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)

Radiation is a well-known etiology for many CNS tumors, including meningiomas, sarcomas and gliomas. However, occurrence of pituitary adenoma after radiation exposure is rare. We report a 21-year-old man with a pituitary adenoma, who was treated with post-operative radiotherapy for pontine glioma at 6 years of age. The role of radiation exposure in the etiology of pituitary adenoma is discussed, along with a literature review of radiation-induced tumors.
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PMID:Can radiation induce pituitary tumors? Giant prolactinoma after radiation exposure. 1882 28

Oligodendrogliomas account for a small subset of all gliomas, but they often are more sensitive to treatment than other glioma subtypes. In addition, oligodendrogliomas are the first central nervous system neoplasm for which a specific molecular abnormality, allelic loss of 1p/19q (1p/19q loss), correlates with patient outcome in large-scale prospective clinical trials. However, the incorporation of 1p/19q status into clinical practice remains controversial. Other molecular alterations found in oligodendrogliomas include hypermethylation of the promoter for the MGMT gene, TP53 mutations, EGFR and platelet-derived growth factor/PDGFR alterations, and 9p and 10q loss.
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PMID:Molecular profiling of oligodendrogliomas: impact on prognosis, treatment, and future directions. 1908 Jul 43

Leptomeningeal (LM) dissemination arises rarely in patients with low-grade gliomas. Few cases of LM dissemination of spinal cord low-grade gliomas have been reported in children. Here, we report a case of an intramedullary spinal cord low-grade glioma occurring in an adult presenting by LM dissemination. A 57-year-old man presented with a history of headaches and visual acuity deterioration. Neurological examination revealed mental confusion, decreasing left limb strength and left positive Babinski sign. Lumbar puncture showed low CSF glucose, high CSF protein and no tumor cells. Spinal MRI revealed an intramedullary spinal lesion with a diffuse leptomeningeal enhancement. A spinal meningeal biopsy showed arachnoiditis with isolated atypical cells which were cytokeratin immunopositive. A differential diagnosis was proposed between arachnoiditis close to an infectious process or close to meningeal carcinomatosis. An intramedullary biopsy was programmed but the patient died 1 month after biopsy. The post-mortem examination showed thickened leptomeninges and an ill-circumscribed intramedullary grey lesion. Histological examination revealed a low-grade glial neoplasm composed of monomorphous spindle "piloid" cells with diffuse dissemination to leptomeninges. Glial fibrillary acidic protein immunostaining showed scattered immunoreactive cells. Clinical and pathological features of this case are unusual. Pathogenesis and prognosis of low-grade gliomas with LM dissemination are poorly understood. This case, like cases occurring in children, cannot easily be classified in the present WHO system of classification of CNS tumors. Spinal low-grade gliomas with LM dissemination may represent a possible distinctive clinico-pathological entity.
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PMID:Leptomeningeal dissemination of low-grade intramedullary gliomas: about one case and review. 1912 71

The incidence of gliomas is increasing worldwide, including India. Of the 18,820 new cases of primary central nervous system (CNS) tumors diagnosed annually in the United States, gliomas account for over 60% with 30-40% of them being glioblastoma multiforme (GBM), 10% being anaplastic astrocytoma (AA), and 10% being low grade gliomas (LGGs). This is in contrast to one study from West Bengal, India, in which only 7.9% of the brain tumors were GBMs, while 46.8% were astrocytomas. Of all adult primary CNS tumors, GBM is the most common and the most malignant with about 7,000 to 8,000 new cases annually in the United States. Given poor outcomes, a number of treatment approaches have been investigated. Common to these approaches is the use of adjuvant radiation therapy, even as surgery alone, with or without chemotherapy, may be the mainstay for some lower grade and low-risk gliomas. Today, treatment typically involves external beam radiation, with concurrent and adjuvant chemotherapy for more aggressive histologies. Although gliomas are relatively uncommon, active research is ongoing. Results of landmark trials along with some of the recently published trials are presented. These trials and management strategies as well as evolving concepts are found by reviewing over 200 articles in the National Library Medical (NLM) database, PubMed, more than 60 of which are refrenced. Specifically, the database is searched using the following keywords, with various combinations: glioma, low-grade, anaplastic, astrocytoma, oligodendroglioma, oligoastrocytoma, glioblastoma multiforme, chemotherapy, radiation, new concepts, phase III, MGMT, CDX-110 (Celldex), temozolomide, 1p/19q deletion, and bevacizumab.
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PMID:Evidence-based adjuvant therapy for gliomas: current concepts and newer developments. 1934 43

The development of effective immunotherapy strategies for glioma requires adequate understanding of the unique immunological microenvironment in the central nervous system (CNS) and CNS tumors. Although the CNS is often considered to be an immunologically privileged site and poses unique challenges for the delivery of effector cells and molecules, recent advances in technology and discoveries in CNS immunology suggest novel mechanisms that may significantly improve the efficacy of immunotherapy against gliomas. In this review, we first summarize recent advances in the CNS and CNS tumor immunology. We address factors that may promote immune escape of gliomas. We also review advances in passive and active immunotherapy strategies for glioma, with an emphasis on lessons learned from recent early-phase clinical trials. We also discuss novel immunotherapy strategies that have been recently tested in non-CNS tumors and show great potential for application to gliomas. Finally, we discuss how each of these promising strategies can be combined to achieve clinical benefit for patients with gliomas.
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PMID:Immunotherapeutic approaches for glioma. 1934 9

Gliomas are the most common tumors of the central nervous system (CNS). Malignant astrocytic gliomas account for 50% of all primary brain tumors. Cells of origin are unknown for the majority of brain tumors: CNS tumors have frequently in their content many histological forms and their classification will depend on what the parts of neoplasm that will be clearly identified at the material taking and further investigation. Current immunohistochemical studies may determine the antigenic structure of a tumor cell, compare it with the antigens expressed by a certain cell type and, thus, classify the tumor by its origin, but there are no antibodies which would correctly identify different types of tumors. The lecture reflects the current classifications of glial tumors: the typical three-leveled classification, the Kernokhan classification, the Duma-Duport classification. A part of the lecture deals with the specific features of genetics and molecular biology of gliomas: recent studies cast any doubt on the existing data on the sources of growth of these tumors.
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PMID:[Glial tumors of the brain: current aspects of their classification and bases for genetic predisposition]. 1938 37

The purpose is to determine the incidence of active and latent human herpesvirus-6 (HHV-6) infection in a large cohort of adult primary and recurrent CNS tumors. We screened a tissue microarray (TMA) containing more than 200 adult primary and recurrent CNS tumors with known clinical information for the presence of HHV-6 DNA by in situ hybridization (ISH) and protein by immunohistochemistry (IHC). One hundred six of 224 (47%) CNS tumors were positive for HHV-6 U57 Major Capsid Protein (MCP) gene by ISH compared to 0/25 non tumor control brain (P = 0.001). Fourteen of 30 (47%) tumors were HHV-6 MCP positive by nested PCR compared to 0/25 non-tumor brain controls (P = 0.001), revealing HHV-6 Variant A in 6 of 14 samples. HHV-6A/B early (p41) and late (gp116/64/54) antigens were detected by IHC in 66 of 277 (24%) (P = 0.003) and 84 of 282 (35%) (P = 0.002) tumors, respectively, suggesting active infection. HHV-6 p41 (P = 0.645) and gp116/64/54 (P = 0.198) antigen detection was independent of recurrent disease. Glial tumors were 3 times more positive by IHC compared to non glial tumors for both HHV-6 gp116/64/54 (P = 0.0002) and HHV-6 p41 (P = 0.004). Kaplan Meier survival analysis showed no effect of HHV-6 gp116/64/54 (P = 0.852) or HHV-6 p41 (P = 0.817) antigen detection on survival. HHV-6 early and late antigens are detected in adult primary and recurrent CNS tumors more frequently in glial tumors. We hypothesize that the glial-tropic features of HHV-6 may play an important modifying role in tumor biology that warrants further investigation.
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PMID:Detection of human herpesvirus-6 in adult central nervous system tumors: predominance of early and late viral antigens in glial tumors. 1942 65

Although the safety of vaccine approaches for central nervous system (CNS) malignancies has been established in early phase clinical trials, the success of a vaccine strategy will depend critically on the ability of effector T cells to home in to CNS tumors and durably exert antitumor effects. Based on our recent studies, efficient CNS tumor homing is a characteristic of cytotoxic T lymphocytes (CTLs) with a type 1 phenotype (Tc1), and this appears to be related to the Tc1 response to the type 1 CXC chemokine ligand (CXCL) 10 [also known as interferon (IFN)-inducible protein (IP)-10] and expression of an integrin receptor very late antigen (VLA)-4 on Tc1. In addition, we have previously shown that direct intratumoral delivery of dendritic cells (DCs) ex vivo engineered to secrete IFN-alpha further enhances Tc1 homing via upregulation of CXCL10/IP-10 in the tumor microenvironment. As a means to induce IFN-alpha and CXCL10/IP-10 in the CNS tumor microenvironment in a clinically feasible manner, we used administration of polyinosinic-polycytidylic acid stabilized by lysine and carboxymethylcellulose (poly-ICLC), a ligand for toll-like receptor 3 and melanoma differentiation-associated gene 5 (MDA5) in combination with vaccinations targeting CTL epitopes derived from glioma-associated antigens (GAAs). The combination of subcutaneous vaccination and i.m. poly-ICLC administration remarkably promoted systemic induction of antigen GAA-specific Tc1s expressing VLA-4 in the CNS tumors and improved the survival of tumor-bearing mice in the absence of detectable autoimmunity. Based on these data, we have implemented a phase I/II vaccination study using type 1 polarizing DCs loaded with GAA peptides in combination with poly-ICLC in patients with recurrent malignant glioma.
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PMID:Brain tumor immunotherapy with type-1 polarizing strategies. 1976 32

Primary malignant brain cancer, one of the most deadly diseases, has a high rate of recurrence after treatment. Studies in the past several years have led to the hypothesis that the root of the recurrence may be brain tumor stem cells (BTSCs), stem-like subpopulation of cells that are responsible for propagating the tumor. Current treatments combining surgery and chemoradiotherapy could not eliminate BTSCs because these cells are highly infiltrative and possess several properties that can reduce the damages caused by radiation or anti-cancer drugs. BTSCs are similar to NSCs in molecular marker expression and multi-lineage differentiation potential. Genetic analyses of Drosophila CNS neoplasia, mouse glioma models, and human glioma tissues have revealed a link between increased NSC self-renewal and brain tumorigenesis. Furthermore, data from various rodent models of malignant brain tumors have provided compelling evidence that multipotent NSCs and lineage-restricted neural progenitor cells (NPCs) could be the cell origin of brain tumors. Thus, the first event of brain tumorigenesis might be the occurrence of oncogenic mutations in the stem cell self-renewal pathway in an NSC or NPC. These mutations convert the NSC or NPC to a BTSC, which then initiates and sustains the growth of the tumor. The self-renewal of BTSCs is controlled by several evolutionarily conserved signaling pathways and requires an intact vascular niche. Targeting these pathways and the vascular niche could be a principle in novel brain tumor therapies aimed to eliminate BTSCs.
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PMID:Brain tumor stem cells. 1985

The central nervous system (CNS) has evolved as an immune-privileged site to protect its vital functions from damaging immune-mediated inflammation. There must be a CNS-adapted system of surveillance that continuously evaluates local changes in the nervous system and communicates to the peripheral immune system during an injury or a disease. Recent advances leading to a better understanding of the CNS disease processes has placed microglia, the CNS-based resident macrophages, at center stage in this system of active surveillance. Evidence points to microglia cells contributing to the immunosuppressive environment of gliomas and actually promoting tumor growth. Microglia accumulation exists in almost every CNS disease process, including CNS tumors. This article discusses the role of microglia in CNS immunity and highlights key advances made in glioma immunology.
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PMID:Microglia and central nervous system immunity. 1994 65


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