Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen primary lymphomas of the central nervous system (CNS) have been studied with an immunoperoxidase technique (PAP) for the demonstration of intracytoplasmic immunoglobulins. The material was obtained by biopsy (10 cases) and at autopsy (6 cases). For comparison, ten other tumors (glial tumors and secondary lymphomas involving the nervous tissue) were simultaneously investigated. In the 16 primary lymphomas, 14 contained intracellular immunoglobulins that were considered "monoclonal" in 9 cases, "probably monoclonal" in 4 cases but "uninterpretable" in the last one. According to the Kiel classification, the 13 malignant lymphomas with intracellular immunoglobulins were classified, morphologically, as immunoblastic sarcomas (9 cases) or immunocytomas (4 cases). No immunoglobulins were detected in 2 cases: 1 lymphoblastic lymphoma and 1 centrocytic lymphoma. Various amounts of intracytoplasmic immunoglobulins were detected in inflammatory cells and glial cells (either reactive or tumoral) but the pattern of staining was consistent with current concepts of polyclonality. Therefore, a diagnosis based on the Kiel classification of lymphomas and the PAP technique will allow a more accurate prognosis on the evolution of primary lymphomas of the CNS with aspect of "high grade" and "low grade" malignancy.
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PMID:[Immunohistochemical study in 16 cases of primary lymphoma of the central nervous system (author's transl)]. 703 25

The presence of natural anti-tumor antibodies (NAA) against fibrosarcoma- and glioma cells was revealed in the normal sera of 10 different strains of rats. By means of a direct cytotoxicity test using guinea-pig complement and an absorption tests, NAA in inbred WKA/Hok rats were observed to be cytotoxically reactive to all investigated syngeneic and allogeneic fibrosarcoma lines and one glioma line, but not to hepatoma, lymphoma, leukemia, and neurinoma lines. Moreover, NAA reactivity to fibrosarcoma cells was significantly absorbed with brain, lung, kidney, skin homogenates, and cultured normal fibroblasts of syngeneic rats, but not with liver homogenates, thymus, spleen, lymph node and red blood cells. NAA were identified as being predominantly IgM and were stables at 56 degree C for 30 min. With the exception of one strain, there were no strain or sex differences in NAA levels among any of the investigated strains of rats. The level of NAA correlated with the in vivo anti-tumor response: when NAA-reactive fibrosarcoma or glioma cells were implanted into syngeneic WKA/Hok rats, groups of rats with high NAA levels suppressed tumor growth and survived longer than groups of rats with low NAA levels, while there was no difference in length of survival days in NAA non-reactive hepatoma or lymphoma cells. When 3-methylcholanthrene was inoculated into these two groups of rats, the tumor incidence in the groups of rats with high NAA level was significantly suppressed as compared to the group of rats with low NAA level. We discuss the mechanism of the induction of NAA in relation to the anti-tumor immunity.
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PMID:[Cytotoxic natural anti-tumor antibodies against fibrosarcoma and glioma cells in rats (author's transl)]. 731 60

Deletions of 9p21-22, that frequently include the alpha-, beta- and omega-IFN gene cluster, are common in malignant diseases such as acute lymphocytic leukemia, malignant melanoma and malignant glioma. There is also evidence to support the role of a gene(s) on chromosome 9p21 in predisposition for familial malignant melanoma. Although initial studies implicated that the IFN genes could serve as tumor suppressor genes, there is now data, mainly based on estimations of minimum region of overlap for the deletions, indicating that the relevant tumor suppressor gene is located centromeric of the alpha-, beta-, omega-IFN gene cluster.
Leuk Lymphoma 1993 Oct
PMID:Chromosome 9 short arm deletions in malignant diseases. 750 46

Myelin basic protein (MBP) in the cerebrospinal fluid (CSF) of patients with brain tumors and other neurological diseases was measured before, during and after various treatments such as surgery, chemotherapy and irradiation. We assessed the significance of changes in the MBP levels during the course of treatment, and speculate on what the elevated level of MBP in brain tumor patients indicates. In meningeal dissemination of malignant tumors, meningeal carcinomatosis from cancer of the systemic organ showed the highest level of MBP followed by meningeal gliomatosis and meningeal lymphoma. Meningeal carcinomatosis and meningeal lymphoma, which have responded to chemotherapy, showed normal levels of MBP after chemotherapy. Six of eight patients with newly diagnosed malignant glioma showed moderate to high levels of MBP (range 4.6-35.5ng/ml) just before intraarterial chemotherapy with VP-16 and CDDP. The level increased in five patients during the course of chemotherapy and then decreased in relation to the degree of tumor reduction by chemotherapy. In the solid type of metastatic brain tumor, five of seven patients with multiple tumors showed high levels of MBP and these levels also returned to normal after treatment in four patients. As for the influence of irradiation, levels of MBP did not increase after irradiation except in three patients who developed radiation necrosis, local extensive edema or atrophic change. In other brain tumors, levels of MBP were high in a patient with a large meningioma with very extensive edema and during an unstable postoperative condition after total removal of a large craniopharyngioma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Myelin basic protein in the cerebrospinal fluid of patients with neurological disease: especially with malignant brain tumors]. 750 61

Unconjugated monoclonal antibodies (mAb) kill tumor cells in vivo by activating immune functions. One of these is ADCC (antibody-dependent cellular cytotoxicity). The efficacy of mAbs might be augmented if the cytotoxic capacity of the effector cells could be increased. In this study the augmenting effect of granulocyte-colony-stimulating factor (G-CSF), granulocyte/macrophage(GM)-CSF and macrophage(M)-CSF was analyzed. Effector cells [peripheral blood mononuclear cells (PBMC) or granulocytes] were activated for 4-6 h by the respective CSF and assayed in an 18-h Cr51-release assay. Human colorectal, lymphoma, glioma and melanoma cell lines were target cells. Mouse mAbs of different isotypes, as well as chimeric and humanized mAbs, were used. mAbs having the human Fc part of the IgG molecule were the most effective. The killing capacity of PBMC as well as of granulocytes was statistically significantly enhanced when mAbs were added. M-CSF and GM-CSF were the best CSF for augmenting the lytic capacity of PBMC in ADCC. G-CSF had no significant effect on PBMC. Spontaneous cytolysis of PBMC was significantly augmented only by M-CSF. Granulocytes were, in general, significantly less effective than PBMC but may be equally effective killer cells together with mouse or human mAbs of the IgG1 isotype, particularly against melanoma cells. Granulocytes may also be significantly stimulated to increased lytic capacity when activated with G-CSF or GM-CSF. On the basis of the present evaluation, clinical trials in tumor patients are warranted, combining mAbs with GM-CSF or M-CSF. Preference might be given to GM-CSF as this cytokine activates both PBMC and granulocytes.
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PMID:Cytotoxicity of white blood cells activated by granulocyte-colony-stimulating factor, granulocyte/macrophage-colony-stimulating factor and macrophage-colony-stimulating factor against tumor cells in the presence of various monoclonal antibodies. 752 59

A patient who developed primary brain lymphoma 6 years following whole brain irradiation due to a low-grade glioma is described. The patient had no evidence of congenital or acquired immunodeficiency state and achieved a good and prompt response to aggressive chemotherapy, including high-dose methotrexate. The previous radiation therapy is implicated in the etiology of the lymphoma because of the geometric coincidence, the relatively long latency period and the different histology. A brief review of current literature is reported.
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PMID:Radiation-induced primary brain lymphoma: a case report. 757 Oct 30

CT findings of 2 patients with primary cerebral lymphoma were presented with a literature review of the CT manifestations of primary cerebral lymphoma. On the plain CT scan, most of lymphomas were either hyper- or isodense, well demarcated, and had variable surrounding edema. The tumors were mostly situated in the deep structures of brain: the basal ganglia, corpus callosum, periventricular white matter and vermis of cerebellum. On the postcontrast CT scan, cerebral lymphomas showed a homogeneous contrast enhancement. Ring enhancement, occasionally gyral enhancement also may be seen. On the CT scan, primary cerebral lymphomas were usually misdiagnosed as glioma, meningioma, metastases and abscess. The difference between lymphoma and the above lesions was discussed.
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PMID:[CT diagnosis of primary cerebral lymphoma--report of 2 cases]. 780 5

Single-photon emission tomography (SPET) with technetium-99m sestamibi (MIBI) was carried out in 61 adult patients with supratentorial expanding brain lesions. Thirty-one patients had pathologically proven malignant glioma. Ten patients had pathologically proven low-grade glioma, while another 12 patients had a clinical diagnosis of low-grade glioma. The other eight patients had a variety of lesions including radiation necrosis (3), abscess (2), ischaemic stroke (2) and primary brain lymphoma (1). SPET was performed 15 min after administration of 740-930 MBq MIBI and transverse, sagittal and coronal views were reconstructed. Using computed tomography or magnetic resonance imaging guidance, a MIBI uptake index was computed as the ratio of counts in the lesion to counts in the contralateral homologous region. In high-grade gliomas, the MIBI index ranged from 1.9 to 6.6 (mean 3.6 +/- 1.4) whereas it ranged from 0.8 to 1.7 (1.1 +/- 0.2) in the pathologically proven low-grade group (P < 0.01). No significant difference was found between the two low-grade groups (1.1 +/- 0.2 vs 1.1 +/- 0.2). No overlap was found between high-grade and low-grade glioma index values. Patients with suspected radiation necrosis, cerebral abscess or ischaemic stroke did not demonstrate high MIBI uptake (0.9-2.2), whereas one patient with brain lymphoma did (3.9). This study suggests that MIBI SPET imaging is of value in distinguishing low-from high-grade supratentorial gliomas in adults.
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PMID:Evaluation of single-photon emission tomography imaging of supratentorial brain gliomas with technetium-99m sestamibi. 782 15

The pathophysiology and treatment of malignant brain tumors (malignant glioma, metastatic brain tumor and malignant lymphoma) were discussed. In order to improve the prognosis of malignant brain tumor patients, many clinical trials have been conducted. The most acceptable treatment for malignant glioma is surgical resection plus radiochemotherapy with ACNU. A multidisciplinary approach to treatment is important for control of metastatic brain tumors. Treatment of malignant lymphoma includes radiotherapy and chemotherapy in combination. Combination chemotherapy with CHOP is more effective for malignant lymphoma.
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PMID:[Treatment of malignant brain tumor]. 806 Jan 32

The molecular interfaces between Gs and the beta-adrenergic receptor were investigated using synthetic peptides corresponding to various regions of its alpha subunit, alpha s. These experiments were carried out on saponin-permeable C6 glioma cells in which the beta-adrenergic receptor appears tightly coupled to Gs. Synthetic site-specific peptides from alpha s (corresponding to amino acids 15-29, 354-372, and 384-394) and alpha i (8-22, 315-324, and 345-455) were tested for their ability to interfere with coupling between the beta-adrenergic receptor and Gs. The two carboxyl-terminal peptides from alpha s blocked beta-adrenergic stimulation of adenylyl cyclase in permeable cells. However, only alpha s-354-372 had this effect in C6 membranes. It is suggested that the partial uncoupling of Gs, which occurs subsequent to cell disruption, may be related to a change in the interaction of the alpha s carboxyl terminus with the beta-adrenoreceptor. Two carboxyl-terminal peptides, 354-372 and 384-394, could also mimic the effect of Gs to increase agonist affinity for the beta-adrenergic receptor. In combination, alpha s-354-372 and alpha s-384-394 increased the ability of isoproterenol to compete with 125I-pindolol binding in a partially additive manner. Synthetic peptides from alpha i and amino-terminal peptides from alpha s had no effect on beta-agonist binding, suggesting a high specificity of peptide effects. Two findings suggest that these peptides bind directly to the beta-adrenergic receptor and stabilize its high agonist affinity conformation. First, GTP and hydrolysis-resistant GTP analogs did not alter the high affinity binding in the presence of high concentrations of the peptides. Second, in S49 lymphoma cyc- cells, which lack Gs, these peptides evoked the high affinity agonist binding state of the beta-receptor. Neither peptide had an effect on antagonist binding affinity, as measured by propranolol displacement of 125I-pindolol. These data suggest that at least two regions on the alpha subunit of Gs participate in high affinity Gs binding to the beta-adrenergic receptor. The fact that these small peptides could mimic the holo-Gs effect on the receptor is rather surprising, and the specificity of the effect suggests that the primary and secondary structure of small regions of alpha s contain much of the information for specific interaction with beta-adrenergic receptors.
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PMID:Synthetic peptides as probes for G protein function. Carboxyl-terminal G alpha s peptides mimic Gs and evoke high affinity agonist binding to beta-adrenergic receptors. 806 88


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