Global histone modification patterns predict risk of prostate cancer recurrence
By D. Seligson, Steve Horvath, T. Shi, Hong Yu, S. Tze, M. Grunstein, S. Kurdistani. Nature, 2005
1,119 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/088c8b45e2b00ff25f836aab16f0d469b9cd94c5
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In Molecular Biology
- Peter A. Jones
- S. Baylin
- Manel Esteller
- D. Reinberg
- J. Simon
- Paul Tempst
- H. Erdjument‐Bromage
- Tony Kouzarides
In Oncology
- Ping Gao
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- Tony Kouzarides
- L. Zou
- Peter A. Jones
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- Huafeng Zhang
Citations in the corpus
- Cancer epigenetics: from mechanism to therapy. (2012, background): “Cell 150, July 6, 2012 ª2012 Elsevier Inc. 17 et al., 2005; Seligson et al., 2005 ), it is also well established that several nonhistone proteins, including many important oncogenes and tumor suppressors such as MYC, p53, and PTEN, are also dynamically acetylated (Choudhary et al., 2009).”
- Recognition of trimethylated histone H3 lysine 4 facilitates the recruitment of transcription postinitiation factors and pre-mRNA splicing. (2007, background): “Global changes in histone methylation and acetylation are associated with cancer and may serve as a predictive indicator of clinical outcome (Seligson et al., 2005).”
- Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “Low levels of histone 3 lysine 4 dimethylation are associated with poor prognosis for patients with prostate (Seligson et al., 2005; Bianco-Miotto et al., 2010), lung (Barlesi et al.”
- A chromatin-mediated reversible drug tolerant state in cancer cell subpopulations (2010, background): “Notably, reduced methylation of H3K4 has been linked to poor prognosis in cancer patients (Seligson et al., 2005).”
- The epigenomics of cancer. (2007, background): “Loss of acetylation at lysine 16 and trimethylation at lysine 20 of histone H4 is a common hallmark of human cancer (Fraga et al., 2005), and global histone modification patterns predict the risk of prostate cancer recurrence (Seligson et al., 2005).”
- Unsupervised Learning With Random Forest Predictors (2006, background): “It has been found that such clusters are clinically meaningful in tumor marker expression studies (Shi et al. 2005; Seligson et al. 2005).”
- Targeting epigenetic regulators for cancer therapy: mechanisms and advances in clinical trials (2019, background): “In tumor tissues, different tumor cells show various patterns of histone modification, genome-wide or in individual genes, indicating that epigenetic heterogeneity exists at a cellular level.(6) Likewise, using molecular biomarkers is thought to be a potential method to divide patients into differen”
- Histone methylation: a dynamic mark in health, disease and inheritance (2012, neutral): “KMT3B (NSD1, STO, SOTOS) H3K36 5q35 NUP98 t(5;11)(q35;p15.”
- 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].”
- Post-Translational Modifications That Drive Prostate Cancer Progression (2021, background): “Globally, hypoacetylation and excessive histone deacetylase activity in prostate cancer cells has been observed [293,294] and global histone modification patterns (acetylation and dimethylation in histones H3 and H4) predict progression, development and risk of prostate cancer recurrence [295,296].”