Glioma causes: Difference between revisions
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==Overview== | ==Overview== | ||
==Causes== | ==Causes== | ||
* Genetic factors | * 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> | :* [[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> | ||
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::* 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> | ::* 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> | ::* 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> | ||
* [[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> | |||
* [[ | |||
==References== | ==References== |
Revision as of 19:22, 21 August 2015
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Causes
- 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]
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.
- ↑ 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.