doi: 10.1093/neuonc/1.1.1pmid: N/A
This content is only available as a PDF. © 1999 by the Society for Neuro-Oncology
doi: 10.1093/neuonc/1.1.1pmid: N/A
This content is only available as a PDF. © 1999 by the Society for Neuro-Oncology
Giese,, Alf;Hagel,, Christian;Kim, Ella, L.;Zapf,, Svenja;Djawaheri,, Jasmin;Berens, Michael, E.;Westphal,, Manfred
doi: 10.1093/neuonc/1.1.3pmid: 11550298
Abstract The capacity of glial tumor cells to migrate and diffusely infiltrate normal brain compromises surgical eradication of the disease. Identification of genes associated with invasion may offer novel strategies for anti-invasive therapies. The gene for TXsyn, an enzyme of the arachidonic acid pathway, has been identified by differential mRNA display as being overexpressed in a glioma cell line selected for migration. In this study TXsyn mRNA expression was found in a large panel of glioma cell lines but not in a strain of human astrocytes. Immunohistochemistry demonstrated TXsyn in the parenchyma of glial tumors and in reactive astrocytes, whereas it could not be detected in quiescent astrocytes and oligodendroglia of normal brain. Glioma cell lines showed a wide range of thromboxane B2 formation, the relative expression of which correlated with migration rates of these cells. Migration was effectively blocked by specific inhibitors of TXsyn, such as furegrelate and dazmegrel. Other TXsyn inhibitors and cyclooxygenase inhibitors were less effective. Treatment with specific inhibitors also resulted in a decrease of intercellular adhesion in glioma cells. These data indicate that TXsyn plays a crucial role in the signal transduction of migration in glial tumors and may offer a novel strategy for anti-invasive therapies. References Aas, A.T., Tonnessen, T.I., Brun, A., and Salford, L.G. ( 1995 ) Growth inhibition of rat glioma cells in vitro and in vivo by aspirin. J. Neurooncol. 24 , 171 -180. Amberger, V.R., Paganetti, P.A., Seulberger, H., Eldering, J.A., and Schwab, M.E. ( 1994 ) Characterization of a membrane-bound metalloendoprotease of rat C6 glioblastoma cells. Cancer Res. 54 , 4017 -4025. Asch, A.S., Leung, L.L., Shapiro, J.R., and Nachmann, R.L ( 1986 ) Human brain glia cells synthesize thrombospondin. Proc. Natl. Acad. Sci. U. S. A. 83 , 2904 -2908. Auch-Schwelk, W., Katusic, Z.S., and Vanhoutte, P.M. 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( 1982 ) Eicosanoids: Prostaglandins, thromboxanes, leukotrienes, and other derivatives of carbon-20 unsaturated fatty acids. J. Neurochem. 38 , 1 -14. Wynalda, M.A., Liggett, W.F., and Fitzpatrick, F.A. ( 1983 ) Sodium 5-(39-pyridinylmethyl) benzofuran-2-carboxylate (U-63557A), a new, selective thromboxane synthase inhibitor: Intravenous and oral pharmacokinetics in dogs and correlation with ex situ thromboxane B2 production. Prostaglandins 26 , 311 -324. Author notes Departments of Neurosurgery [A.G., E.L.K., S.Z., J.D., M.W.] andNeuropathology [C.H.], University Hospital Eppendorf, 20246 Hamburg, Germany;Neuro-Oncology Laboratory [M.E.B.], Barrow Neurological Institute, Phoenix, AZ 85013-4496 © 1999 by the Society for Neuro-Oncology
doi: 10.1093/neuonc/1.1.14pmid: 11554386
The Central Brain Tumor Registry of the United States (CBTRUS) obtained 5 years of incidence data (1990-1994)—including reports on all primary brain and CNS tumors—from 11 collaborating state cancer registries. Data were available for 20,765 tumors located in the brain, meninges, and other CNS sites, including the pituitary and pineal glands. The average annual incidence was estimated at 11.5 cases per 100,000 person-years. The higher incidence of tumors in male patients (12.1 per 100,000 person-years) than in female patients (11.0 per 100,000 person-years) was statistically significant ( P <0.05); the higher incidence in whites (11.6 per 100,000 person-years) compared with blacks (7.8 per 100,000 person-years) was statistically significant ( P <0.05). The most frequently reported histologies were meningiomas (24.0%) and glioblastomas (22.6%). Higher rates for glioblastomas, anaplastic astrocytomas, oligodendrogliomas, anaplastic oligodendrogliomas, ependymomas, mixed gliomas, astrocytomas not otherwise specified, medulloblastomas, lymphomas, and germ cell tumors in male than in female patients were statistically significant ( P <0.05), with relative risks (RR) ranging from 1.3 to 3.4. Meningiomas were the only tumors with a significant excess in females (RR=0.5). We noted higher occurrence rates in whites than in blacks for the following histologies: diffuse astrocytomas, anaplastic astrocytomas, glioblastomas, oligodendrogliomas, ependymomas, mixed gliomas, astrocytomas NOS, medulloblastomas, nerve sheath tumors, hemangioblastomas, and germ cell tumors, with RRs ranging from 1.5 to 3.4. Racial differences in occurrence rates were not observed for predominately benign meningiomas or pituitary tumors. This study represents the largest compilation of data on primary brain and CNS tumors in the United States. Standard reporting definitions and practices must be universally adopted to improve the quality and use of cancer registry data. © 1999 by the Society for Neuro-Oncology « Previous | Next Article » Table of Contents This Article Neuro Oncol (January 1999) 1 (1): 14-25. doi: 10.1093/neuonc/1.1.14 » Abstract Free References Full Text (PDF) Free Classifications Retrospective Clinical Study Epidemiology and Cancer Control Services Article metrics Alert me when cited Alert me if corrected Find similar articles Similar articles in Web of Science Similar articles in PubMed Add to my archive Download citation Request Permissions Citing Articles Load citing article information Citing articles via CrossRef Citing articles via Scopus Citing articles via Web of Science Citing articles via Google Scholar Google Scholar Articles by Surawicz, T. S. Search for related content PubMed PubMed citation Articles by Surawicz, T. S. Articles by McCarthy, B. J. Articles by Kupelian, V. Articles by Jukich, P. J. Articles by Bruner, J. M. Articles by Davis, F. G. Related Content Load related web page information Share Email this article CiteULike Delicious Facebook Google+ Mendeley Twitter What's this? Search this journal: Advanced » Current Issue December 2015 17 (12) Alert me to new issues Published on behalf of Society for Neuro-Oncology The Journal About this journal Editor's Choice Articles Rights & Permissions Dispatch date of the next issue We are mobile – find out more This journal is a member of the Committee on Publication Ethics (COPE) Journals Career Network Impact factor: 6.776 5-Yr impact factor: 6.604 Also affiliated with Japan Society for Neuro-Oncology European Association of Neuro-Oncology Editor-in-Chief Patrick Wen View full editorial board For Authors Instructions to authors Submit now! Self-Archiving Policy Open access options available for authors - visit Oxford Open This journal enables compliance with the NIH Public Access Policy Alerting Services Email table of contents CiteTrack XML RSS feed Corporate Services Advertising sales Reprints Classified Advertising
doi: 10.1093/neuonc/1.1.26pmid: N/A
This content is only available as a PDF. © 1999 by the Society for Neuro-Oncology
doi: 10.1093/neuonc/1.1.27pmid: 11550297
This content is only available as a PDF. © 1999 by the Society for Neuro-Oncology
Gladson, Candece, L.;Guha,, Abhijit;Wong, Albert, J.
doi: 10.1093/neuonc/1.1.30pmid: 11550299
Author notes Department of Pathology, Division of Neuropathology, University of Alabama at Birmingham, Birmingham, AL 35294 [C.L.G.];Department of Neurosurgery, University of Toronto, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, M5T 288 Canada [A.G.]; andDepartment of Microbiology and Immunology, Kimmel Cancer Institute, Thomas Jefferson University, Philadelphia, PA 19107 [A.J.W.] © 1999 by the Society for Neuro-Oncology
doi: 10.1093/neuonc/1.1.43pmid: N/A
This content is only available as a PDF. © 1999 by the Society for Neuro-Oncology
Kleihues,, Paul;Ohgaki,, Hiroko
doi: 10.1093/neuonc/1.1.44pmid: 11550301
Abstract Glioblastomas may develop de novo (primary glioblastomas) or through progression from low-grade or anaplastic astrocytomas (secondary glioblastomas). These subtypes of glioblastoma constitute distinct disease entities that evolve through different genetic pathways, affect patients at different ages, and are likely to differ in prognosis and response to therapy. Primary glioblastomas develop in older patients and typically show EGFR overexpression, PTEN (MMAC1) mutations, CDKN2A (p16) deletions, and less frequently, MDM2 amplification. Secondary glioblastomas develop in younger patients and often contain TP53 mutations as the earliest detectable alteration. These characteristics are derived largely from patients selected on the basis of clinical history and sequential biopsies. Currently available data are insufficient for a substitution of histologic classification and grading of astrocytic tumors by genetic typing alone. More subtypes of glioblastomas may exist with intermediate clinical and genetic profiles, a factor exemplified by the giant-cell glioblastoma that clinically and genetically occupies a hybrid position between primary (de novo) and secondary glioblastomas. Future research should aim at the identification of criteria for a combined clinical, histologic, and genetic classification of astrocytic tumors. References al-Sarraj, S., and Bridges, L.R. ( 1995 ) p53 immunoreactivity in astrocytomas and its relationship to survival. Br. J. Neurosurg. 9 , 143 -149. Albarosa, R., Colombo, B.M., Roz, L., Magnani, I., Pollo, B., Cirenei, N., Giani, C., Conti, A.M., DiDonato, S., and Finocchiaro, G. ( 1996 ) Deletion mapping of gliomas suggest the presence of two small regions for candidate tumor-suppressor genes in a 17-cM interval on chromosome 10q. Am. J. Hum. Genet. 58 , 1260 -1267. Ashley, D.M., and Bigner, D.D. ( 1997 ) Recent advances in the biology of central nervous system tumors. Curr. Opin. 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This content is only available as a PDF. © 1999 by the Society for Neuro-Oncology
Bigner, Sandra, H.;Rasheed, B.K., Ahmed;Wiltshire,, Rodney;McLendon, Roger, E.
doi: 10.1093/neuonc/1.1.52pmid: 11550302
Abstract Morphologic criteria for diagnosing oligodendrogliomas and for classifying them as well-differentiated (World Health Organization grade II) and anaplastic (World Health Organization grade III) are well recognized. Nevertheless, applying these guidelines to specific cases often reveals discrepancies among different observers. In addition, whether a given tumor also contains an astrocytic component may be debatable. Loss of heterozygosity studies have demonstrated that oligodendroglial neoplasms have a high incidence of loss of the 1p and 19q chromosomal arms. Although loss of heterozygosity for portions of 19q are sometimes seen in astrocytic neoplasms, these tumors seldom show complete loss of 19q accompanied by loss of 1p. Loss of 9p or homozygous deletion of the CDKN2 gene or both are associated with anaplastic oligodendrogliomas, whereas loss of 17p or TP53 gene mutations or both are frequent in astrocytomas, but rare in oligodendrogliomas. 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Paleologos, Nina, A.;Cairncross, J., Gregory
doi: 10.1093/neuonc/1.1.61pmid: N/A
Abstract Oligodendrogliomas are rare primary brain tumors. Significant attention has recently been focused on these interesting neoplasms because of their unique chemosensitivity and the durability of some of these responses. Surgery and radiation continue to play important roles in the treatment of oliogodendrogliomas. Molecular genetic analyses have given new insight into the allelic deletions that distinguish these tumors and their progression from indolent to more aggressive forms. In the future, molecular genetic analysis may guide therapeutic decisions concerning patients with oligodendroglioma and may help us learn more about how to best treat other malignant brain neoplasms. References Bailey, P., and Bucy, P.C. ( 1929 ) Oligodendrogliomas of the brain. J. Pathol. 32 , 735 -751. Bailey, P., and Cushing, H. ( 1926 ) Tumors of the Glioma Group . Philadelphia: Lippincott. Bailey, P., and Hiller, G. ( 1924 ) The interstitial tissues of central nervous system: A review. J. Nerv. 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