Epigenetics in cancer.
By Shikhar Sharma, T. Kelly, Peter A. Jones. Carcinogenesis, 2010
4,700 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/d680aaf845f2d24ae6709fd209bb4edf58ef4cbd
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
Citations in the corpus
- The Behaviour of 5-Hydroxymethylcytosine in Bisulfite Sequencing (2010, background): “Changes in DNA methylation status are associated with X-inactivation, imprinting, and the development of primordial germ cells [2–5]; moreover, DNA methylation is highly aberrant in cancer [6–9].”
- DNMT3A Mutations in Acute Myeloid Leukemia (2010, background): “The PMLRARA fusion protein, which is created by t(15;17), physically interacts with DNMT3A, and AML-ETO, which is created by t(8;21), interacts with DNMT1; both fusion proteins alter the methylation of specific promoters.”
- microRNAs in cancer (2013, background): “Aberrant epigenetic changes, such as DNA hypermethylation of tumor-suppressor genes, extensive genomic DNA hypomethylation, and alteration of histone modification patterns, are well-known features of cancer cells (85).”
- Increased methylation variation in epigenetic domains across cancer types (2011, unknown): “Until now, cancer epigenetics has focused on high-density CpG islands, gene promoters, or dispersed repetitive elements 2,3 .”
- Cancer Genetics and Epigenetics: Two Sides of the Same Coin? (2012, background): “There are over 1,000 human miRNAs and, interestingly, these miRNAs frequently target regions related to cancer development (Ryan et al., 2010).”
- The Warburg Effect Dictates the Mechanism of Butyrate Mediated Histone Acetylation and Cell Proliferation (2012, background): “Chromosomal rearrangements that deregulate HATs are a common cause of leukemias (Yang, 2004), and promoter CpG hypermethylation (coupled with histone hypoacetylation) silences tumor-suppressor genes in leukemias and solid tumors (Esteller, 2008).”
- Child health, developmental plasticity, and epigenetic programming. (2011, background): “Poulsen P, Esteller M, Vaag A, Fraga MF 2007 The epigenetic basis of twin discordance in age-related diseases.”
- Mechanisms of diabetic complications. (2013, background): “Recently, these posttranslational modifications, such as DNA and histone methylation, have been suggested as contributors to diabetic complications (119, 489) since they regulate many cellular processes including proliferation, differentiation, and apoptosis in disease states such as cancer (470, 53”
- A decade of exploring the cancer epigenome — biological and translational implications (2011, background): “resulting in an emerging view of what may now be called 'the cancer epigenome', which harbours myriad abnormalities that are based on somatically heritable alterations that are not due to primary DNA sequence change”
- Genomic instability — an evolving hallmark of cancer (2010, background): “The mutation frequency may underestimate the frequency of gene inactivation because gene function can also be repressed by epigenetic mechanism”
- Fusobacterium nucleatum Promotes Chemoresistance to Colorectal Cancer by Modulating Autophagy (2017, unknown): “Siena, 2010; Dallas et al., 2009; Esteller, 2008; Linardou et al., 2008; Van Geelen et al., 2004; Weichert et al., 2008).”
- Epigenetic Determinants of Cancer. (2016, background): “The genes were easily recognized as classic TSGs, known to cause inherited forms of cancer when mutated in the germline of families (Jones and Laird 1999; Jones and Baylin 2002, 2007; Esteller 2008; Shen and Laird 2013).”