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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In our retrospective analysis of 305 patients with primary brain tumors, treated and followed at Rambam Medical Center between 1983-1990, 56% were males; mean age was 43; 47% were Ashkenazi Jews, 22% Sephardi Jews, 22% Arabs and 9% were Jews of unspecified origin. 3-year actuarial survival for all patients was 33.5%, Arabs 51%, Sephardi Jews 40%, Ashkenazi Jews 20%; for those younger than 20, it was 57%, and older than 20, 26%. Diagnoses were: astrocytoma grades I-II, 68%; astrocytoma grade III, 24%; glioblastoma multiforme, 5.5%; medulloblastoma 73%; ependymoma, 75%; oligodendroglioma, 85%; meningioma, 100%; pituitary adenoma, 100%. Survival probability of those with glioblastoma multiforme treated by combined surgery and radiotherapy was superior to that of those treated by surgery alone. In low-grade astrocytoma there was no difference in survival probability between those with combined therapy and those treated by surgery alone. Survival when the diagnosis was based on imaging studies alone without histological confirmation of malignancy, was similar to that of those with glioblastoma: only 3.0% at 3 years. Prognostic factors identified by univariate analysis were histology, age of patient and ethnic origin, and type of treatment.
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PMID:[Primary brain tumors]. 898 15

The ultrastructural pathology of primary brain tumors of glial origin is examined. These are divided into two major groups. The first category comprises astrocytoma with the variants: fibrillary, protoplasmic, gemistocytic, and anaplastic. These are biologically aggressive tumors of a relatively high proliferative potential and include a substantial proportion of cases that transform into the most malignant secondary glioblastoma. The second category, comprised of rather benign tumors of a limited proliferative capacity and a reasonable good prognosis, includes such clinico-pathological entities as pilocytic astrocytoma, pleomorphic xanthoastrocytoma, and subependymal giant cell astrocytoma of tuberous sclerosis. There is no ultrastructural feature, however, which makes it possible to discriminate between major subclasses of astrocytes; but secondary glioblastoma cells, while still retaining the stigmata of neoplastic astrocytes, are characterized by nuclei that seem to be more indented, cisterns of the endoplastic reticulum may be distended, and intranuclear pseudoinclusions are frequently observed. Primary glioblastoma, which probably originates de novo, is characterized by poorly differentiated cells with a paucity of subcellular organelles and no obvious features of astrocytic origin. Granular cell tumor also belongs to neoplasms of astrocytic lineage and the hallmark of this entity is a cell characterized by the presence of numerous membrane-bound, electron-dense autophagic vacuoles. Its malignant analogue is the granular cell glioblastoma. Two subtypes of granular cell glioblastoma have been distinguished. The first is characterized by the presence of numerous granular, electron-dense bodies which correspond to autophagic vacuoles. The second type is characterized by numerous electron-dense, amorphous masses within cellular processes. These electron-dense inclusions are virtually indistinguishable from minute Rosenthal fibers. The pilocytic astrocytoma is virtually indistinguishable at the ultrastructural level from fibrillary astrocytomas but cells tend to be more elongated. Besides Rosenthal fibers, two types of distinctive structures are relatively common in pilocytic astrocytomas: eosinophilic hyaline droplets and round granular bodies, which are composed of large aggregates of electron-dense secondary lysosomes or small electron-dense bodies, respectively. Pleomorphic xanthoastrocytoma is characterized by astrocytes surrounded by basal membranes. It belongs to a peculiar category of astrocytic "desmoplastic" brain tumors occurring in younger patients, the common denominator for which is the presence of basal lamina. The last category in this group is subependymal giant cell astrocytoma, a tumor of bivalent (glial and neuronal) differentiation, the cells of which are characterized by the presence of peculiar crystalloids. The hallmark of oligodendroglioma is the presence of concentric arrays of membranes (so-called membrane laminations, whorls, or scrolls). A fragment of the cytoplasm sequestrated within a particular whorl may contain mitochondria, lysosomes, or abundant glycogen granules. Ependymomas are characterized by a florid picture dominated by the presence of microlumina, cilia with basal bodies (blepharoplasts), microvilli, and long, interdigitating intercellular junctions of the zonulae adherentiae type. Ganglioglioma, the last category covered by this review, is a mixed glio-neuronal tumor. While glial cells are indistinguishable from their counterparts encountered elsewhere (mostly pilocytic astrocytes), the ganglion cells are characterized by abundant intracytoplasmic dense-core vesicles, absence of intermediate filaments, and numerous microtubules. Occasionally a close apposition of ganglion cells and Rosenthal fibers is seen. Dense-core vesicles are pleomorphic and ranged in a diameter from small synaptic vesicles to large lysosome-like neurosecretory granules.
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PMID:Ultrastructural pathology of glial brain tumors revisited: a review. 902 63

Mass lesions of the central nervous system (CNS) that may assume a clear cell appearance are diverse in nature. Primary conditions in this category include oligodendroglioma, hemangioblastoma, germinoma (seminoma), clear cell and chordoid meningioma, pleomorphic xanthoastrocytoma, and lipid-rich glioblastoma. These proliferations usually can be identified by attention to clinical presentation, topographic location, radiographic details, and histological nuances. Occasionally, however, electron microscopy or immunohistological analysis may be necessary. A recommended panel of reagents for the evaluation of clear cell primary CNS lesions include antibodies to glial fibrillary acidic proteins, S-100 protein, epithelial membrane antigen, vimentin, keratins, placental-like alkaline phosphatase, and synaptophysin. This article reviews the salient clinicopathologic attributes of such proliferations, elaborates a practical approach to their diagnosis, and discusses important differential diagnostic considerations. The latter include malformative lesions, infarcts, inflammatory conditions, and secondary lymphomas, carcinomas, and melanomas.
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PMID:Clear cell neoplasms and pseudoneoplastic lesions of the central nervous system. 938 25

For a single-dose toxicity assessment, five patients with recurrent malignant glioma (ages 29-46 years) were treated with intracavitary alloreactive cytotoxic T lymphocytes (CTL) and interleukin-2 (IL-2). The trial tested the hypothesis that alloreactive CTL, sensitized to the major histocompatibility complex (MHC) proteins of the patient, offer selective, targeted killing of glioma cells that express MHC. Patient lymphocytes, which also express MHC, were irradiated and placed into CellMax artificial capillary systems with lymphocytes from MHC-disparate donors and CTL developed over a 2- to 3-week period with a low concentration of IL-2. The CTL largely expressed CD3 and CD11a/CD8 markers and lysed targets displaying patient MHC. CTL were implanted into the tumor bed at surgery and a catheter was used for subsequent infusions. Patients received one to five treatment cycles every other month; one cycle generally consisted of two or three CTL infusates administered within a 1- to 2-week period. Different unrelated donors were used for each cycle. Treatment was well tolerated; transient toxicity at grades 1-3 was recorded by NCI Common Toxicity Scale criteria. Two glioblastoma patients have died; one from tumor recurrence locally and the other from recurrence at a site distant from the treatment. Two of the five patients completed five cycles; one anaplastic oligodendroglioma patient shows no evidence of tumor 30 months from the start of immune therapy and an anaplastic astrocytoma patient shows stable disease 28 months after initiation of therapy. One anaplastic oligodendroglioma patient, who dropped the protocol during her second treatment cycle, has no evidence of tumor 28 months after recurrence.
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PMID:Treatment of recurrent glioma with intracavitary alloreactive cytotoxic T lymphocytes and interleukin-2. 939 Jan 98

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

A total of 26 patients (6 with anaplastic astrocytoma; 20 with glioblastoma) were treated with crisnatol mesylate. All patients had residual or progressive disease following surgery and standard radiotherapy; nine patients had prior chemotherapy. Crisnatol was administered as a 72-hour infusion every 21 days at a starting dose of 2250 mg/m2. Two patients who had not received prior chemotherapy achieved a complete response and remain in continuous complete remission over seven and six years, respectively, post-diagnosis. Two other patients remained stable on crisnatol for 10 months before disease progression. One patient with mixed oligodendroglioma/glioblastoma progressed after 12 months on crisnatol. He survives at 7 years post-diagnosis, with Karnofsky Performance Status of 60 following other therapies. One patient with anaplastic astrocytoma stopped treatment by request after 10 months and remains stable 64 months post diagnosis. Seventeen evaluable patients, including nine patients with prior chemotherapy, progressed after 2-9 courses of therapy. Median survival is 9.25 months, with a one year survival rate of 30% and 2 years survival rate of 17%. Neurotoxicity was acute and dose-limiting. Side effects were tolerable and limited to duration of infusion. Two complete, long-lasting responses to crisnatol mesylate in patients with progressive malignant glioma are encouraging results and warrant further investigation.
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PMID:Long-term response to crisnatol mesylate in patients with glioma. 954 77

Retrospective analysis of case records of 9793 patients with brain tumors operated on at the Burdenko Neurosurgical Institute from 1985 to 1992 was done. 323 patients (3.2%) had postoperative CNS infectious complications with deaths registered in 46 cases. Cholesteatomas and choriopapillomas had the highest complication rates: 12% of all cases and 11.4%, respectively. Variable incidence was observed in the glial tumors group: from 3% in glioblastoma patients to 4.7% in oligodendroglioma patients. Concurrent infections, surgical approaches via parabasal sinuses and CSF leakage at the operation site were considered as risk factors for postoperative CNS infectious complications.
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PMID:[Craniocerebral suppurative-inflammatory complications in nervous system cancer patients in the postoperative period]. 958 45

Over the past few years, although much has been learned about the molecular genetics of central nervous system (CNS) tumors, researchers and pathologists are only beginning to understand the scientific basis of the development of these tumors. Data accumulated so far support the division of glioblastoma into two clinical and molecular subsets. Primary or de novo glioblastomas occur in older patients, are clinically aggressive and exhibit epidermal growth factor receptor amplification or overexpression. Secondary glioblastomas develop from pre-existing low-grade astrocytomas, have a more protracted clinical course, and frequently contain p53 mutations. Both types of tumors show deletions of chromosome 10 and possibly mutations of the PTEN/MMAC1 gene as an endstage event. Oligodendrogliomas have been shown to have genetic abnormalities distinct from those of the astrocytic tumors, commonly involving chromosomes 1p and 19q. As regards meningiomas, loss of chromosome 22q and mutations of the neurofibromatosis type 2 gene are frequent events and loss of chromosome 14q and 10q may be seen in atypical or malignant transformation. Such genetic findings, apart from providing a better understanding of neoplastic transformation in brain tumors, are beginning to form the basis of a new approach to neuro-oncology.
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PMID:The molecular genetics of central nervous system tumors. 964 6

Vascular endothelial growth factor (VEGF) is a hypoxia-inducible angiogenic factor, which is known to be upregulated in most cases of glioblastoma multiforme (GBM). The expression of VEGF and its receptors in ependymomas, oligodendrogliomas, and particularly the expression during anaplastic progression of these three types of gliomas has not been studied extensively. Fifty-six gliomas, consisting of 10 ependymomas, 12 oligodendrogliomas, 3 anaplastic oligodendrogliomas, 6 astrocytomas grade II, 5 anaplastic astrocytomas, and 20 glioblastoma multiformes, were investigated for VEGF and receptor expression using in situ hybridization (ISH) and reverse transcription polymerase chain reaction (RT-PCR). Results showed that VEGF was moderately to strongly expressed in 8 of 10 ependymomas and in all anaplastic oligodendrogliomas and glioblastoma multiforme cases. These tumors displayed similar degrees of extensive necrosis and vascular proliferation, with VEGF expression consistently seen in tumor cells around necrotic areas. The VEGF expression, although present at a lower level, also was shown in 4 of 12 oligodendrogliomas, in 3 of 6 astrocytomas grade II, and in 2 of 5 anaplastic astrocytomas, with a regional rather than diffuse pattern of positive result. The findings from the in situ hybridization study correlated with the expression index, as determined by reverse transcription polymerase chain reaction. Expression of VEGF was correlated significantly with vascular proliferation (p < 10(-5)) and necrosis (p < 10(-5)), as well as with microvessel density (p = 0.002, rs = 0.41). The VEGF receptors, kinase domain region (KDR) and Fms-like-tyrosine kinase (Flt-1), also were upregulated in the tumor vasculature of glioblastoma multiforme, anaplastic oligodendrogliomas, and ependymomas with necrosis, whereas the astrocytomas grade II, anaplastic astrocytomas, and oligodendroglioma tumors tended to express a weak to nondetectable signal. Anaplastic progression in all three types of gliomas is heralded by the occurrence of small zones of VEGF-expressing cells and early vascular proliferation, followed by an accelerated phase of angiogenesis closely associated with VEGF induction around areas of necrosis and with the expression of VEGF receptors in the tumor vasculature.
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PMID:Expression of vascular endothelial growth factor and its receptors in the anaplastic progression of astrocytoma, oligodendroglioma, and ependymoma. 966 44

Despite more than two decades of clinical research with chemotherapy, the outcome of malignant gliomas remains poor. Recent years have seen major advances in elucidation of the biology of these tumors, which in turn have led to the current development of innovative therapeutic strategies. The question confronting us at the end of the 1990s is whether we should continue to use and investigate chemotherapy or whether the time has come for experimental treatments. As a contribution to this debate, we reviewed the abundant literature on chemotherapy of malignant glioma, paying special attention to methodological features. The new treatment approaches based on current knowledge about glioma biology are then briefly summarized. Assessment of more than 20 years of chemotherapy trials is discouraging despite a few areas of modest success. Only patients with specific histology (oligodendroglioma, anaplastic astrocytoma) and good prognostic factors (young age, good performance status) may benefit from chemotherapy, with a possible reversal of neurological dysfunction. However, the real impact on survival is small (anaplastic astrocytoma) or undefined (oligodendroglioma). Furthermore, it is unfortunately obvious that the outcome of glioblastoma patients is not significantly modified by chemotherapy. We believe the time has come to explore the potential of novel biological therapies in glioblastoma patients. This could also be proposed for anaplastic astrocytoma and oligodendroglioma patients after failure of chemotherapy.
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PMID:Malignant glioma: should chemotherapy be overthrown by experimental treatments? 968 Oct 71


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