The fundamental role of epigenetic events in cancer

By Peter A. Jones, S. Baylin. Nature reviews genetics, 2002

5,833 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/34f5ca499d5d8541ac1ac12cef26364a79d31801

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In Molecular Biology

Citations in the corpus

Roles of the EZH2 histone methyltransferase in cancer epigenetics. (2008, background): “The most well-characterized alteration is pG DNA hypermethylation which often accumulates in promoter egions of tumor suppressor genes, thereby contributing to tumor uppressor loss through epigenetic silencing [1].”
Cancer epigenetics. (2005, background): “It is now realized that CpG island hypermethylation is just one facet of an integrated change in chromatin structure and in histone modifications (10,11), including histone H3 and H4 deacetylation (12), histone H3 lysine 9 methylation (13), histone H4 sumoylation (14) and reduced histone H3 lysine 4”
Epigenetics in human disease and prospects for epigenetic therapy (2004, background): “Aberrant de novo methylation of CpG islands is a hallmark of human cancers and is found early during carcinogenesi”
Improved classification of breast cancer by analysis of genetic alterations and gene expression profiling (2011, background): “Differences in gene expression between breast tumor samples can be considered to be the result of genetic (10, 11) and/or epigenetic changes (12).”
The epigenetic progenitor origin of human cancer (2006, background): “In addition, the silencing of tumour-suppressor genes is associated with promoter DNA hypermethylation and chromatin hypoacetylation, which affect diverse genes such as retinoblastoma 1 ( RB1 ), p16 (also known as cyclin-dependent kinase inhibitor 2A ( CDKN2A )), von Hippel–Lindau tumour suppr”
Analysis of repetitive element DNA methylation by MethyLight (2005, background): “Most CpG islands overlap the 50 end of gene regions, including promoters, and are typically unmethylated in normal somatic tissues (4,5).”
The epigenomics of cancer. (2007, background): “The importance of DNA methylation in cancer has been established (Jones and Baylin, 2002; Jones and Laird, 1999), and the focus in the field is changing to include the mechanisms by which other chromatin modifications play a role in cancer development (Figure 1).”
Results of a randomized study of 3 schedules of low-dose decitabine in higher-risk myelodysplastic syndrome and chronic myelomonocytic leukemia. (2007, methodology): “Eligibility criteria included (1) age 16 years or older; (2) diagnosis of MDS with International Prognostic Scoring System (IPSS) intermediate or high risk, or diagnosis of CMML; (3) normal organ functions including creatinine 176.”
Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “Human cancers often exhibit characteristic changes in DNA methylation, including genome-wide hypomethylation and site-specific hypermethylation (Jones and Baylin, 2002; Feinberg and Tycko, 2004).”
A stem cell–like chromatin pattern may predispose tumor suppressor genes to DNA hypermethylation and heritable silencing (2007, background): “Epigenetic modulation of gene expression is essential for normal function of these early cells but is highly abnormal in cancers, which often show aberrant promoter CpG island hypermethylation and transcriptional silencing of tumor suppressor genes and pro-differentiation factor”
DNA methylation and gene silencing in cancer (2005, background): “When DNA is methylated in the promoter region of genes, where transcription is initiated, genes are inactivated and silenced”
Regulation of CXCR4 signaling. (2007, background): “One example is DNA methylation, a modification typically associated with inactivation of tumor suppressors [173].”