|
|
| (13 intermediate revisions by 3 users not shown) |
| Line 1: |
Line 1: |
| __NOTOC__ | | __NOTOC__ |
| {{Glioma}} | | {{Glioma}} |
| | | {{CMG}}{{AE}}{{SR}} |
| {{CMG}} | |
|
| |
|
| ==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== |
| * Genetic factors | | *Common causes of glioma include genetic mutations. |
| :* [[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>
| | *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> |
| :* 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 /> | | **''ERCC1'' |
| | | **''[[ERCC2]]'' |
| ::* 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>
| | **''[[XRCC1]]'' |
| ::* 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>
| | **''MGMT'' |
| ::* 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>
| | **''IDH1'' |
|
| | **''[[IDH2]]'' |
| * [[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> | | **''[[p53]]'' |
| | **''[[EGFR]]'' |
| | **''[[TSC1]]'' |
| | **''[[TSC2]]'' |
| | **''[[RB1]]'' |
| | **''[[APC]]'' |
| | **''hMLH1'' |
| | **''hMSH2'' |
| | **''[[PMS2]]'' |
| | **''[[PTEN]]'' |
| | **''[[NF1]]'' |
| | **''NF2'' |
|
| |
|
| ==References== | | ==References== |
| Line 24: |
Line 35: |
| [[Category:Types of cancer]] | | [[Category:Types of cancer]] |
| [[Category:Neurosurgery]] | | [[Category:Neurosurgery]] |
| [[Category:Oncology]]
| |
| [[Category:Needs content]]
| |
|
| |
|
| {{WikiDoc Help Menu}} | | {{WikiDoc Help Menu}} |
| {{WikiDoc Sources}} | | {{WikiDoc Sources}} |
| | [[Category:Up-To-Date]] |
| | [[Category:Oncology]] |
| | [[Category:Medicine]] |
| | [[Category:Neurology]] |
| | [[Category:Neurosurgery]] |