Literature DB >> 33588926

Genetic and environmental determinants of O6-methylguanine DNA-methyltransferase (MGMT) gene methylation: a 10-year longitudinal study of Danish twins.

Lijie Wang1,2, Afsaneh Mohammadnejad1, Weilong Li1,3, Jesper Lund1,4, Shuxia Li1, Signe Clemmensen1, Maria Timofeeva1, Mette Soerensen1, Jonas Mengel-From1, Kaare Christensen1,5, Jacob Hjelmborg1, Qihua Tan6,7.   

Abstract

BACKGROUND: Epigenetic inactivation of O6-methylguanine DNA-methyltransferase (MGMT) is associated with increased sensitivity to alkylating chemotherapeutic agents in glioblastoma patients. The genetic background underlying MGMT gene methylation may explain individual differences in treatment response and provide a clue to a personalized treatment strategy. Making use of the longitudinal twin design, we aimed, for the first time, to estimate the genetic contributions to MGMT methylation in a Danish twin cohort.
METHODS: DNA-methylation from whole blood (18 monozygotic (MZ) and 25 dizygotic (DZ) twin pairs) repeated 10 years apart from the Longitudinal Study of Aging Danish Twins (LSADT) were used to search for genetic and environmental contributions to DNA-methylation at 170 CpG sites of across the MGMT gene. Both univariate and bivariate twin models were applied. The intraclass correlations, performed on cross-sectional data (246 MZ twin pairs) from an independent study population, the Middle-Aged Danish Twins (MADT), were used to assess the genetic influence at each CpG site of MGMT for replication.
RESULTS: Univariate twin model revealed twelve CpG sites showing significantly high heritability at intake (wave 1, h2 > 0.43), and seven CpG sites with significant heritability estimates at end of follow-up (wave 2, h2 > 0.5). There were six significant CpG sites, located at the gene body region, that overlapped among the two waves (h2 > 0.5), of which five remained significant in the bivariate twin model, which was applied to both waves. Within MZ pair correlation in these six CpGs from MADT demarks top level of genetic influence. There were 11 CpGs constantly have substantial common environmental component over the 10 years.
CONCLUSIONS: We have identified 6 CpG sites linked to the MGMT gene with strong and persistent genetic control based on their DNA methylation levels. The genetic basis of MGMT gene methylation could help to explain individual differences in glioblastoma treatment response and most importantly, provide references for mapping the methylation Quantitative Trait Loci (meQTL) underlying the genetic regulation.

Entities:  

Keywords:  CpG site; DNA methylation; Glioma; Heritability; MGMT; Twin models

Mesh:

Substances:

Year:  2021        PMID: 33588926      PMCID: PMC7885436          DOI: 10.1186/s13148-021-01009-5

Source DB:  PubMed          Journal:  Clin Epigenetics        ISSN: 1868-7075            Impact factor:   6.551


  48 in total

1.  A Danish population-based twin study on general health in the elderly.

Authors:  K Christensen; N V Holm; M McGue; L Corder; J W Vaupel
Journal:  J Aging Health       Date:  1999-02

Review 2.  MGMT: its role in cancer aetiology and cancer therapeutics.

Authors:  Stanton L Gerson
Journal:  Nat Rev Cancer       Date:  2004-04       Impact factor: 60.716

3.  Genome-wide evolutionary analysis of eukaryotic DNA methylation.

Authors:  Assaf Zemach; Ivy E McDaniel; Pedro Silva; Daniel Zilberman
Journal:  Science       Date:  2010-04-15       Impact factor: 47.728

Review 4.  Twin methodology in epigenetic studies.

Authors:  Qihua Tan; Lene Christiansen; Jacob von Bornemann Hjelmborg; Kaare Christensen
Journal:  J Exp Biol       Date:  2015-01-01       Impact factor: 3.312

5.  The MGMT promoter SNP rs16906252 is a risk factor for MGMT methylation in glioblastoma and is predictive of response to temozolomide.

Authors:  Robert W Rapkins; Fan Wang; HuyTram N Nguyen; Timothy F Cloughesy; Albert Lai; Wendy Ha; Anna K Nowak; Megan P Hitchins; Kerrie L McDonald
Journal:  Neuro Oncol       Date:  2015-04-24       Impact factor: 12.300

6.  Detection of MGMT promoter methylation in normal individuals is strongly associated with the T allele of the rs16906252 MGMT promoter single nucleotide polymorphism.

Authors:  Ida L M Candiloro; Alexander Dobrovic
Journal:  Cancer Prev Res (Phila)       Date:  2009-09-29

7.  Relevance of MSP assay for the detection of MGMT promoter hypermethylation in glioblastomas.

Authors:  Kazunari Yachi; Takao Watanabe; Takashi Ohta; Takao Fukushima; Atsuo Yoshino; Akiyoshi Ogino; Yoichi Katayama; Hiroki Nagase
Journal:  Int J Oncol       Date:  2008-09       Impact factor: 5.650

8.  Optimization of quantitative MGMT promoter methylation analysis using pyrosequencing and combined bisulfite restriction analysis.

Authors:  Thomas Mikeska; Christoph Bock; Osman El-Maarri; Anika Hübner; Denise Ehrentraut; Johannes Schramm; Jörg Felsberg; Philip Kahl; Reinhard Büttner; Torsten Pietsch; Andreas Waha
Journal:  J Mol Diagn       Date:  2007-07       Impact factor: 5.568

9.  Extent of MGMT promoter methylation correlates with outcome in glioblastomas given temozolomide and radiotherapy.

Authors:  J Dunn; A Baborie; F Alam; K Joyce; M Moxham; R Sibson; D Crooks; D Husband; A Shenoy; A Brodbelt; H Wong; T Liloglou; B Haylock; C Walker
Journal:  Br J Cancer       Date:  2009-06-16       Impact factor: 7.640

10.  DNA methylation arrays as surrogate measures of cell mixture distribution.

Authors:  Eugene Andres Houseman; William P Accomando; Devin C Koestler; Brock C Christensen; Carmen J Marsit; Heather H Nelson; John K Wiencke; Karl T Kelsey
Journal:  BMC Bioinformatics       Date:  2012-05-08       Impact factor: 3.169

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  1 in total

1.  Prognostic value of O 6-methylguanine-DNA methyltransferase methylation in isocitrate dehydrogenase mutant gliomas.

Authors:  Keng Lam; Blaine S C Eldred; Bryan Kevan; Sean Pianka; Brittany A Eldred; Serendipity Zapanta Rinonos; William H Yong; Linda M Liau; Phioanh L Nghiemphu; Timothy F Cloughesy; Richard M Green; Albert Lai
Journal:  Neurooncol Adv       Date:  2022-03-01
  1 in total

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