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)

In a retrospective study of 73 patients operated on for cerebellar pilocytic astrocytomas, results of treatment, outcome and biological behaviour of residual tumour were analysed. Complete tumour resection proven by CT or MRI scans within 1 year after surgery was achieved only in 69% of cases. In 31% of cases the surgeon's opinion on the extent of surgical resection was not borne out by the result of postoperative neuroimaging. Progression of residual tumour or tumour recurrence appeared in 19% of patients. 1 patient showed metastatic spread along the craniospinal axis, and in 1 patient malignant degeneration appeared during follow-up. Stable residual tumour or regression of residual tumour was seen in 14% of patients. Outcome after surgical treatment, which was combined with irradiation in 10 patients (14%), was favourable in 80% and unfavourable in 20% of patients. This outcome of treatment was not influenced by a second operation for progression of residual tumour or recurrent tumour. Characteristics of patients with tumour progression after the first operation did not differ from those of the whole group. There were 17 reoperations for residual or recurrent tumour, 10 of which took place within 4 years after the initial surgical treatment. Surgery-related morbidity was 15% and mortality 4%. Irradiation to residual tumour in 8 patients was followed by complete regression in 1 patient, progression in 4 patients and no changes in 1 patient. For the remaining 2 patients the effect of irradiation on the residual tumour is unknown. Factors that determine the prognosis are discussed on the basis of this retrospective analysis and the data from the literature. It is concluded that optimal treatment for a cerebellar pilocytic astrocytoma does not consist solely in surgery with the aim of total tumour removal and careful tumour handling in order to avoid spread of tumour cells and subsequent metastases and additional radiation therapy is strictly selected cases, but also in posttreatment follow-up based on direct postoperative neuroimaging, preferably by MRI. An algorithm for postoperative follow-up management is presented.
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PMID:Cerebellar pilocytic astrocytoma: a treatment protocol based upon analysis of 73 cases and a review of the literature. 908 97

A 4-month-old child presented with nystagmus and macrocephaly. He had a large tumor in the suprasellar and hypothalamic region, as well as two smaller similar masses in the posterior fossa and one in the spinal canal. A biopsy of the suprasellar mass revealed it to be a desmoplastic infantile cerebral astrocytoma. Cerebrospinal fluid obtained at surgery before tumor manipulation showed clusters of malignant cells immunopositive for glial fibrillary acidic protein. In our opinion, the smaller tumors were metastases from the large suprasellar primary astrocytoma. Review of all of the previously reported cases of desmoplastic infantile cerebral astrocytoma and of the related neoplastic entity desmoplastic infantile ganglioglioma suggested that this was a unique case, but we still recommend caution with respect to the previously accepted notion that desmoplastic infantile neuroepithelial tumors are virtually benign neoplasms.
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PMID:Desmoplastic infantile astrocytoma with metastases at presentation. 931 Sep 60

A 31-year-old man underwent total resection for a fibrillary astrocytoma in the right frontal lobe followed by 6MV x-ray radiotherapy. The portal field size was a square of 8 cm x 7 cm, and the total dose of irradiation was 50Gy, with single fractions of 2Gy. For the next 6.5 years there was no recurrence of the astrocytoma. At 38 years of age, the patient noticed a subcutaneous mass in the scar of the previous operation and developed generalized convulsive seizures. MRI revealed a dural tumor within the previous radiation field, and the tumor was partially removed. Histologically, it was diagnosed as a leiomyosarcoma. This dural sarcoma satisfies the widely used criteria for definition of radiation-induced malignancies first described by Cahan et al. Both the clinical features and the possible histogenesis of this secondary tumor are briefly discussed.
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PMID:[Radiation-induced leiomyosarcoma of the dura mater: a case report]. 938 72

We have performed immunohistochemical studies of mortalin in normal and tumor human brain sections. In normal brain sections, the expression was seen mainly as being confined to neurons. Normal astrocytes showed undetectable expression of this unique member of the heat shock 70 protein family. Three grades of astrocyte tumors (low-grade astrocytoma, anaplastic astrocytoma, and glioblastoma), however, showed an increasing number of mortalin-positive cells. Other types of brain tumors, such as meningiomas, neurinomas, pituitary adenomas, and metastases, also showed elevated levels of mortalin expression compared to those in the normal brain. Mortalin has earlier been reported to have differential intracellular distribution in normal and transformed cells in vitro. Therefore, we substantiated the present study with immunofluorescence localization of the protein in normal and glioblastoma cells. The observations indicated that the tumors might be expressing a nonpancytosolic mortalin. An increase in number of mortalin-positive cells with malignant progression of brain tumors and its correlation with Ki-67 (a cell proliferation marker)-positive cells further suggested an involvement of nonpancytosolic mortalin(s) in malignant transformation of cells in vivo.
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PMID:Elevated levels of mortalin expression in human brain tumors. 941 64

CD44 belongs to a family of adhesion molecules displayed by a wide range of normal and malignant cells. Several studies implicated its presence as a marker for poor prognosis or metastases, especially in breast and colon cancer. CD44 has been proposed as an invasion marker for glioblastoma. We studied 75 astrocytic tumors with different degrees of anaplasia including juvenile pilocytic astrocytoma (JPA), low-grade astrocytoma (LGA), anaplastic astrocytoma (AA), and glioblastoma multiforme (GBM) to determine whether standard CD44 (CD44s) can be used as a clinically useful marker distinguishing between low- and high-grade gliomas. Archival paraffin-embedded tissues from 19 JPAs, 20 LGAs, 17 AAs, and 19 GBMs were immunostained with standard CD44 monoclonal antibody and compared with glial fibrillary acidic protein, using the streptavidin-complex peroxidase technique. Immunostaining was rated on a three-tiered scale by two observers. The expression of variant-splice forms of CD44 (CD44v) have been variably reported in brain tumors; a subset of these gliomas were tested with anti-CD44v monoclonal antibodies. In the tumors studied, 89% of JPAs, 90% of LGAs, 76% of AAs, and 84% of GBMs have 2+ or 3+ intensity for CD44s. Low- and high-grade gliomas showed no significant difference in staining (P > .05). Therefore, CD44s does not seem to correlate with the grading range of astrocytomas. The overall intensity of CD44s immunostaining usually, but not always, showed concordance with glial fibrillary acidic protein immunostaining, but the distinctive membrane staining of CD44s surface staining revealed fine cytologic detail in tumor cell processes in diagnostic sections. Some very anaplastic tumors were negative for CD44s, and gliomas were immunonegative for CD44v6. If variant chains (CD44v) are not found in gliomas and if this large series of low- and high-grade gliomas show no difference in CD44 expression, other factors must be explored to understand the differential behavior of low- and high-grade astrocytomas.
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PMID:CD44 expression in astrocytic tumors. 943 70

Cadherins are a family of glycoproteins that are associated with cell adhesion mechanisms. They are divided into subclasses. The E- and P-cadherins are regarded as the epithelial subtype. Their expression has been demonstrated in many different carcinoma types. Using immunomorphological techniques, we studied the expression of E-cadherin in a series of 145 human brain tumours with the monoclonal antibody 5H9. Western blot analysis was used to confirm the immunohistochemical data. The tumour types represented were astrocytoma WHO I (n = 7), astrocytoma WHO II (n = 6), astrocytoma WHO III (n = 14), glioblastoma WHO IV (n = 8), oligodendroglioma WHO II (n = 5), ependymoma WHO II (n = 5), choroid plexus papilloma WHO I (n = 5), pineoblastoma WHO IV (n = 5), medulloblastoma WHO IV (n = 5), neurinoma WHO I (n = 5), meningioma WHO I and WHO III (n = 75) and pituitary adenoma WHO I (n = 5). Only choroid plexus papillomas (5/5) and meningiomas showed E-cadherin expression. In benign meningiomas (n = 45; 100%), positive E-cadherin immunoreactivity was found regardless of the histomorphological subtype. E-Cadherin was also expressed in 21 WHO I meningiomas (100%) invading dura, bone, brain, and muscle. In contrast, E-cadherin was absent from the majority of morphologically malignant meningiomas (6/9, 66.6%). In addition, in recurrent meningiomas (n = 9), E-cadherin expression in the recurrent tumours was identical to that in the primary neoplasm except in cases with malignant progression, where the malignant recurrent tumour was E-cadherin negative. In 2 cases of metastasizing meningiomas, no E-cadherin immunoreactivity was found in the primary tumours or their metastases.
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PMID:E-Cadherin in human brain tumours: loss of immunoreactivity in malignant meningiomas. 950 62

Eighty patients with intramedullary spinal cord tumors were treated by microsurgical methods between 1988 and 1996. Twenty-nine patients were diagnosed with astrocytoma, 36 with ependymoma, five with metastasis, four with lipoma, three with dermoid or epidermoid tumor, two with neurofibroma, and one with neuroma. Vascular and infectious lesions (such as abscesses and hemangioblastomas) were excluded. After laminectomy, total removal of the lesion was achieved in 68 of 80 patients and subtotal removal in 12. Postoperative radiation therapy was performed in 13 of 80 patients. The follow-up period ranged from 12 to 92 months (mean 42.2 months). All patients underwent preoperative and postoperative magnetic resonance imaging at intervals ranging from 3 months to 5 years postoperatively. Four patients showed clinical and radiological evidence of local tumor recurrence during the follow-up period. Four patients died 5 months to 15 months postoperatively from the re-expansion of their primary metastatic disease. The operative results at long term (after the 6th postoperative month) were better than the results at short term (before the 6th postoperative month) and revealed clinical improvement in 63, no change in 10, and deterioration in seven patients. We recommend early radical surgery, whenever possible, to be performed when the patient's neurological status is still good. Subtotal removal and irradiation are better for malignant or metastatic tumors. Partial decompressive removal is best for large intramedullary lipomas. Plastic laminotomy with preservation of the intervertebral joints is especially recommended in young or middle-aged patients.
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PMID:Microsurgical treatment of intramedullary spinal cord tumors. 964 Sep 61

Magnetic resonance imaging (MRI) and computed tomography (CT) may not be reliable in the differential diagnosis of tumour necrosis, scar and recurrent tumour. We compared 201Tl-chloride SPET with CT and MRI for the differential diagnosis of these cerebral lesions. Brain SPET was performed in 40 patients after the intravenous injection of 201Tl-chloride. All 40 patients also had a CT or MRI scan, and a histological diagnosis was available for 27 of the patients. For each patient, the ratio of counts in the lesion region of interest (ROI) to counts in the contralateral ROI was calculated and found to be between 0.58 and 9.60. The ratios for high-grade gliomas, metastases and meningiomas were high (> 2.7), especially in tumours with good vascularization. A low ratio (< 1.7) was noted in patients with low-grade astrocytoma, necrosis or ischaemic lesions. There were two exceptional cases of ischaemic lesions in the luxury perfusion stage (ratios of 3.61 and 3.87), as verified by HMPAO-SPET. We found that 201Tl-chloride SPET helps to differentiate between malignant tumours, poorly vascularized benign lesions and necrosis. Differentiation between low-grade astrocytoma and non-malignant lesions was not possible, but there was a trend towards differentiating between low-grade astrocytoma and ischaemic infarction. The timing of the investigation is important to avoid false-positive results in hyperperfused ischaemic tissue.
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PMID:Clinical relevance of 201Tl-chloride SPET in the differential diagnosis of brain tumours. 985 23

The authors report on their experience of lesionectomies close to or in the thalamus, basal ganglia, third ventricle and in the temporal lobe. The resection itself is performed stereotactically, MRI or CT guided, either microscopically or endoscopically through a sleeve designed by one of the authors and named PAN working sleeve. Over the last four years this new minimally invasive technique has been successfully applied in 39 cases. Eighteen patients with 11 astrocytoma (6AA, 5All), 5 cavernoma and 2 metastases (melanoma, adenocarcinoma) of the basal ganglion-thalamus area and the trigonum were resected by means of a frontal or an occipital burr-hole, whereby in some cases there were subtotal resections. With four of these patients an existing hemiparesis increased by one degree (according to the proposal of the British Medical Research Council I-V). Seventeen patients with lesions in the foramen Monroi and in the third ventricle also underwent operation by means of frontal access, and in each case there was a total resection. Two of the patients required a shunt due to a persistent hydrocephalus internus. In one of these cases there was intraventricular bleeding which necessitated an intra-operative craniotomy. Four patients with intractable epilepsy were operated through a burr-hole in the anterior area of the os zygomaticum. Three patients were submitted to a selective resection of mesial structures and one to an anterior temporal lobe resection. To date the four patients have had no further seizures and no deficits have been observed.
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PMID:Minimally invasive lesionectomies through a stereotactically guided working sleeve. 1004 56

Recent reports have suggested that cyst formation accompanying astrocytomas in the central nervous system (CNS) is due to an edematous process caused by blood-brain barrier (BBB) disruption and not a result of necrosis. This study is performed to investigate whether the hypothesis of cyst formation based on BBB disruption also applies to various pathologically different intra-axial gliomatous tumors and metastases. By chemical analysis, using immunokinetic nephelometry, isoelectric focussing, cellulose acetate electrophoresis and a biuretic method, the concentrations of albumin, immunoglobulin G (IgG), IgA, alpha2-macroglobulin, IgM and total protein were measured and proportions of concentrations of these proteins were compared in cyst fluid, blood plasma and cerebrospinal fluid (CSF). Our data, based on the chemical analysis of cyst fluid and blood plasma of 37 patients, including 2 ependymomas (one cerebral; one thoracic), 3 oligodendrogliomas, 4 hemangioblastomas, 5 cerebellar astrocytomas and 1 cervical, 1 giant astrocytoma grade one, 1 gangliocytoma, 1 neuroblastoma and 19 metastases (five lung-; two renal-; three breast-; one melanoma-; one thyroid metastasis and seven metastases of unknown origin) present high protein concentrations in the cysts with a highly similar spectrum of proteins in the tumor cyst fluid and blood plasma, suggesting a BBB disruption followed by exudation of plasma proteins into the brain parenchyma with formation of edema and transition of edematous tissue into a cyst accompanying the tumor. Although histopathologically different types of tumor tissue are involved, data suggests that the pathogenesis of cysts accompanying gliomatous tumors and metastases in the CNS is based on BBB disruption and consequent edema, as is the case in the formation of cysts in anaplastic astrocytomas.
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PMID:The pathogenesis of cysts accompanying intra-axial primary and metastatic tumors of the central nervous system. 1006 1


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