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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Causes
The exact causes of gliomas are not known.
- Genetic factors
- genetic disorders such as neurofibromatosis (type 1 and type 2) and tuberous sclerosis complex are known to predispose to their development.[1]
- DNA damages[2] Excess DNA damages can give rise to mutations through translesion synthesis. Furthermore, incomplete DNA repair can give rise to epigenetic alterations or epimutations.[3][4] Such mutations and epimutations may provide a cell with a proliferative advantage which can then, by a process of natural selection, lead to progression to cancer.[2]
- Epigenetic repression of DNA repair genes is often found in progression to sporadic glioblastoma. For instance, methylation of the DNA repair gene O-6-methylguanine-DNA methyltransferase(MGMT) Promoter was observed in 51.3% to 66% of glioblastoma specimens.[5][6]
- Epigenetic reductions in expression of another DNA repair protein, ERCC1, were found in an assortment of 32 gliomas.[7]
- Mutations in gliomas frequently occur in either isocitrate dehydrogenase (IDH) 1 or 2 genes. One of these mutations (mostly in IDH1) occurs in about 80% of low grade gliomas and secondary high-grade gliomas.[8]
- Environnemental factors
- cytomegalovirus[11][12][13]
- Occupational factors
References
- ↑ Reuss, D; von Deimling, A (2009). "Hereditary tumor syndromes and gliomas". Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer. 171: 83–102. doi:10.1007/978-3-540-31206-2_5. PMID 19322539.
- ↑ 2.0 2.1 Bernstein C, Prasad AR, Nfonsam V, Bernstein H. (2013). DNA Damage, DNA Repair and Cancer, New Research Directions in DNA Repair, Prof. Clark Chen (Ed.), ISBN 978-953-51-1114-6, InTech, http://www.intechopen.com/books/new-research-directions-in-dna-repair/dna-damage-dna-repair-and-cancer
- ↑ Cuozzo C, Porcellini A, Angrisano T, Morano A, Lee B, Di Pardo A, Messina S, Iuliano R, Fusco A (2007). "DNA damage, homology-directed repair, and DNA methylation". PLoS Genet. 3 (7): e110. doi:10.1371/journal.pgen.0030110. PMC 1913100. PMID 17616978.
- ↑ O'Hagan HM, Mohammad HP, Baylin SB. Double strand breaks can initiate gene silencing and SIRT1-dependent onset of DNA methylation in an exogenous promoter CpG island. PLoS Genet 2008;4(8) e1000155. doi:10.1371/journal.pgen.1000155 PMID 18704159
- ↑ Skiriute D, Vaitkiene P, Saferis V, Asmoniene V, Skauminas K, Deltuva VP, Tamasauskas A (2012). "MGMT, GATA6, CD81, DR4, and CASP8 gene promoter methylation in glioblastoma". BMC Cancer. 12: 218. doi:10.1186/1471-2407-12-218. PMC 3404983. PMID 22672670.
- ↑ Spiegl-Kreinecker S, Pirker C, Filipits M, Lötsch D, Buchroithner J, Pichler J, Silye R, Weis S, Micksche M, Fischer J, Berger W (January 2010). "O6-Methylguanine DNA methyltransferase protein expression in tumor cells predicts outcome of temozolomide therapy in glioblastoma patients". Neuro-oncology. 12 (1): 28–36. doi:10.1093/neuonc/nop003. PMC 2940563. PMID 20150365.
- ↑ Chen HY, Shao CJ, Chen FR, Kwan AL, Chen ZP (April 2010). "Role of ERCC1 promoter hypermethylation in drug resistance to cisplatin in human gliomas". Int. J. Cancer. 126 (8): 1944–54. doi:10.1002/ijc.24772. PMID 19626585.
- ↑ Cohen AL, Holmen SL, Colman H (May 2013). "IDH1 and IDH2 mutations in gliomas". Curr Neurol Neurosci Rep. 13 (5): 345. doi:10.1007/s11910-013-0345-4. PMC 4109985. PMID 23532369.
- ↑ "IARC classifies radiofrequency electromagnetic fields as possibly carcinogenic to humans" (PDF) (Press release). IARC. 31 May 2011.
- ↑ Benson, Victoria; Kristin Pirie; Joachim Schüz; Gillian K Reeves; Valerie Beral; Jane Green (23 March 2013). "Mobile phone use and risk of brain neoplasms and other cancers: prospective study". International Journal of Epidemiology. 42 (3): 792–802. doi:10.1093/ije/dyt072. Retrieved 8 May 2013.
- ↑ Michaelis M, Baumgarten P, Mittelbronn M, Driever PH, Doerr HW, Cinatl J, Jr (February 2011). "Oncomodulation by human cytomegalovirus: novel clinical findings open new roads". Medical microbiology and immunology. 200 (1): 1–5. doi:10.1007/s00430-010-0177-7. PMID 20967552.
- ↑ Barami, K (July 2010). "Oncomodulatory mechanisms of human cytomegalovirus in gliomas". Journal of Clinical Neuroscience. 17 (7): 819–23. doi:10.1016/j.jocn.2009.10.040. PMID 20427188.
- ↑ Dziurzynski K, Chang SM, Heimberger AB, Kalejta RF, McGregor Dallas SR, Smit M, Soroceanu L, Cobbs CS; HCMV and Gliomas Symposium (Mar 2012). "Consensus on the role of human cytomegalovirus in glioblastoma". Neuro Oncol. 14 (3): 246–55. doi:10.1093/neuonc/nor227. PMC 3280809. PMID 22319219.
- ↑ Efird, Jimmy T.; Davies, Stephen W.; O'Neal, Wesley T.; Anderson, Ethan J. (2014). "Animal viruses, bacteria, and cancer: a brief commentary". Frontiers in Public Health. 2: 14. doi:10.3389/fpubh.2014.00014. ISSN 2296-2565. PMC 3923154. PMID 24592380.
- ↑ Ruder, Avima M.; Carreón, Tania; Butler, Mary Ann; Calvert, Geoffrey M.; Davis-King, Karen E.; Waters, Martha A.; Schulte, Paul A.; Mandel, Jack S.; Morton, Roscoe F. (Jun 15, 2009). "Exposure to farm crops, livestock, and farm tasks and risk of glioma: the Upper Midwest Health Study". American Journal of Epidemiology. 169 (12): 1479–1491. doi:10.1093/aje/kwp075. ISSN 1476-6256. PMID 19403843.
- ↑ Ostrom, Quinn T.; Bauchet, Luc; Davis, Faith G.; Deltour, Isabelle; Fisher, James L.; Langer, Chelsea Eastman; Pekmezci, Melike; Schwartzbaum, Judith A.; Turner, Michelle C. (Jul 2014). "The epidemiology of glioma in adults: a "state of the science" review". Neuro-Oncology. 16 (7): 896–913. doi:10.1093/neuonc/nou087. ISSN 1523-5866. PMC 4057143. PMID 24842956.