ArticleGut2007
Molecular correlates with MGMT promoter methylation and silencing support CpG island methylator phenotype-low (CIMP-low) in colorectal cancer.
Article in Gut, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 113 citations in OpenAlex.
- KRAS mutation in stage III colon cancer and clinical outcome following intergroup trial CALGB 89803.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Trial
- Impact of MGMT methylation on overall survival in solid tumors: A systematic review and meta-analysis.Experimental and therapeutic medicine · 2026Article
- High MGMT expression identifies aggressive colorectal cancer with distinct genomic features and immune evasion properties.Journal for immunotherapy of cancer · 2025Article
- Preliminary exploration of the effects of environmental factors on the microsatellite status of BRAF-mutated colorectal cancer.World journal of surgical oncology · 2023Article
- Interaction between Microsatellite Instability (MSI) and Tumor DNA Methylation in the Pathogenesis of Colorectal Carcinoma.Cancers · 2021Article
- Molecular subtypes of colorectal cancer: An emerging therapeutic opportunity for personalized medicine.Genes & diseases · 2021Review
- Molecular Features of the Serrated Pathway to Colorectal Cancer: Current Knowledge and Future Directions.Gut and liver · 2021Review
- Molecular Mechanisms of Colon Cancer Progression and Metastasis: Recent Insights and Advancements.International journal of molecular sciences · 2020Review
- An update on the morphology and molecular pathology of serrated colorectal polyps and associated carcinomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019Review
- Review
- A novel DNA methylation panel accurately detects colorectal cancer independently of molecular pathway.Journal of translational medicine · 2018Article
- Mapping clinicopathological entities within colorectal mucinous adenocarcinomas: a hierarchical clustering approach.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2017Article
- What influences preneoplastic colorectal lesion recurrence?Oncotarget · 2017Review
- Frequent CpG island methylation: a risk factor in the progression of traditional serrated adenoma of the colorectum.International journal of clinical and experimental pathology · 2017Article
- SNP rs16906252C>T Is an Expression and Methylation Quantitative Trait Locus Associated with an Increased Risk of Developing MGMT-Methylated Colorectal Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Molecular phenotypes of colorectal cancer and potential clinical applications.Gastroenterology report · 2015Review
- Diagnostic performance of fecal immunochemical test and sigmoidoscopy for advanced right-sided colorectal neoplasms.Digestive diseases and sciences · 2015Article
- Heterogeneous DNA methylation contributes to tumorigenesis through inducing the loss of coexpression connectivity in colorectal cancer.Genes, chromosomes & cancer · 2015Article
- Serrated polyps and their alternative pathway to the colorectal cancer: a systematic review.Gastroenterology research and practice · 2015Review
- Progress and opportunities in molecular pathological epidemiology of colorectal premalignant lesions.The American journal of gastroenterology · 2014Review
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThe CpG island methylator phenotype (CIMP or CIMP-high) with widespread promoter methylation is a distinct epigenetic phenotype in colorectal cancer. In contrast, a phenotype with less widespread promoter methylation (CIMP-low) has not been well characterised. O-6-methylguanine-DNA methyltransferase (MGMT) promoter methylation and silencing have been associated with G>A mutations and microsatellite instability-low (MSI-low).
aimTo examine molecular correlates with MGMT methylation/silencing in colorectal cancer.
methodsUtilising MethyLight technology, we quantified DNA methylation in MGMT and eight other markers (a CIMP-diagnostic panel; CACNA1G, CDKN2A (p16), CRABP1, IGF2, MLH1, NEUROG1, RUNX3 and SOCS1) in 920 population-based colorectal cancers.
resultsTumours with both MGMT methylation and loss were correlated positively with MSI-low (p = 0.02), CIMP-high (>or=6/8 methylated CIMP markers, p = 0.005), CIMP-low (1/8-5/8 methylated CIMP markers, p = 0.002, compared to CIMP-0 with 0/8 methylated markers), KRAS G>A mutation (p = 0.02), and inversely with 18q loss of heterozygosity (p = 0.0002). Tumours were classified into nine MSI/CIMP subtypes. Among the CIMP-low group, tumours with both MGMT methylation and loss were far more frequent in MSI-low tumours (67%, 12/18) than MSI-high tumours (5.6%, 1/18; p = 0.0003) and microsatellite stable (MSS) tumours (33%, 52/160; p = 0.008). However, no such relationship was observed among the CIMP-high or CIMP-0 groups.
conclusionThe relationship between MGMT methylation/silencing and MSI-low is limited to only CIMP-low tumours, supporting the suggestion that CIMP-low in colorectal cancer may be a different molecular phenotype from CIMP-high and CIMP-0. Our data support a molecular difference between MSI-low and MSS in colorectal cancer, and a possible link between CIMP-low, MSI-low, MGMT methylation/loss and KRAS mutation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.