Journal articles on the topic 'Epigenomics and epigenetics'
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Bunnik, Eline M., Marjolein Timmers, and Ineke LLE Bolt. "Ethical Issues in Research and Development of Epigenome-wide Technologies." Epigenetics Insights 13 (January 2020): 251686572091325. http://dx.doi.org/10.1177/2516865720913253.
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To date, few scholarly discussions on ethical implications of epigenetics and epigenomics technologies have focused on the current phase of research and development, in which researchers are confronted with real and practical ethical dilemmas. In this article, a responsible research and innovation approach, using interviews and an expert meeting, is applied to a case of epigenomic test development for cervical cancer screening. This article provides an overview of ethical issues presently facing epigenomics researchers and test developers, and discusses 3 sets of issues in depth: (1) informed consent; (2) communication with donors and/or research participants, and (3) privacy and publication of data and research results. Although these issues are familiar to research ethics, some aspects are new and most require reinterpretation in the context of epigenomics technologies. With this article, we aim to start a discussion of the practical ethical issues rising in research and development of epigenomic technologies and to offer guidance for researchers working in the field of epigenetic and epigenomic technology.
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Leite, Michel Lopes, and Fabricio F. Costa. "Epigenomics, epigenetics, and cancer*." Revista Pan-Amazônica de Saúde 8, no. 4 (November 2017): 23–25. http://dx.doi.org/10.5123/s2176-62232017000400006.
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Peedicayil, J. "Beyond Genomics: Epigenetics and Epigenomics." Clinical Pharmacology & Therapeutics 84, no. 1 (February 27, 2008): 25–26. http://dx.doi.org/10.1038/clpt.2008.26.
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Jirtle, Randy L. "The science of hope: an interview with Randy Jirtle." Epigenomics 14, no. 6 (March 2022): 299–302. http://dx.doi.org/10.2217/epi-2022-0048.
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In this interview, Professor Randy L Jirtle speaks with Storm Johnson, Commissioning Editor for Epigenomics, on his work on genomic imprinting, environmental epigenomics and the fetal origins of disease susceptibility. Professor Randy Jirtle joined the Duke University Department of Radiology in 1977 and headed the Epigenetics and Imprinting Laboratory until 2012. He is now Professor of Epigenetics in the Department of Biological Sciences at North Carolina State University, Raleigh, NC, USA. Jirtle's research interests are in epigenetics, genomic imprinting and the fetal origins of disease susceptibility. He is known for his groundbreaking studies linking environmental exposures early in life to the development of adult diseases through changes in the epigenome and for determining the evolutionary origin of genomic imprinting in mammals. He has published over 200 peer-reviewed articles as well as the books Liver Regeneration and Carcinogenesis: Molecular and Cellular Mechanisms, Environmental Epigenomics in Health and Disease: Epigenetics and Disease Origins and Environmental Epigenomics in Health and Disease: Epigenetics and Complex Diseases. He was honored in 2006 with the Distinguished Achievement Award from the College of Engineering at the University of Wisconsin-Madison. In 2007, he was a featured scientist on the NOVA television program on epigenetics titled ‘Ghost in Your Genes’ and was nominated for Time Magazine's ‘Person of the Year’. He was the inaugural recipient of the Epigenetic Medicine Award in 2008 and received the STARS Lecture Award in Nutrition and Cancer from the National Cancer Institute in 2009. Jirtle was presented the Linus Pauling Award from the Institute of Functional Medicine in 2014. In 2017, ShortCutsTV produced the English documentary ‘Are You What Your Mother Ate? The Agouti Mouse Study’ based on his pioneering epigenetic research. He received the 2018 Northern Communities Health Foundation Visiting Professorship Award at the University of Adelaide, Australia. The Personalized Lifestyle Medicine Institute presented Jirtle with the Research and Innovation Leadership Award in 2019. Dr Jirtle was also given the Alexander Hollaender Award in 2019 at the 50th annual meeting of the Environmental Mutagenesis and Genomics Society.
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Kim, Kyoung-Tae, Young-Seok Lee, and Inbo Han. "The Role of Epigenomics in Osteoporosis and Osteoporotic Vertebral Fracture." International Journal of Molecular Sciences 21, no. 24 (December 11, 2020): 9455. http://dx.doi.org/10.3390/ijms21249455.
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Osteoporosis is a complex multifactorial condition of the musculoskeletal system. Osteoporosis and osteoporotic vertebral fracture (OVF) are associated with high medical costs and can lead to poor quality of life. Genetic factors are important in determining bone mass and structure, as well as any predisposition for bone degradation and OVF. However, genetic factors are not enough to explain osteoporosis development and OVF occurrence. Epigenetics describes a mechanism for controlling gene expression and cellular processes without altering DNA sequences. The main mechanisms in epigenetics are DNA methylation, histone modifications, and non-coding RNAs (ncRNAs). Recently, alterations in epigenetic mechanisms and their activity have been associated with osteoporosis and OVF. Here, we review emerging evidence that epigenetics contributes to the machinery that can alter DNA structure, gene expression, and cellular differentiation during physiological and pathological bone remodeling. A progressive understanding of normal bone metabolism and the role of epigenetic mechanisms in multifactorial osteopathy can help us better understand the etiology of the disease and convert this information into clinical practice. A deep understanding of these mechanisms will help in properly coordinating future individual treatments of osteoporosis and OVF.
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Mladenov, Velimir, Vasileios Fotopoulos, Eirini Kaiserli, Erna Karalija, Stephane Maury, Miroslav Baranek, Na'ama Segal, et al. "Deciphering the Epigenetic Alphabet Involved in Transgenerational Stress Memory in Crops." International Journal of Molecular Sciences 22, no. 13 (July 1, 2021): 7118. http://dx.doi.org/10.3390/ijms22137118.
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Although epigenetic modifications have been intensely investigated over the last decade due to their role in crop adaptation to rapid climate change, it is unclear which epigenetic changes are heritable and therefore transmitted to their progeny. The identification of epigenetic marks that are transmitted to the next generations is of primary importance for their use in breeding and for the development of new cultivars with a broad-spectrum of tolerance/resistance to abiotic and biotic stresses. In this review, we discuss general aspects of plant responses to environmental stresses and provide an overview of recent findings on the role of transgenerational epigenetic modifications in crops. In addition, we take the opportunity to describe the aims of EPI-CATCH, an international COST action consortium composed by researchers from 28 countries. The aim of this COST action launched in 2020 is: (1) to define standardized pipelines and methods used in the study of epigenetic mechanisms in plants, (2) update, share, and exchange findings in epigenetic responses to environmental stresses in plants, (3) develop new concepts and frontiers in plant epigenetics and epigenomics, (4) enhance dissemination, communication, and transfer of knowledge in plant epigenetics and epigenomics.
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Dar, Fayaz Ahmad, Naveed Ul Mushtaq, Seerat Saleem, Reiaz Ul Rehman, Tanvir Ul Hassan Dar, and Khalid Rehman Hakeem. "Role of Epigenetics in Modulating Phenotypic Plasticity against Abiotic Stresses in Plants." International Journal of Genomics 2022 (June 14, 2022): 1–13. http://dx.doi.org/10.1155/2022/1092894.
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Plants being sessile are always exposed to various environmental stresses, and to overcome these stresses, modifications at the epigenetic level can prove vital for their long-term survival. Epigenomics refers to the large-scale study of epigenetic marks on the genome, which include covalent modifications of histone tails (acetylation, methylation, phosphorylation, ubiquitination, and the small RNA machinery). Studies based on epigenetics have evolved over the years especially in understanding the mechanisms at transcriptional and posttranscriptional levels in plants against various environmental stimuli. Epigenomic changes in plants through induced methylation of specific genes that lead to changes in their expression can help to overcome various stress conditions. Recent studies suggested that epigenomics has a significant potential for crop improvement in plants. By the induction and modulation of various cellular processes like DNA methylation, histone modification, and biogenesis of noncoding RNAs, the plant genome can be activated which can help in achieving a quicker response against various plant stresses. Epigenetic modifications in plants allow them to adjust under varied environmental stresses by modulating their phenotypic plasticity and at the same time ensure the quality and yield of crops. The plasticity of the epigenome helps to adapt the plants during pre- and postdevelopmental processes. The variation in DNA methylation in different organisms exhibits variable phenotypic responses. The epigenetic changes also occur sequentially in the genome. Various studies indicated that environmentally stimulated epimutations produce variable responses especially in differentially methylated regions (DMR) that play a major role in the management of stress conditions in plants. Besides, it has been observed that environmental stresses cause specific changes in the epigenome that are closely associated with phenotypic modifications. However, the relationship between epigenetic modifications and phenotypic plasticity is still debatable. In this review, we will be discussing the role of various factors that allow epigenetic changes to modulate phenotypic plasticity against various abiotic stress in plants.
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Chen, Xiangsong, and Dao-Xiu Zhou. "Rice epigenomics and epigenetics: challenges and opportunities." Current Opinion in Plant Biology 16, no. 2 (May 2013): 164–69. http://dx.doi.org/10.1016/j.pbi.2013.03.004.
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Xanthopoulos, Charalampos, and Efterpi Kostareli. "Advances in Epigenetics and Epigenomics in Chronic Lymphocytic Leukemia." Current Genetic Medicine Reports 7, no. 4 (November 27, 2019): 214–26. http://dx.doi.org/10.1007/s40142-019-00178-3.
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Abstract Purpose of Review The development and progression of chronic lymphocytic leukemia (CLL), a highly heterogenous B cell malignancy, are influenced by both genetic and environmental factors. Environmental factors, including pharmacological interventions, can affect the epigenetic landscape of CLL and thereby determine the CLL phenotype, clonal evolution, and clinical outcome. In this review, we critically present the latest advances in the field of CLL epigenomics/epigenetics in order to provide a systematic overview of to-date achievements and highlight the potential of epigenomics approaches in light of novel treatment therapies. Recent Findings Recent technological advances have enabled broad and precise mapping of the CLL epigenome. The identification of CLL-specific DNA methylation patterns has allowed for accurate CLL subtype definition, a better understanding of clonal origin and evolution, and the discovery of reliable biomarkers. More recently, studies have started to unravel the prognostic, predictive, and therapeutic potential of mapping chromatin dynamics and histone modifications in CLL. Finally, analysis of non-coding RNA expression has indicated their contribution to disease pathogenesis and helped to define prognostic subsets in CLL. Summary Overall, the potential of CLL epigenomics for predicting treatment response and resistance is mounting, especially with the advent of novel targeted CLL therapies.
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Hussey, Bethan, Martin R. Lindley, and Sarabjit Mastana. "Epigenetics and epigenomics: the future of nutritional interventions?" Future Science OA 3, no. 4 (November 2017): FSO237. http://dx.doi.org/10.4155/fsoa-2017-0088.
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Rosen, Evan D., Klaus H. Kaestner, Rama Natarajan, Mary-Elizabeth Patti, Richard Sallari, Maike Sander, and Katalin Susztak. "Epigenetics and Epigenomics: Implications for Diabetes and Obesity." Diabetes 67, no. 10 (September 20, 2018): 1923–31. http://dx.doi.org/10.2337/db18-0537.
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Qureshi, Irfan A., and Mark F. Mehler. "Advances in Epigenetics and Epigenomics for Neurodegenerative Diseases." Current Neurology and Neuroscience Reports 11, no. 5 (June 15, 2011): 464–73. http://dx.doi.org/10.1007/s11910-011-0210-2.
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Płonka, Beata. "Nature or Nurture – Will Epigenomics Solve the Dilemma?" Studia Humana 5, no. 2 (June 1, 2016): 13–36. http://dx.doi.org/10.1515/sh-2016-0007.
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AbstractThe concept of “nature and nurture” is used to distinguish between genetic and environmental influences on the formation of individual, mainly behavioral, traits. Different approaches that interpret nature and nurture as completely opposite or complementary aspects of human development have been discussed for decades. The paper addresses the most important points of nature vs nurture debate from the perspective of biological research, especially in the light of the recent findings in the field of epigenetics. The most important biological concepts, such as the trait, phenotype and genotype, as well as the evolution of other crucial notions are presented. Various attempts to find the main source of human variation are discussed - mainly the search for structural variants and the genome-wide association studies (GWAS). A new approach resulting from the discovery of “missing heritability”, as well as the current knowledge about the possible influence of epigenetic mechanisms on human traits are analyzed. Finally, the impact of epigenetic revolution on the society (public attitude, health policy, human rights etc.) is discussed.
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Mathers, John C. "Session 2: Personalised nutrition Epigenomics: a basis for understanding individual differences?" Proceedings of the Nutrition Society 67, no. 4 (October 10, 2008): 390–94. http://dx.doi.org/10.1017/s0029665108008744.
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Epigenetics encompasses changes to marks on the genome that are copied from one cell generation to the next, which may alter gene expression but which do not involve changes in the primary DNA sequence. These marks include DNA methylation (methylation of cytosines within CpG dinucleotides) and post-translational modifications (acetylation, methylation, phosphorylation and ubiquitination) of the histone tails protruding from nucleosome cores. The sum of genome-wide epigenetic patterns is known as the epigenome. It is hypothesised that altered epigenetic marking is a means through which evidence of environmental exposures (including nutritional status and dietary exposure) is received and recorded by the genome. At least some of these epigenetic marks are remembered through multiple cell generations and their effects may be revealed in altered gene expression and cell function. Altered epigenetic marking allows plasticity of phenotype in a fixed genotype. Despite their identical genotypes, monozygotic twins show increasing epigenetic diversity with age and with divergent lifestyles. Differences in epigenetic markings may explain some inter-individual variation in disease risk and in response to nutritional interventions.
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Laird, Peter W. "How epigenomics broke the mold: an interview with Peter W Laird." Epigenomics 14, no. 6 (March 2022): 303–8. http://dx.doi.org/10.2217/epi-2022-0066.
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In this interview, Professor Peter W Laird speaks with Storm Johnson, Commissioning Editor for Epigenomics, on his work to date in the field of cancer epigenetics. Dr Peter W Laird is a Professor at Van Andel Institute (VAI) in Grand Rapids, Michigan. He earned his B.S. and M.S., Cum Laude, from the University of Leiden, The Netherlands. He trained for his PhD with Dr Piet Borst, The Netherlands Cancer Institute, and as a postdoc with Dr Anton Berns, The Netherlands Cancer Institute, and with Dr Rudolf Jaenisch, at the Whitehead Institute for Biomedical Research in Cambridge, MA, USA. He joined the faculty at the University of Southern California in 1996, where he served as the Founding Director of the USC Epigenome Center and also as the Leader of the Epigenetics and Regulation Program of the Norris Comprehensive Cancer Center. In 2014, he relocated to VAI to join Dr Peter Jones in building an internationally acclaimed research center focused on Epigenetics. Dr Laird published the first demonstration of the causal role for DNA methylation in oncogenesis ( Cell, 1995) [ 1 ]. He served as the Principal Investigator for all DNA methylation data production for the Cancer Genome Atlas (TCGA) and led many TCGA analysis efforts. He has been awarded 10 patents related to DNA methylation technology by the United States Patent and Trademark Office, one of which is the basis for the first US FDA-approved blood-based DNA methylation assay for cancer (Epi proColon). His research findings include the report of a close link between DNA methylation and BRAF mutation in colorectal cancer ( Nature Genetics, 2006) [ 2 ], the discovery that embryonic stem cell polycomb repressor targets are predisposed to abnormal DNA methylation in cancer ( Nature Genetics, 2007) [ 3 ], the identification of a novel epigenetic subtype of glioma (G-CIMP), tightly associated with IDH1 mutation ( Cancer Cell, 2010) [ 4 ], and the connection between nuclear architecture, late replication, and domains of epigenetic instability ( Nature Genetics, 2011) [ 5 ], later showing a link with mitotic cell division, thus providing a mechanistic explanation for the loss of DNA methylation in aging and cancer first described four decades ago ( Nature Genetics, 2018) [ 6 ].
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Szyf, Moshe. "The epigenetics of early life adversity and trauma inheritance: an interview with Moshe Szyf." Epigenomics 14, no. 6 (March 2022): 309–14. http://dx.doi.org/10.2217/epi-2021-0483.
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In this interview, Professor Moshe Szyf speaks with Storm Johnson, Commissioning Editor for Epigenomics, on his work to date in the field of social epigenetics. Szyf received his PhD from the Hebrew University and did his postdoctoral fellowship in genetics at Harvard Medical School, joined the Department of Pharmacology and Therapeutics at McGill University in Montreal in 1989 and is a fellow of the Royal Society of Canada and the Academy of Health Sciences of Canada. He is the founding codirector of the Sackler Institute for Epigenetics and Psychobiology at McGill and is a Fellow of the Canadian Institute for Advanced Research Experience-Based Brain and Biological Development program. Szyf was the founder of the first pharma to develop epigenetic pharmacology, Methylgene Inc., and the journal Epigenetics. The Szyf lab proposed two decades ago that DNA methylation is a prime therapeutic target in cancer and other diseases and postulated and provided the first set of evidence that the social environment early in life can alter DNA methylation, launching the emerging field of social epigenetics.
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Baccarelli, Andrea. "ENVIRONMENTAL EPIGENETICS AND AGING." Innovation in Aging 3, Supplement_1 (November 2019): S735. http://dx.doi.org/10.1093/geroni/igz038.2696.
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Abstract The human epigenome is a flexible, environmental sensitive component of human biology that changes over time. Multiple studies have identified prospective changes in epigenetic marks that indicate that the epigenome ages as we grow older. These changes have been leveraged to create multiple indicators of age that may also predict mortality and age-related disease. There is ongoing research to determine the extent to which age-related epigenomics changes are inherent to cell biology and/or driven by lifestyle and environmental factors. In this presentation, I will review the current evidence derived from human aging studies and potential contributions to human health and disease. I will discuss the source of data, methodological challenges for large human studies, limitations and possible future directions.
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Alexander, Sheila A. "The Contributions of Nursing to Genetics, Epigenetics, Genomics, and Epigenomics." Biological Research For Nursing 17, no. 4 (June 17, 2015): 362–63. http://dx.doi.org/10.1177/1099800415586250.
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Kato, Mitsuo, and Rama Natarajan. "Epigenetics and epigenomics in diabetic kidney disease and metabolic memory." Nature Reviews Nephrology 15, no. 6 (March 20, 2019): 327–45. http://dx.doi.org/10.1038/s41581-019-0135-6.
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Li, Shanyi, Hsiao-Chen Dina Kuo, Ran Yin, Renyi Wu, Xia Liu, Lujing Wang, Rasika Hudlikar, Rebecca Mary Peter, and Ah-Ng Kong. "Epigenetics/epigenomics of triterpenoids in cancer prevention and in health." Biochemical Pharmacology 175 (May 2020): 113890. http://dx.doi.org/10.1016/j.bcp.2020.113890.
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Roy, Suchismita, and Praveen Soni. "Unraveling the Epigenetic Landscape for Salt Tolerance in Plants." International Journal of Plant Biology 13, no. 4 (October 13, 2022): 443–62. http://dx.doi.org/10.3390/ijpb13040036.
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In every organism, the expression of genes is regulated in response to the changes in the surrounding environment. The study of epigenetics in plants is essential in view of the improvement of agricultural productivity. Epigenetic modifications can enhance crops’ yield and stress tolerance without making any alteration within their genomic sequences. The routes of epigenetic modifications include processes such as methylation of DNA, modifications of histone proteins, chromatin remodeling, and non-coding RNA-mediated regulation of genes. Genome-wide epigenetic profiles, coined as the epigenome, of several plants have been identified in recent years. In the scope of this review, we are going to discuss progress made in the field of plant epigenomics under the limelight of stress tolerance, especially saline conditions.
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Augusto, Ronaldo de Carvalho, Aki Minoda, and Christoph Grunau. "A simple ATAC-seq protocol for population epigenetics." Wellcome Open Research 5 (June 9, 2020): 121. http://dx.doi.org/10.12688/wellcomeopenres.15552.1.
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We describe here a protocol for the generation of sequence-ready libraries for population epigenomics studies. The protocol is a streamlined version of the Assay for transposase accessible chromatin with high-throughput sequencing (ATAC-seq) that provides a positive display of accessible, presumably euchromatic regions. The protocol is straightforward and can be used with small individuals such as daphnia and schistosome worms, and probably many other biological samples of comparable size, and it requires little molecular biology handling expertise.
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Ehrlich, Melanie. "Risks and rewards of big-data in epigenomics research: an interview with Melanie Ehrlich." Epigenomics 14, no. 6 (March 2022): 351–58. http://dx.doi.org/10.2217/epi-2022-0056.
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Melanie Ehrlich, PhD, is a professor in the Tulane Cancer Center, the Tulane Center for Medical Bioinformatics and Genomics and the Hayward Human Genetics Program at Tulane Medical School, New Orleans, LA. She obtained her PhD in molecular biology in 1971 from the State University of New York at Stony Brook and completed postdoctoral research at Albert Einstein College of Medicine in 1972. She has been working on various aspects of epigenetics, starting with DNA methylation, since 1973. Her group made many first findings about DNA methylation (see below). For example, in 1982 and 1983, in collaboration with Charles Gehrke at the University of Missouri, she was the first to report tissue-specific and cancer-specific differences in overall DNA methylation in humans. In 1985, Xian-Yang Zhang and Richard Wang in her lab discovered a class of human DNA sequences specifically hypomethylated in sperm. In 1998, her group was the first to describe extensive losses of DNA methylation in pericentromeric and centromeric DNA repeats in human cancer. Her lab's many publications on the prevalence of both DNA hypermethylation and hypomethylation in the same cancers brought needed balance to our understanding of the epigenetics of cancer and to its clinical implications [ 1 ]. Besides working on cancer epigenetics, her research group has helped elucidate cytogenetic and gene expression abnormalities in the immunodeficiency, centromeric and facial anomalies (ICF) syndrome, a rare recessive disease often caused by mutations in DNMT3B. Her group also studied the epigenetics and transcriptomics of facioscapulohumeral muscular dystrophy (FSHD), whose disease locus is a tandem 3.3-kb repeat at subtelomeric 4q (that happens to be hypomethylated in ICF DNA [ 2 ]). Her study of FSHD has taken her in the direction of muscle (skeletal muscle, heart and aorta) epigenetics [ 3–6 ]. Recently, she has led research that applies epigenetics much more rigorously than usual to the evaluation of genetic variants from genome-wide association studies (GWAS) of osteoporosis and obesity. In continued collaboration with Sriharsa Pradhan at New England Biolabs and Michelle Lacey at Tulane University, she has compared 5-hydroxymethylcytosine and 5-methylcytosine clustering in various human tissues [ 7 ] and is studying myoblast methylomes that they generated by a new high-resolution enzymatic technique (enzymatic methyl-seq).
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Biémont, C. "From genotype to phenotype. What do epigenetics and epigenomics tell us?" Heredity 105, no. 1 (June 16, 2010): 1–3. http://dx.doi.org/10.1038/hdy.2010.66.
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Agarwal, Gaurav, Himabindu Kudapa, Abirami Ramalingam, Divya Choudhary, Pallavi Sinha, Vanika Garg, Vikas K. Singh, et al. "Epigenetics and epigenomics: underlying mechanisms, relevance, and implications in crop improvement." Functional & Integrative Genomics 20, no. 6 (October 21, 2020): 739–61. http://dx.doi.org/10.1007/s10142-020-00756-7.
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Pinel, Clémence. "When more data means better results: Abundance and scarcity in research collaborations in epigenetics." Social Science Information 59, no. 1 (January 16, 2020): 35–58. http://dx.doi.org/10.1177/0539018419895456.
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Drawing upon ethnographic findings from an epigenetics research laboratory in the United Kingdom, this article explores practices of research collaborations in the field of epigenetics, and epigenomics research consortia in particular. I demonstrate that research consortia are key scientific infrastructures that enable the aggregation of masses of data deemed necessary for the production of results and the fostering of epistemic value. Building on Science and Technology Studies (STS) scholarship on value production, and the concept of asset, I show that the production of valuable research within epigenomics research consortia rests on the active organisation and management of abundance and scarcity. It involves shaping and standardising the masses of data gathered in consortia, while it also entails research teams enclosing their data within their laboratories’ walls. As they do so, research teams construct data into scarce and monopolised assets, which they can put to productive use in collaborative endeavours against a revenue. In addition to contributing empirical and critical insights into the ways epigenetics knowledge is formed and negotiated in specific research contexts, this article offers conceptual tools to examine and problematise knowledge production practices in data-intensive research more broadly. In particular, it points out that while contemporary big biology is marked by the generalised imperative to ‘share’ data and ‘open’ science, collaborative endeavours within research consortia are built around forms of exclusions.
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Augusto, Ronaldo de Carvalho, Oliver Rey, Céline Cosseau, Cristian Chaparro, Jérémie Vidal-Dupiol, Jean-François Allienne, David Duval, et al. "A simple ATAC-seq protocol for population epigenetics." Wellcome Open Research 5 (January 7, 2021): 121. http://dx.doi.org/10.12688/wellcomeopenres.15552.2.
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We describe here a protocol for the generation of sequence-ready libraries for population epigenomics studies, and the analysis of alignment results. We show that the protocol can be used to monitor chromatin structure changes in populations when exposed to environmental cues. The protocol is a streamlined version of the Assay for transposase accessible chromatin with high-throughput sequencing (ATAC-seq) that provides a positive display of accessible, presumably euchromatic regions. The protocol is straightforward and can be used with small individuals such as daphnia and schistosome worms, and probably many other biological samples of comparable size (~10,000 cells), and it requires little molecular biology handling expertise.
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Ramos, Paula S. "Epigenetics of scleroderma: Integrating genetic, ethnic, age, and environmental effects." Journal of Scleroderma and Related Disorders 4, no. 3 (July 3, 2019): 238–50. http://dx.doi.org/10.1177/2397198319855872.
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Scleroderma or systemic sclerosis is thought to result from the interplay between environmental or non-genetic factors in a genetically susceptible individual. Epigenetic modifications are influenced by genetic variation and environmental exposures, and change with chronological age and between populations. Despite progress in identifying genetic, epigenetic, and environmental risk factors, the underlying mechanism of systemic sclerosis remains unclear. Since epigenetics provides the regulatory mechanism linking genetic and non-genetic factors to gene expression, understanding the role of epigenetic regulation in systemic sclerosis will elucidate how these factors interact to cause systemic sclerosis. Among the cell types under tight epigenetic control and susceptible to epigenetic dysregulation, immune cells are critically involved in early pathogenic events in the progression of fibrosis and systemic sclerosis. This review starts by summarizing the changes in DNA methylation, histone modification, and non-coding RNAs associated with systemic sclerosis. It then discusses the role of genetic, ethnic, age, and environmental effects on epigenetic regulation, with a focus on immune system dysregulation. Given the potential of epigenome editing technologies for cell reprogramming and as a therapeutic approach for durable gene regulation, this review concludes with a prospect on epigenetic editing. Although epigenomics in systemic sclerosis is in its infancy, future studies will help elucidate the regulatory mechanisms underpinning systemic sclerosis and inform the design of targeted epigenetic therapies to control its dysregulation.
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Pfeifer, Gerd P. "The ups and downs of DNA methylation: an interview with Gerd Pfeifer." Epigenomics 14, no. 6 (March 2022): 339–43. http://dx.doi.org/10.2217/epi-2021-0485.
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In this interview, Professor Gerd Pfeifer speaks with Storm Johnson, Commissioning Editor for Epigenomics, on his work to date in the field of DNA methylation. Dr Pfeifer received a PhD degree from the University of Frankfurt, Germany. After postdoctoral work, he became a faculty member at the Beckman Research Institute of the City of Hope (Duarte, CA) in 1991. He is currently a full professor at the Van Andel Institute in Grand Rapids, MI. Dr. Pfeifer has served on several NIH advisory committees and has published over 300 research papers. Dr Pfeifer's research interests are cancer etiology, molecular carcinogenesis and epigenetics. His expertise is in cellular and molecular biology. His lab currently works on epigenetic mechanisms of gene regulation in cancer and other diseases.
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Silva, Tiago C., Antonio Colaprico, Catharina Olsen, Fulvio D'Angelo, Gianluca Bontempi, Michele Ceccarelli, and Houtan Noushmehr. "TCGA Workflow: Analyze cancer genomics and epigenomics data using Bioconductor packages." F1000Research 5 (June 29, 2016): 1542. http://dx.doi.org/10.12688/f1000research.8923.1.
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Biotechnological advances in sequencing have led to an explosion of publicly available data via large international consortia such as The Cancer Genome Atlas (TCGA), The Encyclopedia of DNA Elements (ENCODE), and The NIH Roadmap Epigenomics Mapping Consortium (Roadmap). These projects have provided unprecedented opportunities to interrogate the epigenome of cultured cancer cell lines as well as normal and tumor tissues with high genomic resolution. The bioconductor project offers more than 1,000 open-source software and statistical packages to analyze high-throughput genomic data. However, most packages are designed for specific data types (e.g. expression, epigenetics, genomics) and there is no comprehensive tool that provides a complete integrative analysis harnessing the resources and data provided by all three public projects. A need to create an integration of these different analyses was recently proposed. In this workflow, we provide a series of biologically focused integrative downstream analyses of different molecular data. We describe how to download, process and prepare TCGA data and by harnessing several key bioconductor packages, we describe how to extract biologically meaningful genomic and epigenomic data and by using Roadmap and ENCODE data, we provide a workplan to identify candidate biologically relevant functional epigenomic elements associated with cancer. To illustrate our workflow, we analyzed two types of brain tumors : low-grade glioma (LGG) versus high-grade glioma (glioblastoma multiform or GBM). This workflow introduces the following Bioconductor packages: AnnotationHub, ChIPSeeker, ComplexHeatmap, pathview, ELMER, GAIA, MINET, RTCGAtoolbox, TCGAbiolinks.
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Silva, Tiago C., Antonio Colaprico, Catharina Olsen, Fulvio D'Angelo, Gianluca Bontempi, Michele Ceccarelli, and Houtan Noushmehr. "TCGA Workflow: Analyze cancer genomics and epigenomics data using Bioconductor packages." F1000Research 5 (December 28, 2016): 1542. http://dx.doi.org/10.12688/f1000research.8923.2.
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Biotechnological advances in sequencing have led to an explosion of publicly available data via large international consortia such as The Cancer Genome Atlas (TCGA), The Encyclopedia of DNA Elements (ENCODE), and The NIH Roadmap Epigenomics Mapping Consortium (Roadmap). These projects have provided unprecedented opportunities to interrogate the epigenome of cultured cancer cell lines as well as normal and tumor tissues with high genomic resolution. The Bioconductor project offers more than 1,000 open-source software and statistical packages to analyze high-throughput genomic data. However, most packages are designed for specific data types (e.g. expression, epigenetics, genomics) and there is no one comprehensive tool that provides a complete integrative analysis of the resources and data provided by all three public projects. A need to create an integration of these different analyses was recently proposed. In this workflow, we provide a series of biologically focused integrative analyses of different molecular data. We describe how to download, process and prepare TCGA data and by harnessing several key Bioconductor packages, we describe how to extract biologically meaningful genomic and epigenomic data. Using Roadmap and ENCODE data, we provide a work plan to identify biologically relevant functional epigenomic elements associated with cancer. To illustrate our workflow, we analyzed two types of brain tumors: low-grade glioma (LGG) versus high-grade glioma (glioblastoma multiform or GBM). This workflow introduces the following Bioconductor packages: AnnotationHub, ChIPSeeker, ComplexHeatmap, pathview, ELMER, GAIA, MINET, RTCGAToolbox, TCGAbiolinks.
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Šrut, Maja. "Environmental Epigenetics in Soil Ecosystems: Earthworms as Model Organisms." Toxics 10, no. 7 (July 20, 2022): 406. http://dx.doi.org/10.3390/toxics10070406.
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One of the major emerging concerns within ecotoxicology is the effect of environmental pollutants on epigenetic changes, including DNA methylation, histone modifications, and non-coding RNAs. Epigenetic mechanisms regulate gene expression, meaning that the alterations of epigenetic marks can induce long-term physiological effects that can even be inherited across generations. Many invertebrate species have been used as models in environmental epigenetics, with a special focus on DNA methylation changes caused by environmental perturbations (e.g., pollution). Among soil organisms, earthworms are considered the most relevant sentinel organisms for anthropogenic stress assessment and are widely used as standard models in ecotoxicological testing of soil toxicity. In the last decade, several research groups have focused on assessing the impact of environmental stress on earthworm epigenetic mechanisms and tried to link these mechanisms to the physiological effects. The aim of this review is to give an overview and to critically examine the available literature covering this topic. The high level of earthworm genome methylation for an invertebrate species, responsiveness of epigenome to environmental stimuli, availability of molecular resources, and the possibility to study epigenetic inheritance make earthworms adequate models in environmental epigenomics. However, there are still many knowledge gaps that need to be filled in, before we can fully explore earthworms as models in this field. These include detailed characterization of the methylome using next-generation sequencing tools, exploration of multigenerational and transgenerational effects of pollutants, and information about other epigenetic mechanisms apart from DNA methylation. Moreover, the connection between epigenetic effects and phenotype has to be further explored.
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Lee, Daniel Y. "Cancer Epigenomics and Beyond: Advancing the Precision Oncology Paradigm." Journal of Immunotherapy and Precision Oncology 3, no. 4 (October 7, 2020): 147–56. http://dx.doi.org/10.36401/jipo-20-18.
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ABSTRACT How cancers are characterized and treated has evolved over the past few decades. Major advances in genomics tools and techniques have revealed interlinked regulatory pathways of cancers with unprecedented detail. Early discoveries led to success with rationally targeted small molecules and more recently with immunomodulatory agents, setting the stage for precision oncology. However, drug resistance to every agent has thus far proven intractable, sending us back to fill the gaps in our rudimentary knowledge of tumor biology. Epigenetics is emerging as a fundamental process in every hallmark of cancer. Large-scale interrogation of the cancer epigenome continues to reveal new mechanisms of astounding complexity. In this review, I present selected experimental and clinical examples that have shaped our understanding of cancer at the molecular level. Translation of our collective erudition into revolutionary diagnostic and treatment strategies will advance the precision oncology paradigm.
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Kelsey, Karl. "Epigenetics, environment and epidemiology: an interview with Karl Kelsey." Epigenomics 14, no. 6 (March 2022): 323–26. http://dx.doi.org/10.2217/epi-2022-0008.
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In this interview, Professor Karl Kelsey speaks with Storm Johnson, Commissioning Editor for Epigenomics, on his work to date in the field of environmental epigenomics and epidemiology. Dr Karl Kelsey, MD, MOH is a Professor of Epidemiology and Pathology and Laboratory Medicine at Brown University. He is the Founding Director of the Center for Environmental Health and Technology and Head of the Environmental Health Section at the Department of Epidemiology. Dr Kelsey is interested in the application of laboratory-based biomarkers in environmental disease, with experience in chronic disease epidemiology and tumor biology. The goals of his work include a mechanistic understanding of individual susceptibility to exposure-related cancers. In addition, his laboratory is interested in tumor biology, investigating somatic alterations in tumor tissue from the patients who have developed exposure-related cancers. This work involves the use of an epidemiologic approach to characterize epigenetic and genetic alteration of genes in the causal pathway for malignancy. Active work includes several studies of individual susceptibility to cancer. Dr Kelsey's laboratory mainly investigates susceptibility to smoking-related lung cancer and studies multi-racial and ethnic populations. In addition, the laboratory is also involved with the study of inherited susceptibility to brain tumors and pancreatic cancer. Major case control studies that are ongoing in the laboratory include studies designed to understand inherited and acquired susceptibility in head and neck cancers. The laboratory is also involved in a case control study of asbestos-associated mesothelioma, arsenic exposure, cigarette smoking and bladder cancer. Considerable work is being devoted to understanding the mechanisms of action of both asbestos and arsenic including their ability to affect promoter methylation and gene silencing in carcinogenesis. Recent laboratory studies includes an interest in using newly developed DNA methylation biomarkers to probe immune profiles from archived blood. Dr Kelsey received his MD from the University of Minnesota and Masters of Occupational Health from Harvard University.
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Goodrich, Jaclyn. "Insights on exposure-induced disease susceptibility: an interview with Jaclyn Goodrich." Epigenomics 14, no. 6 (March 2022): 319–21. http://dx.doi.org/10.2217/epi-2022-0046.
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In this interview, Dr Jaclyn Goodrich speaks with Storm Johnson, Commissioning Editor for Epigenomics, on her work to date on environmental epigenetics and the impact of toxic exposures on susceptible populations. Jaclyn Goodrich is a research assistant professor of environmental health sciences at the University of Michigan School of Public Health (Ann Arbor, MI, USA). She obtained a doctorate in toxicology and completed postdoctoral training in environmental epigenomics at the University of Michigan. The overarching goal of her current research program is to identify environmental factors that modify the epigenome and increase risk for disease throughout the life course. She primarily conducts epidemiological studies to investigate the impact of toxic exposures on susceptible populations including children and occupationally exposed workers. She has coauthored more than 70 publications and is an active member of the Society of Toxicology and the Environmental Mutagenesis and Genomics Society.
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Figueroa, Maria Eugenia, John Greally, Ruud Delwel, and Ari M. Melnick. "Genome-Wide Epigenetics in Myeloid Leukemias." Blood 112, no. 11 (November 16, 2008): sci—35—sci—35. http://dx.doi.org/10.1182/blood.v112.11.sci-35.sci-35.
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Abstract While the role of genetic alterations in cancer is well-recognized, epigenetic deregulation has only recently been identified as a hallmark of malignant transformation. The term “epigenetic” refers to a heritable regulation of gene expression that is not dependent on changes in the DNA sequence. These epigenetic modifications – including but not limited to DNA methylation and covalent modifications of histone tails – play a crucial role in determining chromatin structure and gene expression. Abnormal epigenetic regulation can lead to aberrant chromatin structure and deregulation of transcriptional activity. Epigenetic lesions can affect cancer-related genes, such as CDKN2B, CDKN2A, RB, and BRCA1, and it is not rare for epigenetic lesions to accompany genetic mutations of these and other genes, suggesting that epigenetic deregulation can form a part of the multi-step process of oncogenesis. An alteration in the distribution of DNA methylation has been demonstrated in AML as well as in other malignancies. Generally, intergenic DNA methylation is reported to decrease and promoter methylation to increase. Hypomethylation of DNA can lead to genomic instability and further increase the number of genetic lesions, while promoter hypermethylation has been associated with aberrant silencing of tumor suppressor genes. Altered levels of acetylation at specific histone residues were also shown to be associated with aberrant chromatin structure and gene deregulation in AML. Several oncogenic transcription factors and fusion proteins, such as PML-RARalpha, and AML1-ETO, can introduce aberrant epigenetic programming in myeloid cells through recruitment of epigenetic modifying enzymes to their target genes. However, the emerging field of epigenomic profiling has yielded evidence that epigenetic deregulation in AML is more profound and cannot always be linked to the presence of a given fusion protein. The mechanisms leading to genome-wide epigenetic deregulation still remain largely unidentified, although environmental factors and aging can contribute to this process. Current epigenetic profiling studies have revealed that DNA methylation or histone modification patterns can identify biologically distinct forms of AML that may not be readily identified through other methods. New data suggest that specific DNA methylation profiles may be associated with response to therapeutic agents, including epigenetic-targeted drugs. Numerous epigenetic candidate biomarkers have been recently described in both myeloid and lymphoid malignancies. Integrative analysis of DNA methylation, histone modifications, and gene expression may synergize to identify in far greater depth than single platform studies differences in gene regulation among leukemias. Overall, the emerging field of epigenomics provide a new opportunity to more accurately identify biological variation and therapeutically target acute myeloid leukemias.
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Wu, Renyi, Lujing Wang, Ran Yin, Rasika Hudlikar, Shanyi Li, Hsiao‐Chen D. Kuo, Rebecca Peter, et al. "Epigenetics/epigenomics and prevention by curcumin of early stages of inflammatory‐driven colon cancer." Molecular Carcinogenesis 59, no. 2 (December 9, 2019): 227–36. http://dx.doi.org/10.1002/mc.23146.
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Dudley, K. J., K. Revill, R. N. Clayton, and W. E. Farrell. "Pituitary tumours: all silent on the epigenetics front." Journal of Molecular Endocrinology 42, no. 6 (February 9, 2009): 461–68. http://dx.doi.org/10.1677/jme-09-0009.
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Investigation of the epigenome of sporadic pituitary tumours is providing a more detailed understanding of aberrations that characterise this tumour type. Early studies, in this and other tumour types adopted candidate-gene approaches to characterise CpG island methylation as a mechanism responsible for or associated with gene silencing. However, more recently, investigators have adopted approaches that do not require a priori knowledge of the gene and transcript, as example differential display techniques, and also genome-wide, array-based approaches, to ‘uncover’ or ‘unmask’ silenced genes. Furthermore, through use of chromatin immunoprecipitation as a selective enrichment technique; we are now beginning to identify modifications that target the underlying histones themselves and that have roles in gene-silencing events. Collectively, these studies provided convincing evidence that change to the tumour epigenome are not simply epiphenomena but have functional consequences in the context of pituitary tumour evolution. Our ability to perform these types of studies has been and is increasingly reliant upon technological advances in the genomics and epigenomics arena. In this context, other more recent advances and developing technologies, and, in particular, next generation or flow cell re-sequencing techniques offer exciting opportunities for our future studies of this tumour type.
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Karlsson, Oskar. "Epigenetics in the Anthropocene: an interview with Oskar Karlsson." Epigenomics 14, no. 6 (March 2022): 315–18. http://dx.doi.org/10.2217/epi-2022-0044.
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In this interview, Oskar Karlsson speaks with Storm Johnson, commissioning editor for Epigenomics, on his work to date in the field of toxicological origins of disease and gene–environment interactions. Oskar Karlsson, is an associate professor at the Science for Life Laboratory (SciLifeLab), Department of Environmental Science, Stockholm University, Sweden. Dr. Karlsson earned a PhD in toxicology at the Department of Pharmaceutical Bioscience, Uppsala University, and has also worked at Centre of Molecular Medicine, Karolinska Institute, as well as Harvard University School of Public Health. His research combines experimental model systems, computational and omics tools, and epidemiological studies to investigate the influence of environmental exposures on wildlife and human health, and underlying molecular mechanisms. In particular, his research focuses on developmental origins of health and disease with an emphasis on environmental exposures and epigenetic mechanisms. The projects concern the effects of exposures such as endocrine disrupting chemicals, flame retardants, pesticides, metals and particulate air pollution, as well as drugs, psycho-social stressors and ethnical disparities. Ongoing efforts include studies of paternal epigenetic inheritance in the ERC-funded project PATER.
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Shema, Efrat. "Abstract PR006: Single-molecule and single-cell epigenetics: Decoding the epigenome for cancer research and diagnostics." Cancer Research 82, no. 23_Supplement_2 (December 1, 2022): PR006. http://dx.doi.org/10.1158/1538-7445.cancepi22-pr006.
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Abstract Genes and genomic elements are packaged by chromatin structures that regulate their activity. We developed a novel high-throughput single-molecule imaging technology to decode combinatorial modifications on millions of individual nucleosomes. We apply this technology to image nucleosomes and delineate their combinatorial epigenetic patterns, and how these patterns are deregulated in cancer. In addition, we adapt single-cell technologies based on CyTOF to profile the global levels of multiple histone modifications in single cells, thus revealing epigenetic heterogeneity in cancer. Our research focuses on pediatric gliomas harboring lysine to methionine substitution of residue 27 on histone H3 (K27M). We provide evidence for widespread effects of the H3-K27M oncohistone on multiple core epigenetic pathways, and highlight the capability of single-molecule and single-cell tools to reveal mechanisms of chromatin deregulation and heterogeneity in cancer. We also harness the single-molecule technology as a novel liquid biopsy approach, by comprehensively profiling combinatorial epigenetic marks of plasma-isolated nucleosomes. Applying this analysis to a cohort of plasma samples detect colorectal cancer at high accuracy and sensitivity, even at early stages. Finally, combining this proteomic analysis with single-molecule DNA sequencing reveals the tissue-of-origin of the tumor. Citation Format: Efrat Shema. Single-molecule and single-cell epigenetics: Decoding the epigenome for cancer research and diagnostics. [abstract]. In: Proceedings of the AACR Special Conference: Cancer Epigenomics; 2022 Oct 6-8; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2022;82(23 Suppl_2):Abstract nr PR006.
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Al Jowf, Ghazi I., Clara Snijders, Bart P. F. Rutten, Laurence de Nijs, and Lars M. T. Eijssen. "The Molecular Biology of Susceptibility to Post-Traumatic Stress Disorder: Highlights of Epigenetics and Epigenomics." International Journal of Molecular Sciences 22, no. 19 (October 4, 2021): 10743. http://dx.doi.org/10.3390/ijms221910743.
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Exposure to trauma is one of the most important and prevalent risk factors for mental and physical ill-health. Excessive or prolonged stress exposure increases the risk of a wide variety of mental and physical symptoms. However, people differ strikingly in their susceptibility to develop signs and symptoms of mental illness after traumatic stress. Post-traumatic stress disorder (PTSD) is a debilitating disorder affecting approximately 8% of the world’s population during their lifetime, and typically develops after exposure to a traumatic event. Despite that exposure to potentially traumatizing events occurs in a large proportion of the general population, about 80–90% of trauma-exposed individuals do not develop PTSD, suggesting an inter-individual difference in vulnerability to PTSD. While the biological mechanisms underlying this differential susceptibility are unknown, epigenetic changes have been proposed to underlie the relationship between exposure to traumatic stress and the susceptibility to develop PTSD. Epigenetic mechanisms refer to environmentally sensitive modifications to DNA and RNA molecules that regulate gene transcription without altering the genetic sequence itself. In this review, we provide an overview of various molecular biological, biochemical and physiological alterations in PTSD, focusing on changes at the genomic and epigenomic level. Finally, we will discuss how current knowledge may aid us in early detection and improved management of PTSD patients.
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Sabedot, Thais, Michael Wells, Indrani Datta, Tathiane Malta, Ana Valeria Castro, Laila M. Poisson, Roel Verhaak, Antonio Iavarone, and Houtan Noushmehr. "EPCO-29. EPIGENOMICS OF THE GLIOMA LONGITUDINAL ANALYSIS (GLASS) CONSORTIUM." Neuro-Oncology 22, Supplement_2 (November 2020): ii75. http://dx.doi.org/10.1093/neuonc/noaa215.308.
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Abstract Adult diffuse gliomas are central nervous system (CNS) tumors that arise from the malignant transformation of glial cells. Nearly all gliomas will recur despite standard treatment however, current histopathological grading fails to predict which of them will relapse and/or progress. The Glioma Longitudinal AnalySiS (GLASS) consortium is a large-scale collaboration that aims to investigate the molecular profiling of matched primary and recurrent glioma samples from multiple institutions in order to better understand the dynamic evolution of these tumors. At this time, the cohort comprises 946 samples across 11 institutions and among those, 864 have DNA methylation data available. The current molecular classification based on 7 subtypes published by TCGA in 2016 was applied to the dataset. Among the IDH wildtype tumors, 33% (16/49) of the patients showed a change of subtype upon recurrence, whereas most of them (9/16) were Classic-like at the primary stage but changed to either Mesenchymal-like or PA-like at the recurrent level. Among the IDH mutant tumors, 15% (22/142) showed a change of subtype at recurrent stage, in which 16 out of 22 progressed from G-CIMP-high to G-CIMP-low. Although some tumors progressed to a different subtype upon recurrence, an unsupervised analysis showed that the samples tend to cluster by patient instead of by subtype. By estimating the copy number alterations of these tumors using DNA methylation, the overall copy number profile of the recurrent samples remains similar to their primary counterpart. From this initial analysis using epigenomic data, we were able to characterize some aspects of glioma evolution and how the DNA methylation is associated with the progression of these tumors to different subtypes. These findings corroborate the importance of epigenetics in gliomas and can potentially lead to the identification of new biomarkers that can reflect tumor burden and predict its development.
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Binoy, Ashly, Dhrithi Bhat, Jahnavi G. Bhat, Sarvesha Babu M, Manjunatha Reddy, and Sumathra Manokaran. "Nutrigenomics in Lifestyle Disorders: A Review." ECS Transactions 107, no. 1 (April 24, 2022): 9249–64. http://dx.doi.org/10.1149/10701.9249ecst.
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In the era of increasing unhealthy dietary and lifestyle habits, maintaining a healthy diet is really important to prevent a broad spectrum of diseases. Lifestyle diseases occur due to certain unhealthy daily habits (smoking, unhealthy diet, and physical inactivity) that lead to inappropriate relationships with the environment. The consumption of food in an improper quantity and lacking in quality can have adverse effects on an individual’s health. Diet can bring about certain changes in genes which can be studied in the areas of nutrigenomics, nutrigenetics, epigenetics, epigenomics, and transcriptomics. This can help us understand how genetic makeup responds to nutrition in terms of transcription and translation processes. In this review, the effect of nutrition on gene expressions related to lifestyle disorders such as metabolic syndrome, CVD, and asthma is discussed.
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McCarrey, John R., and Keren Cheng. "Germ cells: ENCODE’s forgotten cell type." Biology of Reproduction 105, no. 3 (July 10, 2021): 761–66. http://dx.doi.org/10.1093/biolre/ioab135.
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Abstract More than a decade ago, the ENCODE and NIH Epigenomics Roadmap consortia organized large multilaboratory efforts to profile the epigenomes of >110 different mammalian somatic cell types. This generated valuable publicly accessible datasets that are being mined to reveal genome-wide patterns of a variety of different epigenetic parameters. This consortia approach facilitated the powerful and comprehensive multiparametric integrative analysis of the epigenomes in each cell type. However, no germ cell types were included among the cell types characterized by either of these consortia. Thus, comprehensive epigenetic profiling data are not generally available for the most evolutionarily important cells, male and female germ cells. We discuss the need for reproductive biologists to generate similar multiparametric epigenomic profiling datasets for both male and female germ cells at different developmental stages and summarize our recent effort to derive such data for mammalian spermatogonial stem cells and progenitor spermatogonia.
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Bhamidipati, Theja, Mithun Sinha, Chandan K. Sen, and Kanhaiya Singh. "Laser Capture Microdissection in the Spatial Analysis of Epigenetic Modifications in Skin: A Comprehensive Review." Oxidative Medicine and Cellular Longevity 2022 (February 9, 2022): 1–12. http://dx.doi.org/10.1155/2022/4127238.
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Each cell in the body contains an intricate regulation for the expression of its relevant DNA. While every cell in a multicellular organism contains identical DNA, each tissue-specific cell expresses a different set of active genes. This organizational property exists in a paradigm that is largely controlled by forces external to the DNA sequence via epigenetic regulation. DNA methylation and chromatin modifications represent some of the classical epigenetic modifications that control gene expression. Complex tissues like skin consist of heterogeneous cell types that are spatially distributed and mixed. Furthermore, each individual skin cell has a unique response to physiological and pathological cues. As such, it is difficult to classify skin tissue as homogenous across all cell types and across different environmental exposures. Therefore, it would be prudent to isolate targeted tissue elements prior to any molecular analysis to avoid a possibility of confounding the sample with unwanted cell types. Laser capture microdissection (LCM) is a powerful technique used to isolate a targeted cell group with extreme microscopic precision. LCM presents itself as a solution to tackling the problem of tissue heterogeneity in molecular analysis. This review will cover an overview of LCM technology, the principals surrounding its application, and benefits of its application to the newly defined field of epigenomics, in particular of cutaneous pathology. This presents a comprehensive review about LCM and its use in the spatial analysis of skin epigenetics. Within the realm of skin pathology, this ability to isolate tissues under specific environmental stresses, such as oxidative stress, allows a far more focused investigation.
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Ge, Xinzhou, Haowen Zhang, Lingjue Xie, Wei Vivian Li, Soo Bin Kwon, and Jingyi Jessica Li. "EpiAlign: an alignment-based bioinformatic tool for comparing chromatin state sequences." Nucleic Acids Research 47, no. 13 (April 24, 2019): e77-e77. http://dx.doi.org/10.1093/nar/gkz287.
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AbstractThe availability of genome-wide epigenomic datasets enables in-depth studies of epigenetic modifications and their relationships with chromatin structures and gene expression. Various alignment tools have been developed to align nucleotide or protein sequences in order to identify structurally similar regions. However, there are currently no alignment methods specifically designed for comparing multi-track epigenomic signals and detecting common patterns that may explain functional or evolutionary similarities. We propose a new local alignment algorithm, EpiAlign, designed to compare chromatin state sequences learned from multi-track epigenomic signals and to identify locally aligned chromatin regions. EpiAlign is a dynamic programming algorithm that novelly incorporates varying lengths and frequencies of chromatin states. We demonstrate the efficacy of EpiAlign through extensive simulations and studies on the real data from the NIH Roadmap Epigenomics project. EpiAlign is able to extract recurrent chromatin state patterns along a single epigenome, and many of these patterns carry cell-type-specific characteristics. EpiAlign can also detect common chromatin state patterns across multiple epigenomes, and it will serve as a useful tool to group and distinguish epigenomic samples based on genome-wide or local chromatin state patterns.
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Stel, Jente, and Juliette Legler. "The Role of Epigenetics in the Latent Effects of Early Life Exposure to Obesogenic Endocrine Disrupting Chemicals." Endocrinology 156, no. 10 (August 4, 2015): 3466–72. http://dx.doi.org/10.1210/en.2015-1434.
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Recent research supports a role for exposure to endocrine-disrupting chemicals (EDCs) in the global obesity epidemic. Obesogenic EDCs have the potential to inappropriately stimulate adipogenesis and fat storage, influence metabolism and energy balance and increase susceptibility to obesity. Developmental exposure to obesogenic EDCs is proposed to interfere with epigenetic programming of gene regulation, partly by activation of nuclear receptors, thereby influencing the risk of obesity later in life. The goal of this minireview is to briefly describe the epigenetic mechanisms underlying developmental plasticity and to evaluate the evidence of a mechanistic link between altered epigenetic gene regulation by early life EDC exposure and latent onset of obesity. We summarize the results of recent in vitro, in vivo, and transgenerational studies, which clearly show that the obesogenic effects of EDCs such as tributyltin, brominated diphenyl ether 47, and polycyclic aromatic hydrocarbons are mediated by the activation and associated altered methylation of peroxisome proliferator-activated receptor-γ, the master regulator of adipogenesis, or its target genes. Importantly, studies are emerging that assess the effects of EDCs on the interplay between DNA methylation and histone modifications in altered chromatin structure. These types of studies coupled with genome-wide rather than gene-specific analyses are needed to improve mechanistic understanding of epigenetic changes by EDC exposure. Current advances in the field of epigenomics have led to the first potential epigenetic markers for obesity that can be detected at birth, providing an important basis to determine the effects of developmental exposure to obesogenic EDCs in humans.
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Xu, Siyuan, Siqing Wang, Shenghui Xing, Dingdang Yu, Bowen Rong, Hai Gao, Mengyao Sheng, et al. "KDM5A suppresses PML-RARα target gene expression and APL differentiation through repressing H3K4me2." Blood Advances 5, no. 17 (August 27, 2021): 3241–53. http://dx.doi.org/10.1182/bloodadvances.2020002819.
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Abstract Epigenetic abnormalities are frequently involved in the initiation and progression of cancers, including acute myeloid leukemia (AML). A subtype of AML, acute promyelocytic leukemia (APL), is mainly driven by a specific oncogenic fusion event of promyelocytic leukemia–RA receptor fusion oncoprotein (PML-RARα). PML-RARα was reported as a transcription repressor through the interaction with nuclear receptor corepressor and histone deacetylase complexes leading to the mis-suppression of its target genes and differentiation blockage. Although previous studies were mainly focused on the connection of histone acetylation, it is still largely unknown whether alternative epigenetics mechanisms are involved in APL progression. KDM5A is a demethylase of histone H3 lysine 4 di- and tri-methylations (H3K4me2/3) and a transcription corepressor. Here, we found that the loss of KDM5A led to APL NB4 cell differentiation and retarded growth. Mechanistically, through epigenomics and transcriptomics analyses, KDM5A binding was detected in 1889 genes, with the majority of the binding events at promoter regions. KDM5A suppressed the expression of 621 genes, including 42 PML-RARα target genes, primarily by controlling the H3K4me2 in the promoters and 5′ end intragenic regions. In addition, a recently reported pan-KDM5 inhibitor, CPI-455, on its own could phenocopy the differentiation effects as KDM5A loss in NB4 cells. CPI-455 treatment or KDM5A knockout could greatly sensitize NB4 cells to all-trans retinoic acid–induced differentiation. Our findings indicate that KDM5A contributed to the differentiation blockage in the APL cell line NB4, and inhibition of KDM5A could greatly potentiate NB4 differentiation.
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Dauncey, M. J. "Recent advances in nutrition, genes and brain health." Proceedings of the Nutrition Society 71, no. 4 (May 3, 2012): 581–91. http://dx.doi.org/10.1017/s0029665112000237.
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Molecular mechanisms underlying brain structure and function are affected by nutrition throughout the life cycle, with profound implications for health and disease. Responses to nutrition are in turn influenced by individual differences in multiple target genes. Recent advances in genomics and epigenomics are increasing understanding of mechanisms by which nutrition and genes interact. This review starts with a short account of current knowledge on nutrition–gene interactions, focusing on the significance of epigenetics to nutritional regulation of gene expression, and the roles of SNP and copy number variants (CNV) in determining individual responses to nutrition. A critical assessment is then provided of recent advances in nutrition–gene interactions, and especially energy status, in three related areas: (i) mental health and well-being, (ii) mental disorders and schizophrenia, (iii) neurological (neurodevelopmental and neurodegenerative) disorders and Alzheimer's disease. Optimal energy status, including physical activity, has a positive role in mental health. By contrast, sub-optimal energy status, including undernutrition and overnutrition, is implicated in many disorders of mental health and neurology. These actions are mediated by changes in energy metabolism and multiple signalling molecules, e.g. brain-derived neurotrophic factor (BDNF). They often involve epigenetic mechanisms, including DNA methylation and histone modifications. Recent advances show that many brain disorders result from a sophisticated network of interactions between numerous environmental and genetic factors. Personal, social and economic costs of sub-optimal brain health are immense. Future advances in understanding the complex interactions between nutrition, genes and the brain should help to reduce these costs and enhance quality of life.
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Singh, Amit K., Roshni Roy, Mary Kaileh, Dimitra Sarantopoulou, Dena Hernandez, Sampath Arepalli, Arsun Bektas, et al. "Unique and shared molecular features of human B and T lymphocyte memory differentiation." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 168.11. http://dx.doi.org/10.4049/jimmunol.208.supp.168.11.
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Abstract Long-term immunity against infections and effective response to vaccination are dependent on remarkable and unique feature of lymphocytes referred as “memory generation”. Despite having multiple mice studies focused on naïve to memory transition of lymphocytes our understanding of human naïve and memory properties is limited. In this study we explored epigenetics (DNA methylation and accessible chromatin), transcriptomics and activation induced gene expression of FACS sorted naïve and memory subsets of B, CD4 T and CD8 T lymphocytes of healthy donors from GESTALT cohort. Shared and specific methylomes between B and T lymphocyte subsets were identified. The relationship between DNA methylation, chromatin accessibility and transcriptome through ATAC-Seq and RNA-Seq data from the same donors is established. Through in-silico analyses and by utilizing data from Roadmap Epigenomics project and ChromHMM, we further identified differentiation-specific connections between DNA methylation, chromatin accessibility, and histone modifications. Transcription factor motif analyses identifies presence of ARNT, OCT and NF-κB motifs around sites hypomethylated in B memory while ETS motifs are in memory-associated hyper-methylated sites. Interestingly, OCT motifs were also significantly enriched in B memory specific accessible chromatin. To understand the extent to which these epigenetic changes effected lymphocytes, we activated naïve and memory subsets of B and CD4+ T lymphocytes in vitro and assayed early and late gene expression changes. These findings will provide the foundation for future studies related to dysregulation of memory cell differentiation in aging and infections. Supported by Intramural Research Program of the National Institute on Aging.