CpG island methylator phenotype underlies sporadic microsatellite instability and is tightly associated with BRAF mutation in colorectal cancer

By D. Weisenberger, K. Siegmund, Mihaela Campan, Joanne P Young, T. Long, M. Faasse, G. Kang, M. Widschwendter, D. Weener, D. Buchanan and 11 more. Nature Genetics, 2006

2,015 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/5dd5569317dce11237e3cbb3463e5c14208a0241

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In Molecular Biology

1. Manel Esteller
2. Peter A. Jones
3. S. Baylin
4. Peter W. Laird
5. Bradley E. Bernstein
6. Hui Shen
7. Alexander Meissner
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In Oncology

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In Pathology and Forensic Medicine

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4. Peter A. Jones
5. S. Baylin
6. D. Hanahan

Citations in the corpus

• Epigenetics and Colorectal Cancer (2011, result): “The panel of genes for defining CIMP still remains to be standardized, thus the criteria used to identify CIMP tumors can vary across studies, which makes generalizing results across studies difficult”
• Colorectal carcinoma: Pathologic aspects. (2012, background): “Third, BRAF mutation is almost exclusively seen in sporadic MSI tumors that are presumed to develop through the serrated tumorigenic pathway, but has never been reported in Lynch syndrome (138).”
• CLONAL EVOLUTION IN CANCER (2012, background): “and between different types of abnormality (for example, single-base sequence changes versus balanced chromosomal rearrangements and gene fusions), and mutation rates will increase by the instigation of genetic instabilit”
• Colorectal Carcinoma: A General Overview and Future Perspectives in Colorectal Cancer (2017, background): “One example of the combined effect of genetics and epigenetics in the colorectal cancer development process is the presence of BRAF mutations as well as microsatellite instability in many CIMP tumours [30].”
• CpG island methylator phenotype, microsatellite instability, BRAF mutation and clinical outcome in colon cancer (2008, methodology): “Among patients who do not manifest hereditary nonpolyposis colorectal cancer (HNPCC), MSI-high is often the consequence of promoter methylation (and subsequent silencing) of MLH1, a DNA mismatch repair gene.[8] In fact, CIMP and BRAF tests are used to exclude HNPCC among patients who exhibit MSI-hig”
• The epigenomics of cancer. (2007, neutral): “The existence of CIMP has been challenged (Yamashita et al., 2003), but recent studies by Weisenberger et al. (2006) showing that a subset of CpG islands is coordinately methylated in tumors argues, in our opinion, for the reality of such a phenotype.”
• The Consensus Molecular Subtypes of Colorectal Cancer (2015, methodology): “is supported by grants from the Dutch Cancer Society (UVA2011-4969, UVA2014-7245), Worldwide Cancer Research (14-1164), the Maag Lever Darm Stichting (MLDS-CDG 14-03) and the European Research Council (ERG-StG 638193).”
• Lessons from the cancer genome. (2013, neutral): “Most CRC-CIMP tumors show high microsatellite instability (MSI) (Ogino et al., 2006; Weisenberger et al., 2006); this is likely due to the fact that such tumors typically have hypermethylation (and hence repression) of the MLH locus, whose loss of expression results in MSI.”