Glioma causes: Difference between revisions

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{{Glioma}}  
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==Overview==
==Overview==
Common causes of glioma include genetic mutations (''ERCC1'', ''[[ERCC2]]'', ''[[XRCC1]]'', ''MGMT'', ''IDH1'', ''[[IDH2]]'', ''[[p53]]'', ''[[EGFR]]'', ''[[TSC1]]'', ''[[TSC2]]'', ''[[RB1]]'', ''[[APC]]'', ''hMLH1'', ''hMSH2'', ''[[PMS2]]'', ''[[PTEN]]'', ''[[NF1]]'', and ''NF2'').<ref name=ddd>Pathology of glioma. Wikipedia. https://en.wikipedia.org/wiki/Glioma</ref><ref name="pmid16932614">{{cite journal| author=Schwartzbaum JA, Fisher JL, Aldape KD, Wrensch M| title=Epidemiology and molecular pathology of glioma. | journal=Nat Clin Pract Neurol | year= 2006 | volume= 2 | issue= 9 | pages= 494-503; quiz 1 p following 516 | pmid=16932614 | doi=10.1038/ncpneuro0289 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16932614  }} </ref>


==Causes==
==Causes==
The exact causes of gliomas are not known.
*Common causes of glioma include genetic mutations.
* Genetic factors
*The various genes include:<ref name=ddd>Pathology of glioma. Wikipedia. https://en.wikipedia.org/wiki/Glioma</ref><ref name="pmid16932614">{{cite journal| author=Schwartzbaum JA, Fisher JL, Aldape KD, Wrensch M| title=Epidemiology and molecular pathology of glioma. | journal=Nat Clin Pract Neurol | year= 2006 | volume= 2 | issue= 9 | pages= 494-503; quiz 1 p following 516 | pmid=16932614 | doi=10.1038/ncpneuro0289 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16932614 }} </ref>
:* [[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>
**''ERCC1''
:* 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 />
**''[[ERCC2]]''
 
**''[[XRCC1]]''
::* 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> 
**''MGMT''
::* 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>  
**''IDH1''
::* 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> 
**''[[IDH2]]''
 
**''[[p53]]''
* Environnemental factors
**''[[EGFR]]''
:* [[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>
**''[[TSC1]]''
<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> 
**''[[TSC2]]''
* [[cytomegalovirus]]<ref>{{cite journal|authors=Michaelis M, Baumgarten P, Mittelbronn M, Driever PH, Doerr HW, Cinatl J, Jr |title=Oncomodulation by human cytomegalovirus: novel clinical findings open new roads.|journal=Medical microbiology and immunology|date=February 2011|volume=200|issue=1|pages=1–5|pmid=20967552|doi=10.1007/s00430-010-0177-7}}</ref><ref>{{cite journal|last=Barami|first=K|title=Oncomodulatory mechanisms of human cytomegalovirus in gliomas.|journal=Journal of Clinical Neuroscience |date=July 2010|volume=17|issue=7|pages=819–23|pmid=20427188|doi=10.1016/j.jocn.2009.10.040}}</ref><ref>{{cite journal|journal=Neuro Oncol |date=Mar 2012 |volume=14 |issue=3 |pages=246–55 |doi=10.1093/neuonc/nor227 |title=Consensus on the role of human cytomegalovirus in glioblastoma |authors=Dziurzynski K, Chang SM, Heimberger AB, Kalejta RF, McGregor Dallas SR, Smit M, Soroceanu L, Cobbs CS; HCMV and Gliomas Symposium |pmid=22319219 |pmc=3280809 }}</ref>
**''[[RB1]]''
* Occupational factors
**''[[APC]]''
:* 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>
**''hMLH1''
:* Architects
**''hMSH2''
:* Surveyors
**''[[PMS2]]''
:* Retail workers
**''[[PTEN]]''
:* Butchers
**''[[NF1]]''
:* 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>
**''NF2''


==References==
==References==
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Latest revision as of 23:37, 26 November 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2]

Overview

Common causes of glioma include genetic mutations (ERCC1, ERCC2, XRCC1, MGMT, IDH1, IDH2, p53, EGFR, TSC1, TSC2, RB1, APC, hMLH1, hMSH2, PMS2, PTEN, NF1, and NF2).[1][2]

Causes

References

  1. 1.0 1.1 Pathology of glioma. Wikipedia. https://en.wikipedia.org/wiki/Glioma
  2. 2.0 2.1 Schwartzbaum JA, Fisher JL, Aldape KD, Wrensch M (2006). "Epidemiology and molecular pathology of glioma". Nat Clin Pract Neurol. 2 (9): 494–503, quiz 1 p following 516. doi:10.1038/ncpneuro0289. PMID 16932614.


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