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==Overview== | |||
==Risk factors== | |||
* Occupational factors | |||
:* Farmers<ref>{{Cite journal|title = Animal viruses, bacteria, and cancer: a brief commentary|url = http://www.ncbi.nlm.nih.gov/pubmed/24592380|journal = Frontiers in Public Health|date = 2014|issn = 2296-2565|pmc = 3923154|pmid = 24592380|pages = 14|volume = 2|doi = 10.3389/fpubh.2014.00014|first = Jimmy T.|last = Efird|first2 = Stephen W.|last2 = Davies|first3 = Wesley T.|last3 = O'Neal|first4 = Ethan J.|last4 = Anderson}}</ref><ref>{{Cite journal|title = Exposure to farm crops, livestock, and farm tasks and risk of glioma: the Upper Midwest Health Study|url = http://www.ncbi.nlm.nih.gov/pubmed/19403843/|journal = American Journal of Epidemiology|date = Jun 15, 2009|issn = 1476-6256|pmid = 19403843|pages = 1479-1491|volume = 169|issue = 12|doi = 10.1093/aje/kwp075|first = Avima M.|last = Ruder|first2 = Tania|last2 = Carreón|first3 = Mary Ann|last3 = Butler|first4 = Geoffrey M.|last4 = Calvert|first5 = Karen E.|last5 = Davis-King|first6 = Martha A.|last6 = Waters|first7 = Paul A.|last7 = Schulte|first8 = Jack S.|last8 = Mandel|first9 = Roscoe F.|last9 = Morton}}</ref> | |||
:* Architects | |||
:* Surveyors | |||
:* Retail workers | |||
:* Butchers | |||
:* Engineers<ref name=":0">{{Cite journal|title = The epidemiology of glioma in adults: a "state of the science" review|url = http://www.ncbi.nlm.nih.gov/pubmed/24842956|journal = Neuro-Oncology|date = Jul 2014|issn = 1523-5866|pmc = 4057143|pmid = 24842956|pages = 896-913|volume = 16|issue = 7|doi = 10.1093/neuonc/nou087|first = Quinn T.|last = Ostrom|first2 = Luc|last2 = Bauchet|first3 = Faith G.|last3 = Davis|first4 = Isabelle|last4 = Deltour|first5 = James L.|last5 = Fisher|first6 = Chelsea Eastman|last6 = Langer|first7 = Melike|last7 = Pekmezci|first8 = Judith A.|last8 = Schwartzbaum|first9 = Michelle C.|last9 = Turner}}</ref> | |||
* Environnemental factors | |||
:* [[electromagnetic radiation]] <ref>{{cite press release |title=IARC classifies radiofrequency electromagnetic fields as possibly carcinogenic to humans |url=http://www.iarc.fr/en/media-centre/pr/2011/pdfs/pr208_E.pdf |publisher=IARC |date=31 May 2011 }}</ref> | |||
<ref>{{cite journal|last=Benson|first=Victoria|author2=Kristin Pirie |author3=Joachim Schüz |author4=Gillian K Reeves |author5=Valerie Beral |author6=Jane Green |title=Mobile phone use and risk of brain neoplasms and other cancers: prospective study|journal=International Journal of Epidemiology|date=23 March 2013|volume=42|issue=3|pages=792–802|doi=10.1093/ije/dyt072|url=http://ije.oxfordjournals.org/content/42/3/792|accessdate=8 May 2013}}</ref> | |||
* Genetic factors | |||
:* [[genetic disorders]] such as [[neurofibromatosis]] (type 1 and type 2) and [[tuberous sclerosis complex]] are known to predispose to their development.<ref>{{cite journal|last=Reuss|first=D|author2=von Deimling, A|title=Hereditary tumor syndromes and gliomas.|journal=Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer|year=2009|volume=171|pages=83–102|pmid=19322539|doi=10.1007/978-3-540-31206-2_5}}</ref> | |||
:* DNA damages<ref name=Bernstein>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</ref> Excess DNA damages can give rise to mutations through [[Mutation#Error prone replication by-pass|translesion synthesis]]. Furthermore, incomplete DNA repair can give rise to [[Epigenetics|epigenetic]] alterations or epimutations.<ref>{{cite journal | author = Cuozzo C, Porcellini A, Angrisano T, Morano A, Lee B, Di Pardo A, Messina S, Iuliano R, Fusco A | last10 = Santillo | first10 = MR | last11 = Muller | first11 = MT | last12 = Chiariotti | first12 = L | last13 = Gottesman | first13 = ME | last14 = Avvedimento | first14 = EV | year = 2007 | title = DNA damage, homology-directed repair, and DNA methylation | url = | journal = PLoS Genet | volume = 3 | issue = 7| page = e110 | doi = 10.1371/journal.pgen.0030110 | pmid = 17616978 | pmc=1913100}}</ref><ref>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</ref> 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.<ref name=Bernstein /> | |||
::* Epigenetic repression of DNA repair genes is often found in progression to [[Cancer#Heredity|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.<ref name="pmid22672670">{{cite journal |author=Skiriute D, Vaitkiene P, Saferis V, Asmoniene V, Skauminas K, Deltuva VP, Tamasauskas A |title=MGMT, GATA6, CD81, DR4, and CASP8 gene promoter methylation in glioblastoma |journal=BMC Cancer |volume=12 |issue= |pages=218 |year=2012 |pmid=22672670 |pmc=3404983 |doi=10.1186/1471-2407-12-218 |url=http://www.biomedcentral.com/1471-2407/12/218}}</ref><ref name=Spiegel>{{cite journal |author=Spiegl-Kreinecker S, Pirker C, Filipits M, Lötsch D, Buchroithner J, Pichler J, Silye R, Weis S, Micksche M, Fischer J, Berger W |title=O6-Methylguanine DNA methyltransferase protein expression in tumor cells predicts outcome of temozolomide therapy in glioblastoma patients |journal=Neuro-oncology |volume=12 |issue=1 |pages=28–36 |date=January 2010 |pmid=20150365 |pmc=2940563 |doi=10.1093/neuonc/nop003 |url=http://neuro-oncology.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=20150365}}</ref> | |||
::* Epigenetic reductions in expression of another DNA repair protein, ERCC1, were found in an assortment of 32 gliomas.<ref name="pmid19626585">{{cite journal |author=Chen HY, Shao CJ, Chen FR, Kwan AL, Chen ZP |title=Role of ERCC1 promoter hypermethylation in drug resistance to cisplatin in human gliomas |journal=Int. J. Cancer |volume=126 |issue=8 |pages=1944–54 |date=April 2010 |pmid=19626585 |doi=10.1002/ijc.24772 |url=http://dx.doi.org/10.1002/ijc.24772}}</ref> | |||
::* 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.<ref name=Cohen>{{cite journal |author=Cohen AL, Holmen SL, Colman H |title=IDH1 and IDH2 mutations in gliomas |journal=Curr Neurol Neurosci Rep |volume=13 |issue=5 |pages=345 |date=May 2013 |pmid=23532369 |doi=10.1007/s11910-013-0345-4 |url=http://dx.doi.org/10.1007/s11910-013-0345-4 |pmc=4109985}}</ref> | |||
==References== | ==References== | ||
Revision as of 19:21, 21 August 2015
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Risk factors
- Occupational factors
- Environnemental factors
- Genetic factors
- genetic disorders such as neurofibromatosis (type 1 and type 2) and tuberous sclerosis complex are known to predispose to their development.[6]
- DNA damages[7] Excess DNA damages can give rise to mutations through translesion synthesis. Furthermore, incomplete DNA repair can give rise to epigenetic alterations or epimutations.[8][9] 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.[7]
- 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.[10][11]
- Epigenetic reductions in expression of another DNA repair protein, ERCC1, were found in an assortment of 32 gliomas.[12]
- 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.[13]
References
- ↑ 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.
- ↑ "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.
- ↑ 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.
- ↑ 7.0 7.1 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.