Epigenetic gene silencing in cancer – a mechanism for early oncogenic pathway addiction?

By S. Baylin, Joyce Ohm. Nature Reviews. Cancer, 2006

1,708 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/1cb8e936cbd289b9ef3e704d2143b76d32617eef

How researchers see this paper

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In Molecular Biology

1. Peter A. Jones
2. S. Baylin
3. Manel Esteller
4. T. Kelly
5. J. You
6. Shikhar Sharma
7. D. Nguyen
8. Ricky W. Johnstone

Citations in the corpus

• MeInfoText: associated gene methylation and cancer information from text mining (2008, background): “In addition, the initiation of the process of abnormal promoter methylation may associate with chro-matin-remodelling complexes [5,9].”
• Epigenetics in cancer. (2010, background): “These pre-invasive immortal stem cells are selected for and then form a pool of abnormal precursor cells that can undergo further genetic mutations leading to tumorigenesis [4,125] .”
• Genetic determinants of cancer metastasis (2007, background): “One example is provided by the EZH2 component of the Polycomb complexes, which catalyse histone modifications and promote DNA methylation in mammalian stem cell”
• The epigenomics of cancer. (2007, background): “As recently reviewed (Baylin and Ohm, 2006), the increases in SIRT1 may prolong cell survival through multiple mechanisms, including downmodulation of p53 function through deacetylation of this target protein.”
• Cancer Genetics and Epigenetics: Two Sides of the Same Coin? (2012, background): “…Selection of Mutations in Key Signaling Pathways Direct evidence for a close epigenetic-genetic cooperation is apparent in the colon cancer cell line HCT116 in which one allele ofMLH1 and CDKN2A is genetically mutated, whereas the other allele is silenced by DNA methylation (Baylin and Ohm, 2006).”
• Mitf regulation of Dia1 controls melanoma proliferation and invasiveness. (2006, background): “These genetic lesions and stable epigenetic modifications, such as histone and DNA methylation, would be inherited by the metastatic progeny and dictate alterations in gene expression compatible with metastatic potential (for a review, see Baylin and Ohm 2006).”