Glioma causes

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

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.[1] Different oncogenes can cooperate in the development of gliomas.[2]

Gliomas have been correlated to the electromagnetic radiation from cell phones, and a link between the cancer and cell phone usage was considered possible,[3] though several large studies have found no conclusive evidence. Experiments designed to test such a link gave negative results.[4] Most glioblastomas are infected with cytomegalovirus, which speeds the development of tumors.[5][6][7] 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.[8][9] 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.[10] Most studies have found that pesticide exposure is probably not a cause of glioma, though a minority of studies have found an association.[10][11]

Germ-line (inherited) polymorphisms of the DNA repair genes ERCC1, ERCC2 (XPD) and XRCC1 increase the risk of glioma.[12] 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.[13] Excess DNA damages can give rise to mutations through translesion synthesis. Furthermore, incomplete DNA repair can give rise to epigenetic alterations or epimutations.[14][15] 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.[13]

Epigenetic repression of DNA repair genes is often found in progression to sporadic glioblastoma. For instance, methylation of the DNA repair gene MGMT promoter was observed in 51.3% to 66% of glioblastoma specimens.[16][17] 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.[17] Zhang et al.[18] found, in the glioblastomas without methylated MGMT 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).

Epigenetic reductions in expression of another DNA repair protein, ERCC1, were found in an assortment of 32 gliomas.[19] 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 microRNAs that affect ERCC1 expression.[13]

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.[20][21][22] 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.[23] Wang et al.[24] 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 methylation. Thus, mutations in IDH1 and IDH2 generate a “DNA CpG island methylator phenotype or CIMP”[25][26] 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.[23] 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.[27]

References

  1. ↑ 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. ↑ Radner H, El-Shabrawi Y, Eibl RH, Brüstle O, Kenner L, Kleihues P, Wiestler OD (1993). "Tumor induction by ras and myc oncogenes in fetal and neonatal brain: modulating effects of developmental stage and retroviral dose". Acta Neuropathologica. 86 (5): 456–465. doi:10.1007/bf00228580. PMID 8310796.
  3. ↑ "IARC classifies radiofrequency electromagnetic fields as possibly carcinogenic to humans" (PDF) (Press release). IARC. 31 May 2011.
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ 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.
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 10.0 10.1 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.
  11. ↑ "CDC - Women's Safety and Health Issues at Work: Job Area: Agriculture - NIOSH Workplace Safety and Health Topic". www.cdc.gov. Retrieved 2015-06-20.
  12. ↑ Adel Fahmideh M, Schwartzbaum J, Frumento P, Feychting M (June 2014). "Association between DNA repair gene polymorphisms and risk of glioma: A systematic review and meta-analysis". Neuro-oncology. 16 (6): 807–14. doi:10.1093/neuonc/nou003. PMID 24500421.
  13. ↑ 13.0 13.1 13.2 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
  14. ↑ 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.
  15. ↑ 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
  16. ↑ 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.
  17. ↑ 17.0 17.1 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.
  18. ↑ Zhang W, Zhang J, Hoadley K, Kushwaha D, Ramakrishnan V, Li S, Kang C, You Y, Jiang C, Song SW, Jiang T, Chen CC (June 2012). "miR-181d: a predictive glioblastoma biomarker that downregulates MGMT expression". Neuro-oncology. 14 (6): 712–9. doi:10.1093/neuonc/nos089. PMC 3367855. PMID 22570426.
  19. ↑ 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.
  20. ↑ Narayanan L, Fritzell JA, Baker SM, Liskay RM, Glazer PM (April 1997). "Elevated levels of mutation in multiple tissues of mice deficient in the DNA mismatch repair gene Pms2". Proc. Natl. Acad. Sci. U.S.A. 94 (7): 3122–7. doi:10.1073/pnas.94.7.3122. PMC 20332. PMID 9096356.
  21. ↑ Hegan DC, Narayanan L, Jirik FR, Edelmann W, Liskay RM, Glazer PM (December 2006). "Differing patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6". Carcinogenesis. 27 (12): 2402–8. doi:10.1093/carcin/bgl079. PMC 2612936. PMID 16728433.
  22. ↑ Tutt AN, van Oostrom CT, Ross GM, van Steeg H, Ashworth A (March 2002). "Disruption of Brca2 increases the spontaneous mutation rate in vivo: synergism with ionizing radiation". EMBO Rep. 3 (3): 255–60. doi:10.1093/embo-reports/kvf037. PMC 1084010. PMID 11850397.
  23. ↑ 23.0 23.1 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.
  24. ↑ 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 (June 2013). "Mutations in isocitrate dehydrogenase 1 and 2 occur frequently in intrahepatic cholangiocarcinomas and share hypermethylation targets with glioblastomas". Oncogene. 32 (25): 3091–100. doi:10.1038/onc.2012.315. PMC 3500578. PMID 22824796.
  25. ↑ Toyota M, Ahuja N, Ohe-Toyota M, Herman JG, Baylin SB, Issa JP (July 1999). "CpG island methylator phenotype in colorectal cancer". Proc. Natl. Acad. Sci. U.S.A. 96 (15): 8681–6. doi:10.1073/pnas.96.15.8681. PMC 17576. PMID 10411935.
  26. ↑ Mojarad EN, Kuppen PJ, Aghdaei HA, Zali MR (2013). "The CpG island methylator phenotype (CIMP) in colorectal cancer". Gastroenterol Hepatol Bed Bench. 6 (3): 120–128. PMC 4017514. PMID 24834258.
  27. ↑ Watanabe T, Nobusawa S, Kleihues P, Ohgaki H (April 2009). "IDH1 mutations are early events in the development of astrocytomas and oligodendrogliomas". Am. J. Pathol. 174 (4): 1149–53. doi:10.2353/ajpath.2009.080958. PMC 2671348. PMID 19246647.


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