow-up study of 77 cases showed 31.2% of survival rate in 6 months, 18.2% in one-year and 5.2% in two-years. Only four patients survived more than 3 years after treatment. The direct causes of death in cases of total removal were attributed in recurrence of primary lesion or remote metastases to other organs. This study revealed that the prognosis of the patient with metastatic brain tumor was influenced by existence of intracranial hypertension due to brain edema or metastatic tumor itself and metastases to other organs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Results of the surgical treatment of metastatic brain tumors]. 405 62

In a prospective study, the effect of dexamethasone treatment on brain edema was evaluated by computed tomography (CT) in 14 patients with intracranial neoplasm. A CT study was made immediately prior to the beginning of the treatment and at various intervals for 8 to 19 days thereafter. The volume and attenuation of the edema were measured and related to the time after the start of treatment. In five cases of meningioma, only minor changes were shown; the edema volume either decreased or increased slightly or did not change at all. In four gliomas, a substantial decrease was noted in the edema volume in two cases and a smaller decrease was observed in two cases. In three metastases, a linear decrease in edema volume was noted during the entire follow-up, reducing it to one-fourth of the initial volume after 2 weeks of treatment. In one case of acoustic neuroma and in one undiagnosed lesion, a marked decrease in edema volume was also noted. The attenuation of the remaining edema was constant during the entire treatment time.
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PMID:Effect of dexamethasone treatment on peritumoral brain edema: evaluation by computed tomography. 628 15

A surgical case of multiple cerebral metastases from choriocarcinoma was reported, who was a 26 year-old female. She had received treatment of hydatid mole on April 1979, and admitted to our hospital for the consciousness disturbance and right hemiparesis. CT scan showed two high density tumors with marked brain edema. Emergency craniotomy was performed and five tumors were completely removed. Following the operation, symptoms of increased intracranial pressure and disturbance of consciousness were markedly improved in about a week. She received radiation therapy. After radiochemotherapy, a metastatic lung tumor was removed. Now her chorionic gonadotropin titers remain normal and she is able to perform all her household responsibilities despite a mild right hemiparesis. Recently, surgical treatment has been getting done for cerebral metastasis of choriocarcinoma. Because most of the metastatic cerebral lesions occur in relatively easy position for the operation. If symptoms of cerebral metastasis appear, we should performed surgical treatment as soon as possible.
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PMID:[Choriocarcinoma: cerebral metastasis from choriocarcinoma--a successfully surgical treated case]. 668 65

The direct and indirect immunofluorescent methods were used to demonstrate the serum proteins in vasogenic brain edema on paraffin embedded formalin fixed human brains with carcinoma metastases. Applying these techniques extravasated albumin was detected within the tumor and in the surrounding neuropil. In the remote part of the peritumorous area the cytoplasma of neurons and astrocytes were stained specifically. The specific immunostaining clearly demonstrates the plasma origin of proteins in human peritumorous edema similarly to the experimental vasogenic brain edema. The immunofluorescent technique seems to be very useful to investigate the human brain edema on necropsy material as well.
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PMID:The application of immunofluorescent antibody method in research of human brain edema. 676 64

In the present study, the immunofluorescent and immunoperoxidase methods were applied to demonstrate the serum proteins in vasogenic brain edema (6). Using these techniques on paraffin embedded formalin fixed human brains with carcinoma metastases, albumin was identified specifically in the edema fluid, while human immunoglobulin (IgG, IgA, IgM) were not detectable. The localisation and spreading of edema fluid clearly show the presence of the vasogenic type of brain edema under human pathological conditions. The astrocytes containing albumin confirm the conception concerning their role in the resolution of brain edema in human pathology, as well. The immunohistological techniques seem to be useful to investigate the human brain edema on necropsy material.
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PMID:Specific demonstration of albumin by immunohistological techniques in human vasogenic brain edema. 701 17

Metastatic brain tumors are almost always associated with vasogenic brain edema, which in turn plays a pivotal role in the evolution of neurological morbidity associated with these lesions. Attention has recently focused on a group of proteinaceous vascular permeability factors (VPF's) that are capable of inducing angiogenesis and promoting increased capillary permeability. To test the hypothesis that metastatic brain tumors expressing VPF's are associated with peritumoral cerebral edema, a rabbit polyclonal immunoglobulin (Ig) G anti-VPF was used to immunostain pathological specimens of metastatic cerebral tumors obtained from 22 patients who underwent surgery at Yale-New Haven Hospital. Magnetic resonance (MR) imaging was used to correlate VPF staining in tumor tissue with the occurrence of peritumoral brain edema. A histological study of the microvasculature was then conducted by immunostaining the specimens for endothelial cell factor VIII surface antigen, using two gliosis specimens as controls. Results revealed 21 of 22 tumors stained positively for VPF's; the negative-VPF tumor was a melanoma that exhibited no peritumoral edema. Twenty of 22 tumors had MR imaging-evident vasogenic edema. The presence and intensity of VPF immunostaining of microvascular features were noted and compared. Factor VIII staining demonstrated tumor vascularity to be most abundant in VPF-rich regions of tumor. The authors therefore report a high correlation between the presence of VPF's and the occurrence of peritumoral brain edema associated with cerebral metastases.
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PMID:Vascular permeability factor in brain metastases: correlation with vasogenic brain edema and tumor angiogenesis. 752 34

Tumor necrosis is a common feature of malignant neoplasms. The pathogenesis of tumor necrosis remains poorly documented. Recent evidence has shown a correlation between the presence of tumor necrosis and low content of tissue plasminogen activator in brain tumors and significantly higher levels of plasminogen activator inhibitor-1 (PAI-1) in human glioblastomas. We subjected fresh brain tumor tissue samples (n = 197) to an enzyme-linked immunosorbent assay to determine PAI-1 content. The results were correlated with the presence of edma and necrosis on imaging studies. The samples studied were from normal brain (n = 10), low-grade gliomas (n = 26), meningiomas (n = 47), acoustic neuromas (n = 18), glioblastomas (n = 45), metastases (n = 45), and areas of tumor necrosis (n = 6). The benign tumor samples (n = 96) had 3.5 times less PAI-1 than did the malignant tumors (n = 101). Tumor necrosis samples contained 3.8 times more PAI-1 than did the nonnecrotic malignant tumor samples (P < 0.000001). The benign meningioma samples showed a similar ratio compared with their malignant counterparts (0.35 versus 1.59 ng/mg, respectively, P = 0.0004). Regression analysis results showed a strong correlation between PAI-1 and necrosis (r = 0.47, P < 0.0000028) and, to a lesser extent, brain edema (r = 0.26, P = 0.001). A negative correlation between PAI-1 and tissue plasminogen activator levels almost reached statistical significance (P = 0.07). There was no correlation between PAI-1 content and the tumor size, duration of symptoms, or the sex or age of the patients. The results of this study indicate that malignant transformation is associated with a significant increase in PAlI1 and that PAI-1 may play an integral role in the pathogenesis of tissue necrosis, perhaps via the inhibition of tissue plasminogen activator and the promotion of microthrombosis.
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PMID:Plasminogen activator inhibitor-1 in brain tumors: relation to malignancy and necrosis. 773 19


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