Book ChapterDOI
Epidemiology of brain tumors.
TLDR
Significant correlation between G:C --> A:T transitions in the TP53 gene and promoter methylation of the O6 -methylguanine-DNA methyltransferase (MGMT) gene in glio-mas have been reported in several studies, suggesting the possible involvement of O6-methylguAnine DNA adducts, which may be produced by exogenous or endogenous alkylating agents in the development of gliomas.Abstract:
Gliomas account for more than 70% of all brain tumors, and of these, glioblastoma is the most frequent and malignant histologic type (World Health Organization [WHO] grade IV). There is a tendency toward a higher incidence of gliomas in highly developed, industrialized countries. Some reports indicate that Caucasians have a higher incidence than African or Asian populations. With the exception of pilocytic astrocytomas (WHO grade I), the prognosis of glioma patients is still poor. Fewer than 3% of glioblastoma patients are still alive at 5 years after diagnosis, older age being the most significant and consistent prognostic factor of poorer outcome. Gliomas are components of several inherited tumor syndromes, but the prevalence of these syndromes is very low. Many environmental and lifestyle factors including several occupations, environmental carcinogens, and diet have been reported to be associated with an elevated glioma risk, but the only factor unequivocally associated with an increased risk is therapeutic X-irradiation. In particular, children treated with X-irradiation for acute lymphoblastic leukemia show a significantly elevated risk of developing gliomas and primitive neuroectodermal tumors, often within 10 years after therapy. Significant correlation between G:C --> A:T transitions in the TP53 gene and promoter methylation of the O6 -methylguanine-DNA methyltransferase (MGMT) gene in glio-mas have been reported in several studies, suggesting the possible involvement of O6-methylguanine DNA adducts, which may be produced by exogenous or endogenous alkylating agents in the development of gliomas.read more
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Journal ArticleDOI
Bevacizumab plus Radiotherapy–Temozolomide for Newly Diagnosed Glioblastoma
Olivier Chinot,Wolfgang Wick,Warren P. Mason,Roger Henriksson,Frank Saran,Ryo Nishikawa,Antoine F. Carpentier,Khê Hoang-Xuan,Petr Kavan,Dana Cernea,Alba A. Brandes,Magalie Hilton,Lauren E. Abrey,Timothy F. Cloughesy +13 more
TL;DR: The addition of bevacizumab to radiotherapy-temozolomide did not improve survival in patients with glioblastoma, and the glucocorticoid requirement was lower.
Journal ArticleDOI
The epidemiology of glioma in adults: a "state of the science" review.
Quinn T. Ostrom,Luc Bauchet,Faith G. Davis,Isabelle Deltour,James L. Fisher,Chelsea Eastman Langer,Melike Pekmezci,Judith A. Schwartzbaum,Michelle C. Turner,Kyle M. Walsh,Margaret Wrensch,Jill S. Barnholtz-Sloan +11 more
TL;DR: A “state of the science” review of current research into causes and risk factors for gliomas in adults is provided.
Journal ArticleDOI
Annual Report to the Nation on the Status of Cancer, 1975–2007, Featuring Tumors of the Brain and Other Nervous System
Betsy A. Kohler,Elizabeth Ward,Bridget J. McCarthy,Maria J. Schymura,Lynn A. G. Ries,Christie R. Eheman,Ahmedin Jemal,Robert N. Anderson,Umed A. Ajani,Brenda K. Edwards +9 more
TL;DR: The decrease in cancer incidence and mortality reflects progress in cancer prevention, early detection, and treatment, however, major challenges remain, including increasing incidence rates and continued low survival for some cancers.
Journal ArticleDOI
Glioblastoma Multiforme: A Review of its Epidemiology and Pathogenesis through Clinical Presentation and Treatment
Farina Hanif,Farina Hanif,Kanza Muzaffar,Kahkashan Perveen,Saima Mehmood Malhi,Shabana Usman Simjee +5 more
TL;DR: It was found that radiation and certain genetic syndromes are the only risk factors identified to date for GBM, and the pathogenesis to involve aberrations of multiple signaling pathways through multiple genetic mutations and altered gene expression.
Journal ArticleDOI
IDH mutations in glioma and acute myeloid leukemia
TL;DR: The prevalence of IDH mutations in cancer is surveyed and current mechanistic understanding ofIDH mutations with implications for diagnostic and therapeutic development for the treatment of gliomas and AML is explored.
References
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Journal ArticleDOI
IARC Monographs on the Evaluation of Carcinogenic Risks to Humans
TL;DR: This timely monograph is a distillation of knowledge of hepatitis B, C and D, based on a review of 1000 studies by a small group of scientists, and it is concluded that hepatitis D virus cannot be classified as a human carcinogen.
Book
Cancer Incidence in Five Continents
Freddie Bray,J. Ferlay,Mathieu Laversanne,David H. Brewster,C. Gombe Mbalawa,B. Kohler,Marion Piñeros,Eva Steliarova-Foucher,Rajaraman Swaminathan,Sebastien Antoni,Isabelle Soerjomataram,David Forman +11 more
TL;DR: The aim of this study was to establish a database of histological groups and to provide a level of consistency and quality of data that could be applied in the design of future registries.
Journal ArticleDOI
Genetic pathways to glioblastoma: a population-based study.
Hiroko Ohgaki,Pierre Dessen,Benjamin Jourde,Sonja Horstmann,Tomofumi Nishikawa,Pier-Luigi Di Patre,Christoph Burkhard,Danielle Schüler,Nicole Probst-Hensch,Paulo César Maiorka,Nathalie Baeza,Paola Pisani,Yasuhiro Yonekawa,M. Gazi Yaşargil,Urs M. Lütolf,Paul Kleihues +15 more
TL;DR: A population-based study on glioblastomas in the Canton of Zurich, Switzerland, suggests that the acquisition of TP53 mutations in these glooblastoma subtypes occurs through different mechanisms.
Journal ArticleDOI
Chronic infections and inflammatory processes as cancer risk factors : possible role of nitric oxide in carcinogenesis
Hiroshi Ohshima,Helmut Bartsch +1 more
TL;DR: Nitric oxide (NO) and other oxygen radicals produced in infected and inflamed tissues could contribute to the process of carcinogenesis by different mechanisms, which are discussed on the basis of authors' studies on liver fluke infection and cholangiocarcinoma development.
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