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| __NOTOC__ | | __NOTOC__ |
| {{Glioma}} | | {{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> |
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| ==Causes== | | ==Causes== |
| The exact causes of gliomas are not known. Hereditary [[genetic disorders]] such as [[neurofibromatoses]] (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> Different oncogenes can cooperate in the development of gliomas.<ref>{{cite journal |author=Radner H, El-Shabrawi Y, Eibl RH, Brüstle O, Kenner L, Kleihues P, Wiestler OD |title=Tumor induction by ras and myc oncogenes in fetal and neonatal brain: modulating effects of developmental stage and retroviral dose |journal=Acta Neuropathologica |volume=86 |issue=5 |pages=456–465 |year=1993 |pmid=8310796 |doi= 10.1007/bf00228580|pmc=}}</ref>
| | *Common causes of glioma include genetic mutations. |
| | | *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> |
| Gliomas have been correlated to the [[electromagnetic radiation]] from [[cell phones]], and a link between the cancer and cell phone usage was considered possible,<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> though several large studies have found no conclusive evidence. Experiments designed to test such a link gave negative results.<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> Most glioblastomas are infected with [[cytomegalovirus]], which speeds the development of tumors.<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> Though some studies have shown that [[farmers]] have higher rates of gliomas compared to the general population, exposure to farm animals or manure is not associated with glioma.<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> Later studies have not found an association between farming and gliomas; similar conflicting data concerns [[teachers]] and glioma. More consistent data shows that architects, surveyors, retail workers, butchers, and engineers have higher rates of gliomas.<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> Most studies have found that pesticide exposure is probably not a cause of glioma, though a minority of studies have found an association.<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><ref>{{Cite web|title = CDC - Women's Safety and Health Issues at Work: Job Area: Agriculture - NIOSH Workplace Safety and Health Topic|url = http://www.cdc.gov/niosh/topics/women/agriculture.html|website = www.cdc.gov|accessdate = 2015-06-20}}</ref>
| | **''ERCC1'' |
| | | **''[[ERCC2]]'' |
| Germ-line (inherited) polymorphisms of the DNA repair genes ''[[ERCC1]]'', ''[[ERCC2]]'' (''XPD'') and ''[[XRCC1]]'' increase the risk of glioma.<ref name="pmid24500421">{{cite journal |author=Adel Fahmideh M, Schwartzbaum J, Frumento P, Feychting M |title=Association between DNA repair gene polymorphisms and risk of glioma: A systematic review and meta-analysis |journal=Neuro-oncology |volume=16 |issue=6 |pages=807–14 |date=June 2014 |pmid=24500421 |doi=10.1093/neuonc/nou003 |url=http://neuro-oncology.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=24500421}}</ref> This indicates that altered or deficient repair of DNA damage contributes to the formation of gliomas. DNA damages are a likely major primary cause of progression to cancer in general.<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 />
| | **''[[XRCC1]]'' |
| | | **''MGMT'' |
| [[Cancer epigenetics|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 (genetics)|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> In addition, in some glioblastomas, the MGMT protein is deficient due to another type of epigenetic alteration. MGMT protein expression may also be reduced due to increased levels of a [[microRNA]] that inhibits the ability of the ''MGMT'' [[messenger RNA]] to produce the MGMT protein.<ref name=Spiegel /> Zhang et al.<ref name="pmid22570426">{{cite journal |author=Zhang W, Zhang J, Hoadley K, Kushwaha D, Ramakrishnan V, Li S, Kang C, You Y, Jiang C, Song SW, Jiang T, Chen CC |title=miR-181d: a predictive glioblastoma biomarker that downregulates MGMT expression |journal=Neuro-oncology |volume=14 |issue=6 |pages=712–9 |date=June 2012 |pmid=22570426 |pmc=3367855 |doi=10.1093/neuonc/nos089 |url=http://neuro-oncology.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=22570426}}</ref> found, in the glioblastomas without methylated ''MGMT'' [[Promoter (genetics)|promoters]], that the level of microRNA miR-181d is inversely correlated with protein expression of MGMT and that the direct target of miR-181d is the ''MGMT'' mRNA 3’UTR (the three prime untranslated region of ''MGMT'' messenger RNA). | | **''IDH1'' |
| | | **''[[IDH2]]'' |
| 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> For 17 of the 32 (53%) of the gliomas tested, ERCC1 protein expression was reduced or absent. In the case of 12 gliomas (37.5%) this reduction was due to methylation of the ''ERCC1'' promoter. For the other 5 gliomas with reduced ERCC1 protein expression, the reduction could have been due to epigenetic alterations in [[microRNA]]s that affect ''ERCC1'' expression.<ref name=Bernstein />
| | **''[[p53]]'' |
| | | **''[[EGFR]]'' |
| When expression of DNA repair genes is reduced, DNA damages accumulate in cells at a higher than normal level, and such excess damages cause increased frequencies of mutation.<ref name=Narayanan>{{cite journal | author = Narayanan L, Fritzell JA, Baker SM, Liskay RM, Glazer PM | title = Elevated levels of mutation in multiple tissues of mice deficient in the DNA mismatch repair gene Pms2 | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 94 | issue = 7 | pages = 3122–7 |date=April 1997 | pmid = 9096356 | pmc = 20332 | doi = 10.1073/pnas.94.7.3122 }}</ref><ref name=Hegan>{{cite journal | author = Hegan DC, Narayanan L, Jirik FR, Edelmann W, Liskay RM, Glazer PM | title = Differing patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6 | journal = Carcinogenesis | volume = 27 | issue = 12 | pages = 2402–8 |date=December 2006 | pmid = 16728433 | pmc = 2612936 | doi = 10.1093/carcin/bgl079 }}</ref><ref name=Tutt>{{cite journal | author = Tutt AN, van Oostrom CT, Ross GM, van Steeg H, Ashworth A | title = Disruption of Brca2 increases the spontaneous mutation rate in vivo: synergism with ionizing radiation | journal = EMBO Rep. | volume = 3 | issue = 3 | pages = 255–60 |date=March 2002 | pmid = 11850397 | pmc = 1084010 | doi = 10.1093/embo-reports/kvf037 }}</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> Wang et al.<ref name="pmid22824796">{{cite journal |author=Wang P, Dong Q, Zhang C, Kuan PF, Liu Y, Jeck WR, Andersen JB, Jiang W, Savich GL, Tan TX, Auman JT, Hoskins JM, Misher AD, Moser CD, Yourstone SM, Kim JW, Cibulskis K, Getz G, Hunt HV, Thorgeirsson SS, Roberts LR, Ye D, Guan KL, Xiong Y, Qin LX, Chiang DY |title=Mutations in isocitrate dehydrogenase 1 and 2 occur frequently in intrahepatic cholangiocarcinomas and share hypermethylation targets with glioblastomas |journal=Oncogene |volume=32 |issue=25 |pages=3091–100 |date=June 2013 |pmid=22824796 |pmc=3500578 |doi=10.1038/onc.2012.315 |url=http://dx.doi.org/10.1038/onc.2012.315}}</ref> pointed out that ''IDH1'' and ''IDH2'' mutant cells produce an excess metabolic intermediate, 2-hydroxyglutarate, which binds to catalytic sites in key enzymes that are important in altering [[histone]] and DNA [[Promoter (genetics)|promoter]] methylation. Thus, mutations in ''IDH1'' and ''IDH2'' generate a “DNA CpG island methylator phenotype or CIMP”<ref name="pmid10411935">{{cite journal |author=Toyota M, Ahuja N, Ohe-Toyota M, Herman JG, Baylin SB, Issa JP |title=CpG island methylator phenotype in colorectal cancer |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=96 |issue=15 |pages=8681–6 |date=July 1999 |pmid=10411935 |pmc=17576 |doi= 10.1073/pnas.96.15.8681|url=http://www.pnas.org/cgi/pmidlookup?view=long&pmid=10411935}}</ref><ref name="pmid24834258">{{cite journal |author=Mojarad EN, Kuppen PJ, Aghdaei HA, Zali MR |title=The CpG island methylator phenotype (CIMP) in colorectal cancer |journal=Gastroenterol Hepatol Bed Bench |volume=6 |issue=3 |pages=120–128 |year=2013 |pmid=24834258 |pmc=4017514 |doi= |url=}}</ref> that causes promoter hypermethylation and concomitant silencing of tumor suppressor genes such as DNA repair genes ''MGMT'' and ''ERCC1''. On the other hand, Cohen et al.<ref name=Cohen /> pointed out that mutations in ''IDH1'' or ''IDH2'' can cause increased oxidative stress. Increased oxidative damage to DNA could be mutagenic. Thus, ''IDH1'' or ''IDH2'' mutations act as driver mutations in glioma carcinogenesis, though it is not clear by which role they are primarily acting. A study, involving 51 patients with brain gliomas who had two or more biopsies over time, showed that mutation in the ''IDH1'' gene occurred prior to the occurrence of a ''p53'' mutation or a 1p/19q loss of heterozygosity, indicating that an ''IDH1'' mutation is an early driver mutation.<ref name="pmid19246647">{{cite journal |author=Watanabe T, Nobusawa S, Kleihues P, Ohgaki H |title=IDH1 mutations are early events in the development of astrocytomas and oligodendrogliomas |journal=Am. J. Pathol. |volume=174 |issue=4 |pages=1149–53 |date=April 2009 |pmid=19246647 |pmc=2671348 |doi=10.2353/ajpath.2009.080958 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9440(10)60974-1}}</ref>
| | **''[[TSC1]]'' |
| | **''[[TSC2]]'' |
| | **''[[RB1]]'' |
| | **''[[APC]]'' |
| | **''hMLH1'' |
| | **''hMSH2'' |
| | **''[[PMS2]]'' |
| | **''[[PTEN]]'' |
| | **''[[NF1]]'' |
| | **''NF2'' |
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| ==References== | | ==References== |
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