Loss of acetylation at Lys16 and trimethylation at Lys20 of histone H4 is a common hallmark of human cancer
By M. Fraga, Esteban Ballestar, A. Villar‐Garea, M. Boix-Chornet, J. Espada, Gunnar Schotta, T. Bonaldi, Claire E Haydon, S. Ropero, K. Petrie and 13 more. Nature Genetics, 2005
1,906 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/2af9281dd2608feff4a73a188036e2e3a57fdfe6
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Citations in the corpus
- Histone acetyltransferase complexes: one size doesn't fit all (2007, background): “First, a global loss of H4K16 acetylation has been linked to tumorigenesi”
- DNA hypomethylation and human diseases. (2007, background): “In addition to genome wide DNA methylation changes Fraga and coworkers [155] examined changes in histone modification in cancer cell lines and primary tumors; they found significant”
- DNA methyltransferases control telomere length and telomere recombination in mammalian cells (2006, background): “It is worth noting that the observation of subtelomeric DNA hypomethylation associated with elongated telomeres in mouse DNMT-deficient cells resembles the observed hypomethylation of subtelomeric DNA sequences in some, but not all human cancer cell”
- Human HDAC1 and HDAC2 function in the DNA-damage response to promote DNA non-homologous end-joining (2010, positive): “, possibly to promote effective DNA repair by regulating histone acetylations, including H4K16A”
- Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “Similarly, the loss of histone 4 lysine 16 acetylation or histone 4 lysine 20 trimethylation is a common hallmark of human cancers (Fraga et al., 2005).”
- DNA methylation and histone modifications: teaming up to silence genes. (2005, background): “Recent evidence indicates that loss of H4K20me3 at constitutive heterochromatin in certain cancer cells, possibly involving the Suv4–20h enzymes, is associated with hypomethylation of DNA at these sequences [36 ].”
- Histone Modifications and Cancer. (2016, background): “The presence of H4K20me3, accompanied by the loss of H4K16 acetylation, constitutes a common H4 cancer “epigenetic signature” predominantly at DNA repetitive sequences (Fraga et al. 2005).”
- Reversal of histone lysine trimethylation by the JMJD2 family of histone demethylases. (2006, background): “Such a hypothesis is also supported by the recent studies that implicate histone methylation regulation in tumorigenesis (Canaani et al., 2004; Fraga et al., 2005; Hess, 2004b; Jaju et al., 2001; Pogribny et al., 2006).”
- Chromatin replication and epigenome maintenance (2012, background): “The chromatin changes that are observed in cancer include loss of H4K16ac and H4K20me3 over repetitive region”
- Combination therapy in combating cancer (2017, background): “Consequently, HDACi are able to effectively inhibit the invasiveness and aggressiveness of cancer phenotypes that express this Lys16 mutation amongst other HDAC mutations [97].”
- The role of histone deacetylases (HDACs) in human cancer (2007, background): “Moreover, these changes occur early in tumorogenesis, as shown by the data from a mouse model of multistage skin cancer tumorogenesis, which indicates that the global loss of monoacetylated and trimethylated forms of histone H4 is a crucial event in cancer development (Fraga et al., 2005).”
- Pharmacologic disruption of Polycomb-repressive complex 2-mediated gene repression selectively induces apoptosis in cancer cells. (2007, background): “These alterations include both DNA hypermethylation and chromatin modifications such as histone methylation and deacetylation (Jones and Baylin 2002; Feinberg and Tycko 2004; Fraga et al. 2005; Baylin and Ohm 2006).”
- Roles of the EZH2 histone methyltransferase in cancer epigenetics. (2008, background): “Particular global paterns of acetylation and methylation of histones H3 and H4 are ssociated with multiple cancer types and, in the case of prostate ancer, these modification patterns distinguish disease subtypes nd can predict patient outcome [9,10].”
- The world of protein acetylation. (2016, background): “Loss of acetylation at K16 of H4 was found to be present in several humanneoplasms, implicating it as a hallmark for cancer [386].”
- Sirtuins: critical regulators at the crossroads between cancer and aging (2007, background): “Importantly, loss of H4-K16 acetylation is a hallmark of human tumors (Fraga et al., 2005), and while this could be due to a loss of HAT association or function, it could also reflect overexpression of SIRT1 in tumors.”