MGMT methylation analysis of glioblastoma on the Infinium methylation BeadChip identifies two distinct CpG regions associated with gene silencing and outcome, yielding a prediction model for comparisons across datasets, tumor grades, and CIMP-status

[1]  G. Reifenberger,et al.  Predictive impact of MGMT promoter methylation in glioblastoma of the elderly , 2012, International journal of cancer.

[2]  Didier Frappaz,et al.  Temozolomide versus standard 6-week radiotherapy versus hypofractionated radiotherapy in patients older than 60 years with glioblastoma: the Nordic randomised, phase 3 trial. , 2012, The Lancet. Oncology.

[3]  G. Reifenberger,et al.  Temozolomide chemotherapy alone versus radiotherapy alone for malignant astrocytoma in the elderly: the NOA-08 randomised, phase 3 trial. , 2012, The Lancet. Oncology.

[4]  R. Mirimanoff,et al.  Presence of an oligodendroglioma-like component in newly diagnosed glioblastoma identifies a pathogenetically heterogeneous subgroup and lacks prognostic value: central pathology review of the EORTC_26981/NCIC_CE.3 trial , 2012, Acta Neuropathologica.

[5]  Ferenc A. Jolesz,et al.  Radiogenomic Mapping of Edema/Cellular Invasion MRI-Phenotypes in Glioblastoma Multiforme , 2011, PloS one.

[6]  Pieter Wesseling,et al.  A Hypermethylated Phenotype Is a Better Predictor of Survival than MGMT Methylation in Anaplastic Oligodendroglial Brain Tumors: A Report from EORTC Study 26951 , 2011, Clinical Cancer Research.

[7]  G. Reifenberger,et al.  Promoter methylation and expression of MGMT and the DNA mismatch repair genes MLH1, MSH2, MSH6 and PMS2 in paired primary and recurrent glioblastomas , 2011, International journal of cancer.

[8]  E. Domany,et al.  The Wnt inhibitory factor 1 (WIF1) is targeted in glioblastoma and has a tumor suppressing function potentially by induction of senescence. , 2011, Neuro-oncology.

[9]  K. Aldape,et al.  RTOG 0525: A randomized phase III trial comparing standard adjuvant temozolomide (TMZ) with a dose-dense (dd) schedule in newly diagnosed glioblastoma (GBM). , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[10]  J. Herman,et al.  Analysis of Promoter CpG Island Hypermethylation in Cancer: Location, Location, Location! , 2011, Clinical Cancer Research.

[11]  D. Pearson,et al.  A distinct region of the MGMT CpG island critical for transcriptional regulation is preferentially methylated in glioblastoma cells and xenografts , 2011, Acta Neuropathologica.

[12]  T. Ryken,et al.  Comprehensive Analysis of MGMT Promoter Methylation: Correlation with MGMT Expression and Clinical Response in GBM , 2011, PloS one.

[13]  J. Licht,et al.  Leukemic IDH1 and IDH2 mutations result in a hypermethylation phenotype, disrupt TET2 function, and impair hematopoietic differentiation. , 2010, Cancer cell.

[14]  J. Mosser,et al.  DNA methylation in glioblastoma: impact on gene expression and clinical outcome , 2010, BMC Genomics.

[15]  Xiao Zhang,et al.  Comparison of Beta-value and M-value methods for quantifying methylation levels by microarray analysis , 2010, BMC Bioinformatics.

[16]  R. Stupp,et al.  Extent and Patterns of MGMT Promoter Methylation in Glioblastoma- and Respective Glioblastoma-Derived Spheres , 2010, Clinical Cancer Research.

[17]  R. Stupp,et al.  Cilengitide in newly diagnosed glioblastoma with MGMT promoter methylation: Protocol of a multicenter, randomized, open-label, controlled phase III trial (CENTRIC). , 2010 .

[18]  R. Wilson,et al.  Identification of a CpG island methylator phenotype that defines a distinct subgroup of glioma. , 2010, Cancer cell.

[19]  R. Gilbertson,et al.  To infinium, and beyond! , 2010, Cancer cell.

[20]  S. Gabriel,et al.  Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1. , 2010, Cancer cell.

[21]  M. J. van den Bent,et al.  MGMT promoter methylation is prognostic but not predictive for outcome to adjuvant PCV chemotherapy in anaplastic oligodendroglial tumors: a report from EORTC Brain Tumor Group Study 26951. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[22]  G. Reifenberger,et al.  NOA-04 randomized phase III trial of sequential radiochemotherapy of anaplastic glioma with procarbazine, lomustine, and vincristine or temozolomide. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[23]  K. Hoang-Xuan,et al.  Identification of regions correlating MGMT promoter methylation and gene expression in glioblastomas. , 2009, Neuro-oncology.

[24]  R. Mirimanoff,et al.  Effects of radiotherapy with concomitant and adjuvant temozolomide versus radiotherapy alone on survival in glioblastoma in a randomised phase III study: 5-year analysis of the EORTC-NCIC trial. , 2009, The Lancet. Oncology.

[25]  J. Herman,et al.  Correlation of O6-methylguanine methyltransferase (MGMT) promoter methylation with clinical outcomes in glioblastoma and clinical strategies to modulate MGMT activity. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[26]  M. Delorenzi,et al.  Validation of real-time methylation-specific PCR to determine O6-methylguanine-DNA methyltransferase gene promoter methylation in glioma. , 2008, The Journal of molecular diagnostics : JMD.

[27]  E. Domany,et al.  Stem cell-related "self-renewal" signature and high epidermal growth factor receptor expression associated with resistance to concomitant chemoradiotherapy in glioblastoma. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[28]  C. Gallagher.  Extending the Linear Model With R: Generalized Linear, Mixed Effects and Nonparametric Regression Models , 2007 .

[29]  K. Hoang-Xuan,et al.  MGMT prognostic impact on glioblastoma is dependent on therapeutic modalities , 2007, Journal of Neuro-Oncology.

[30]  J. Faraway.  Extending the Linear Model with R: Generalized Linear, Mixed Effects and Nonparametric Regression Models , 2005 .

[31]  R. Mirimanoff,et al.  MGMT gene silencing and benefit from temozolomide in glioblastoma. , 2005, The New England journal of medicine.

[32]  Martin J. van den Bent,et al.  Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. , 2005, The New England journal of medicine.

[33]  J. Issa.  CpG island methylator phenotype in cancer , 2004, Nature Reviews Cancer.

[34]  Luca Regli,et al.  Clinical Trial Substantiates the Predictive Value of O-6-Methylguanine-DNA Methyltransferase Promoter Methylation in Glioblastoma Patients Treated with Temozolomide , 2004, Clinical Cancer Research.

[35]  M. Emi,et al.  Silencing effect of CpG island hypermethylation and histone modifications on O6-methylguanine-DNA methyltransferase (MGMT) gene expression in human cancer , 2003, Oncogene.

[36]  V. Muggeo.  Estimating regression models with unknown break‐points , 2003, Statistics in medicine.

[37]  David R. Anderson,et al.  Model selection and multimodel inference : a practical information-theoretic approach , 2003 .

[38]  Christina Gloeckner,et al.  Modern Applied Statistics With S , 2003 .

[39]  Eric R. Ziegel,et al.  Generalized Linear Models , 2002, Technometrics.

[40]  Reto Meuli,et al.  Promising survival for patients with newly diagnosed glioblastoma multiforme treated with concomitant radiation plus temozolomide followed by adjuvant temozolomide. , 2002, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[41]  Frank E. Harrell,et al.  Regression Modeling Strategies: With Applications to Linear Models, Logistic Regression, and Survival Analysis , 2001 .

[42]  Scar,et al.  Inactivation of the DNA-repair gene MGMT and the clinical response of gliomas to alkylating agents. , 2000, The New England journal of medicine.

[43]  B. Kaina,et al.  Apoptosis induced by DNA damage O6-methylguanine is Bcl-2 and caspase-9/3 regulated and Fas/caspase-8 independent. , 2000, Cancer research.

[44]  J. Herman,et al.  CpG island methylator phenotype in colorectal cancer. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[45]  J. Herman,et al.  Inactivation of the DNA repair gene O6-methylguanine-DNA methyltransferase by promoter hypermethylation is a common event in primary human neoplasia. , 1999, Cancer research.

[46]  D. Hosmer,et al.  Applied Logistic Regression , 1991 .

[47]  P. Potter,et al.  Characterization of the promoter region of the human O6-methylguanine-DNA methyltransferase gene. , 1991, Nucleic acids research.

[48]  D. Collett.  Modelling Binary Data , 1991 .

[49]  W. Patefield,et al.  An Efficient Method of Generating Random R × C Tables with Given Row and Column Totals , 1981 .

[50]  R Core Team,et al.  R: A language and environment for statistical computing. , 2014 .

[51]  P. Laird,et al.  Genome-scale analysis of aberrant DNA methylation in colorectal cancer. , 2012, Genome research.

[52]  J. Uhm.  IDH1 mutation is sufficient to establish the glioma hypermethylator phenotype , 2012 .

[53]  G. Reifenberger,et al.  MGMT promoter methylation in malignant gliomas: ready for personalized medicine? , 2010, Nature Reviews Neurology.

[54]  Amy E. Hawkins,et al.  Comprehensive genomic characterization defines human glioblastoma genes and core pathways , 2009 .