Relevant bibliographies by topics / Epigenomics and epigenetics

Academic literature on the topic 'Epigenomics and epigenetics'

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Published: 10 December 2022
Last updated: 28 January 2023

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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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Dissertations / Theses on the topic "Epigenomics and epigenetics"

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Baker, Katie. "The chromatin landscape of barley : gene expression, evolution and epigenetics." Thesis, University of Dundee, 2015. https://discovery.dundee.ac.uk/en/studentTheses/13a096cd-f45b-4e34-babd-ccb3ff3607ca.

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Barley (Hordeum vulgare) is an economically important crop species with a large diploid genome. Around a half of the barley genome and a fifth of the genes are constrained within a low-recombining pericentromeric (LR-PC) region. I explored the LR-PC gene component with a genomic investigation of gene expression, diversity and evolution. Chromatin environments were also explored in the LR and high recombining (HR) regions by surveying the genic and genomic distributions of nine histone modifications. Firstly, regions of HR and LR were identified and compared for gene evolution, expression and diversity. LR regions of the barley genome were found to be restrictive for gene evolution and diversity, but not gene expression. I employed a bioinformatics approach to identify ancient gene pairs in barley to determine the long-term effects of residency in those regions upon gene evolution. Gene pair loss in LR regions was found to be elevated relative to the HR regions. Applying the same method to rice and Brachypodium distachyon revealed the same situation, suggesting a universal process in the grasses for loss of gene pairs in LR regions. The chromosomal distributions of transposable elements (TEs) were also explored and examined for correlations with recombination rate. Secondly, I developed a chromatin immunoprecipitation followed by Next Generation Sequencing (ChIP-seq) protocol for the investigation of histone modifications in barley seedlings. A protocol was optimised for the fixation, extraction and sonication of barley chromatin. The protocol was applied using antibodies against 13 different histone modifications. Following DNA library construction and Illumina sequencing, a bioinformatics pipeline was devised to analyse the sequence data. NGS reads were mapped to a custom assembly of the barley cultivar Morex reference genome sequence before peak calling. Genomic and genic locations were determined for the covalently modified histones. Four modifications were discarded from further study on the basis of low peak numbers or unexpected chromosomal locations. The remaining nine modifications were classified into four groups based on chromosomal distributions. Groupings were closely mirrored by peak sharing relationships between the modifications except histone H3 lysine-27 tri-methylation (H3K27me3). In addition, chromatin states representing local chromatin environments were defined in the barley genome using the peak sharing data. Mapping the states onto the genome revealed a striking chromatin structure of the gene-rich chromosome arms. A telomere-proximal region bearing high levels of H3K27me3-containing states was found adjacent to an interior gene-rich region characterised by active chromatin states lacking H3K27me3. The LTR retroelement-rich interior was found to be associated with repressive chromatin states. The histone modification status of TE classes were also probed revealing unexpected differences relating to the genomic and genic distributions of these elements. Finally, a genome browser was created to host the information publicly.
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Drong, Alexander Werner. "Comprehensive assessment of the role of DNA methylation in obesity and type 2 diabetes." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:c2df87d9-9929-4eb1-8c44-61452b88ea3c.

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Obesity and type 2 diabetes (T2D) are major risk factors for cardiovascular and other diseases and are currently undergoing an increase in global prevalence. The work presented in my thesis addresses the role epigenetics, specifically DNA methylation, plays in the susceptibility to obesity and T2D and deals with methodological issues in the analysis of DNA methylation data. I first combined epigenome-wide DNA methylation data across 38 adipose tissue samples with corresponding SNP and mRNA data for the same subjects. At 5% false discovery rate (FDR), methylation of 149 regions associated with at least one cis-SNP. When 19 of the 149 regions were tested for association in an additional 181 independent samples, five regions replicated. These results indicate a genetic influence on DNA methylation in adipose tissue. I then analysed 90 epigenome-wide methylation samples taken from 15 South Asian controls and 30 T2D cases participating in the LOLIPOP study at two time points ∼7 years apart. I found global differences at both follow-up and baseline between the normal glucose tolerant and T2D groups, as well as strong differences with aging. I further used the main EpiMigrant data from 2,687 individuals, with 36 samples measured in duplicate to assess approaches to quality control, data normalisation and batch correction through control probe adjustment. A null hypothesis for epigenome-wide association studies (EWAS) by permutation testing and I investigated the effects of correlation between individual methylation markers. Using the developed methods, I carried out an EWAS of body mass index (BMI) with subsequent meta-analysis amongst 10,261 individuals of European and South Asian ancestry. DNA methylation markers at 187 genetic loci were associated with BMI. Mendelian randomisation experiments suggested that association of DNA methylation with BMI is the consequence of BMI. Lastly, I tested haplotypes of 85 SNPs currently known to be associated with T2D and 118 SNPs associated with obesity traits for an enrichment of CpG creating or abrogating SNPs and found that 9 T2D and 23 obesity SNPs showed a significant difference in CpG count between the SNP alleles as established by permutation testing. Amongst these is FTO, a locus which has been previously been shown to have a haplotype-specific methylation effect. My work provides novel insights into the role of DNA methylation in metabolic diseases. The methods that I developed to robustly detect association are flexible and scalable and will further be useful for larger, future EWAS.
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Nordor, Akpéli. "Toward the identification of cancer/placenta epigenetic switches." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB097.

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Les cellules placentaires portent un génome différent du génome maternel, puisque 50% de leurs gènes proviennent du génome paternel. Cependant, comme les cellules cancéreuses après la transformation néoplasique, elles réussissent à envahir les tissus de leur hôte, échapper à son système immunitaire et induire une angiogenèse afin d’établir la grossesse. Les cellules cancéreuses et placentaires arborent aussi une différence majeure : alors que de tels mécanismes typiques des cancers sont incontrôlés dans les cellules cancéreuses, ils sont spatialement et temporairement contrôlés dans les cellules placentaires saines. Ainsi, le recherche sur le « concept cancer/placenta » – l’utilisation du placenta pour mieux comprendre le cancer – peut aboutir à l’identification de biomarqueurs et d’approches thérapeutiques innovantes en oncologie, tout comme en gynécologie-obstétrique. Par exemple, les efforts de recherche portant sur l’expression des gènes CGB, codant pour la sous-unité ß de l’hormone chorionique gonadotrope humaine, dans les cellules cancéreuses et placentaires a mené au développement d’un biomarqueur largement utilisé pour la prise en charge de multiples cancers. Il est aussi intéressant de noter que ce même biomarqueur est aussi utilisé pour le dépistage d’aneuploïdies fœtales. De même, le clonage d’INSL4, codant pour le précurseur du peptide placentaire précoce ressemblant à l’insuline (pro-EPIL), dans des cellulaires placentaires précoces, a mené au développement d’un biomarqueur faisant actuellement l’objet d’études cliniques. Avec l’émergence de l’épigénétique, des études de la méthylation de l’ADN, la caractéristique épigénétique la mieux comprise, ont montré que les loci de gènes CGB et INSL4 sont hypométhylés dans les cellules cancéreuses et placentaires ; ce qui pourrait refléter l’hypométhylation globale caractéristique de ces deux types cellulaires. Par conséquent, le projet doctoral présenté dans cette thèse a exploré les modifications des paysages épigénétiques des cellules placentaires au cours de la grossesse et des cellules cancéreuses au cours de la transformation néoplasique. Ce projet a contribué initialement au développement d’un test d’immunoanalyse qui détecte l’hCGß de type II, spécialement codée par un sous-groupe de gènes CGB et détectée dans le sérum de patients atteints de cancers non-placentaires et de trisomie 21 fœtale. Ce test d’immunoanalyse, avec un test similaire développé pour la détection de pro-EPIL, a aussi été utilisé pour des études de preuve de concept précoces quant à l’effet de la méthylation de l’ADN sur l’expression de l’hCGß de type II et de pro-EPIL dans des surnageants de culture cellulaire. En fin de compte, ce projet a mené à la première comparaison directe et pan-génomique de la méthylation de l’ADN dans des cellules cancéreuses au cours de la transformation néoplasique et dans des cellulaires placentaires au cours de la grossesse. Cette étude a porté sur des données, disponibles publiquement, générées à partir de biopsies de 13 types de tumeurs, de villosités choriales (tissus placentaires) et d’autres tissus sains. Elle a également porté sur des données originales générées par nos soins à partir d’échantillons placentaires uniques : des cellules cytotrophoblastiques isolées de villosités choriales ex vivo. Toutes les données inclus dans cette étude ont été générées sur une plateforme de puces à ADN pour la mesure de la méthylation au niveau de 485 512 sites CpG pour chaque échantillon. En combinant, des logiciels innovants reposant sur la puissance d’algorithmes de lissage statistique et sur un solide rationnel biologique, cette étude a ainsi contribué à l’identification de motifs d’hypométhylation à l’échelle du mégabase distinguant les cellules placentaires du début de la grossesse de celles de la fin de la grossesse tout comme ils distinguent les cellules cancéreuses des cellules normales. (...)
Placental cells carry a genome different from the maternal genome, as 50% of it originate from the paternal genome. However, like cancer cells after neoplastic transformation, they successfully invade their host tissues, escape its immune system and induce angiogenesis in order to establish the pregnancy. Cancer and placental cells also display a major discrepancy: while such hallmarks of cancer mechanisms are uncontrolled in cancer cells, they are spatially and temporally controlled in healthy placental cells. Thus, research on the “cancer/placenta concept” – the use of the placenta to better understand cancer – can lead to innovative biomarkers and therapeutic approaches in oncology as well as in gynecology and obstetrics. For example, research efforts on the expression of the CGB genes, encoding for the human chorionic gonadotropin beta subunit (hCGß), in cancer and placental cells have led to the development of a biomarker widely used for the management of various cancers. Interestingly, this same biomarker is also used for the screening of fetal aneuploidies. Likewise, the cloning of INSL4, encoding for the precursor of the early placenta insulin-like peptide (pro-EPIL) in early pregnancy placental cells, has led to the development of a biomarker currently investigated in the clinical setting. Following the rise of epigenetic, studies on DNA methylation, the most well understood epigenetic mark, showed that the loci of CGB genes and INSL4 are hypomethylated in cancer and placental cells, which may reflect a global hypomethylation also characteristic of these cells. Therefore, the doctoral project presented in this dissertation had explored modifications in the epigenetic landscape of placental cells throughout pregnancy and cancer cells throughout neoplastic transformation. This project initially contributed to the development of an immunoassay detecting type II hCGß, specifically encoded by a subset of CGB genes and detected in the serum of patients with non-placental cancers and fetal Down Syndrome. This immunoassay, along with another one directed to pro-EPIL, was also used for an early proof of concept study regarding the effect of DNA methylation on the expression of type II hCGß and pro-EPIL in cell culture supernatants. Ultimately, this project led to the first direct genome-wide comparison of DNA methylation in cancer cells throughout neoplastic transformation and in placental cells throughout pregnancy. It included publically available data generated from biopsies of 13 types of tumors, chorionic villi (placental tissues) and other normal tissues. It also included original data generated from unique placental samples: villous cytotrophoblastic cells isolated ex vivo from chorionic villi. All datasets were generated on a microarray platform measuring DNA methylation at 485,512 CpG sites in each sample. Combining innovative software that leverages the power of statistical smoothing algorithms and a strong biological rationale, this study thus contributed to the identification of megabase-scale patterns of hypomethylation distinguishing early pregnancy from late pregnancy placenta cells as they distinguish normal from cancers cells. Strikingly, the affected genomic regions encompassed genes related to hallmarks of cancer mechanisms such as epithelial-mesenchymal transition (EMT), innate and acquired immune response, and hypoxia. Taken together, these results suggest the hypothesis that patterns of DNA methylation might contribute to “cancer/placenta epigenetic switches” allowing placental implantation and neoplastic transformation when turned “on”, while preventing the placenta to degenerate into an aggressive tumor when turned “off”
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Hernando, Herráez Irene 1985. "Evolutionary insights into human DNA methylation." Doctoral thesis, Universitat Pompeu Fabra, 2015. http://hdl.handle.net/10803/392140.

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DNA methylation is a crucial epigenetic modification involved in numerous biological processes. However, despite its functional importance, the evolutionary history of this modification and the mechanisms diving such changes are poorly understood. The aim of this thesis is to provide a better understanding of DNA methylation in the context of human recent evolution. We identified and described hundreds of regions presenting a human-specific DNA methylation pattern compared to great apes. We also analyzed for the first time the relationship between DNA methylation changes and sequence evolution at both nucleotide and protein level. In summary, this research reveals new insights into the evolutionary properties of DNA methylation and the interpretation of inter-species non-coding variation
La metilación del ADN es una modificación epigenética implicada en numerosos procesos biológicos. Sin embargo, a pesar de su relevancia funcional, se sabe muy poco sobre su historia evolutiva y los mecanismos que generan estos cambios. El objetivo de esta tesis es proporcionar una mejor compresión de la metilación del ADN en el contexto de la evolución humana reciente. Hemos identificado y descrito cientos de regiones que presentan un patrón de metilación especifico de humanos. Así mismo, hemos analizado por primera vez la relación entre los cambios en metilación y la evolución de la secuencia tanto a nivel nucleotídico como proteico. En resumen, esta investigación revela nuevos conocimientos sobre las propiedades evolutivas de la metilación del ADN y la interpretación de la variación no codificante entre especies.
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Yen, Angela. "Computational epigenomics : gene regulation, comparative methodologies, and epigenetic patterns." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/105953.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Electrical Engineering and Computer Science, 2016.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references (pages 203-225).
One of the fundamental aims of biology is to determine what lies at the root of differences across individuals, species, diseases, and cell types. Furthermore, the sequencing of genomes has revolutionized the ways in which scientists can investigate biological processes and disease pathways; new genome-wide, high-throughput experiments require computer scientists with a biological understanding to analyze and interpret the data to improve our understanding about life science. This provides us with a key opportunity to use computational techniques for new biological discoveries. While genetic variation plays an important role in influence phenotype, sequence alone cannot account for all differences: for example, different types of cells in an individual have varying function and attributes, but identical genetic makeup. This highlights the importance of studying epigenetic changes, which are dynamic chemical changes to and around the DNA. While the DNA of every cell in an individual is the same, the epigenetic context for that DNA varies from cell to cell. In this way, these epigenetic differences play a crucial role in gene regulation, with epigenetic changes both causing and recording regulatory mechanisms. In this thesis, we combine the power of computational, statistical, and data science approaches with the new wave of epigenetic data at a genome-wide level in a number of ways. First, in chapter 2, we demonstrate the importance of computational analysis at an epigenomic level by identifying an epigenomic signature of the olfactory receptor gene family that gives insight into the mechanism behind monogenic gene regulation. Next, in chapter 3, we explain our development of ChromDiff, a novel statistical and information theoretic computational methodology to identify chromatin state differences in groups of samples. In our methodology, we use correction for external covariates to isolate the relevant signal, and as a result, we find that our method outperforms existing computational methods, with further validation through randomized simulations. In chapter 4, we apply our methodology to characteristics including sex, developmental age, and tissue type, we unveil relevant chromatin states and genes that distinguish the groups of epigenomes, with further validation of our results through differential expression analysis and gene set enrichment. In chapter 5, we show the power of integrative analysis through the combination of DNA methylation data with chromatin state profiles, cell types, sample groups, experimental technologies, and histone mark data to reveal insightful epigenetic patterns and relationships. Finally, in chapter 6, we identify "hidden" or "unknown" covariates in epigenomic data by using agnostic principal component analysis on our samples to discover similarities between our known covariates and the identified components. In summation, our research highlights the importance of both algorithm development and method application for epigenomic questions, reaffirming the importance of interdisciplinary research that brings together cutting-edge techniques in computer science with appropriate biological hypotheses and data. While questions and analysis must be carefully paired in an informed manner to produce meaningful, interpretable, and believable results in computational biology, our work here provides a sampling of the vast potential for scientific discovery at the intersection of the fields of computer science and biology.
by Angela Yen.
Ph. D.
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Severson, Paul Leamon. "Epigenomic Actions of Environmental Arsenicals." Diss., The University of Arizona, 2013. http://hdl.handle.net/10150/299122.

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Epigenetic dysfunction is a known contributor in carcinogenesis, and is emerging as a mechanism involved in toxicant-induced malignant transformation for environmental carcinogens such as arsenicals. In addition to aberrant DNA methylation of single genes, another manifestation of epigenetic dysfunction in cancer is agglomerative DNA methylation, which can participate in long-range epigenetic silencing that targets many neighboring genes and has been shown to occur in several types of clinical cancers. Using in vitro model systems of toxicant-induced malignant transformation, we found hundreds of aberrant DNA methylation events that emerge during malignant transformation, some of which occur in an agglomerative fashion. In an arsenite-transformed prostate epithelial cell line, the protocadherin (PCDH), HOXC and HOXD gene family clusters are targeted for agglomerative DNA methylation. Aberrant DNA methylation in general occurred more often within H3K27me3 stem cell domains. We found a striking association between enrichment of H3K9me3 stem cell domains and toxicant-induced agglomerative DNA methylation. Global gene expression profiling of the arsenite-transformed prostate epithelial cells showed that gene expression changes and DNA methylation changes were negatively correlated, but less than 10% of the hypermethylated genes were down-regulated. These studies confirm that a majority of the DNA hypermethylation events occur at transcriptionally repressed, H3K27me3 marked genes. In contrast to aberrant DNA methylation targeting H3K27me3 pre-marked silent genes, we found that actively expressed ZNF genes marked with H3K9me3 on their 3' ends, are preferred targets of DNA methylation linked gene silencing. H3K9me3 mediated gene silencing of ZNF genes was widespread, occurring at individual ZNF genes on multiple chromosomes and across ZNF gene family clusters. At ZNF gene promoters, H3K9me3 and DNA hypermethylation replaced H3K4me3, resulting in a widespread down-regulation of ZNF gene expression which accounted for 8% of all the down-regulated genes in the arsenical-transformed cells. In summary, these studies associate arsenical exposure with agglomerative DNA methylation of gene family clusters and widespread silencing of ZNF genes by DNA hypermethylation-linked H3K9me3 spreading, further implicating epigenetic dysfunction as a driver of arsenical-induced carcinogenesis.
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Wang, Jianrong. "Computational algorithm development for epigenomic analysis." Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/48984.

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Multiple computational algorithms were developed for analyzing ChIP-seq datasets of histone modifications. For basic ChIP-seq data processing, the problems of ambiguous short sequence read mapping and broad peak calling of diffuse ChIP-seq signals were solved by novel statistical methods. Their performance was systematically evaluated compared with existing approaches. The potential utility of finding meaningful biological information was demonstrated by the applications on real datasets. For biological question driven data mining, several important topics were selected for algorithm developments, including hypothesis-driven insulator prediction, unbiased chromatin boundary element discovery and combinatorial histone modification signature inference. The integrative computational pipeline for insulator prediction not only produced a list of putative insulators but also recovered specific associated chromatin and functional features. Selected predictions have been experimentally validated. The unbiased chromatin boundary element prediction algorithm was feature-free and had the capability to discover novel types of boundary elements. The predictions found a set of chromatin features and provided the first report of tRNA-derived boundary elements in the human genome. The combinatorial chromatin signature algorithm employed chromatin profile alignments for unsupervised inferences of histone modification patterns. The signatures were associated with various regulatory elements and functional activities. Both the computational advantages and the biological discoveries were discussed.
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Bhasin, Jeffrey M. "Methylome Sequencing Reveals the Context-Specific Functions of DNA Methylation in Indolent Versus Aggressive Prostate Cancer." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case148120498969955.

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Zhu, Yan. "Microfluidic Technology for Low-Input Epigenomic Analysis." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/83402.

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Epigenetic modifications, such as DNA methylation and histone modifications, play important roles in gene expression and regulation, and are highly involved in cellular processes such as stem cell pluripotency/differentiation and tumorigenesis. Chromatin immunoprecipitation (ChIP) is the technique of choice for examining in vivo DNA-protein interactions and has been a great tool for studying epigenetic mechanisms. However, conventional ChIP assays require millions of cells for tests and are not practical for examination of samples from lab animals and patients. Automated microfluidic chips offer the advantage to handle small sample sizes and facilitate rapid reaction. They also eliminate cumbersome manual handling. In this report, I will talk about three different projects that utilized microfluidic immunoprecipitation followed by next genereation sequencing technologies to enable low input and high through epigenomics profiling. First, I examined RNA polymerase II transcriptional regulation with microfluidic chromatin immunoprecipitation followed by next generation sequencing (ChIP-seq) assays. Second, I probed the temporal dynamics in the DNA methylome during cancer development using a transgenic mouse model with microfluidic methylated DNA immunoprecipitation followed by next generation sequencing (MeDIP-seq) assays. Third, I explored negative enrichment of circulating tumor cells (CTCs) followed by microfluidic ChIP-seq technology for studying temporal dynamic histone modification (H3K4me3) of patient-derived tumor xenograft on an immunodeficient mouse model during the course of cancer metastasis. In the first study, I adapted microfluidic ChIP-seq devices to achieve ultrahigh sensitivity to study Pol2 transcriptional regulation from scarce cell samples. I dramatically increased the assay sensitivity to an unprecedented level (~50 K cells for pol2 ChIP-seq). Importantly, this is three orders of magnitude more sensitive than the prevailing pol2 ChIP-seq assays. I showed that MNase digestion provided better ChIP-seq signal than sonication, and two-steps fixation with MNase digestion provided the best ChIP-seq quality followed by one-step fixation with MNase digestion, and lastly, no fixation with MNase digestion. In the second study, I probed dynamic epigenomic changes during tumorigenesis using mice often require profiling epigenomes using a tiny quantity of tissue samples. Conventional epigenomic tests do not support such analysis due to the large amount of materials required by these assays. In this study, I developed an ultrasensitive microfluidics-based methylated DNA immunoprecipitation followed by next-generation sequencing (MeDIP-seq) technology for profiling methylomes using as little as 0.5 ng DNA (or ~100 cells) with 1.5 h on-chip process for immunoprecipitation. This technology enabled me to examine genome-wide DNA methylation in a C3(1)/SV40 T-antigen transgenic mouse model during different stages of mammary cancer development. Using this data, I identified differentially methylated regions and their associated genes in different periods of cancer development. Interestingly, the results showed that methylomic features are dynamic and change with tumor developmental stage. In the last study, I developed a negative enrichment of CTCs followed by ultrasensitive microfluidic ChIP-seq technology for profiling histone modification (H3K4Me3) of CTCs to resolve the technical challenges associated with CTC isolation and difficulties related with tools for profiling whole genome histone modification on tiny cell samples.
Ph. D.
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Gerrard, Diana Lea. "Characterization Of Epigenetic Plasticity And Chromatin Dynamics In Cancer Cell Models." ScholarWorks @ UVM, 2019. https://scholarworks.uvm.edu/graddis/1060.

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Cancer progression is driven by cumulative changes that promote and maintain the malignant phenotype. Epigenetic alterations are central to malignant transformation and to the development of therapy resistance. Changes in DNA methylation, histone acetylation and methylation, noncoding RNA expression and higher-order chromatin structures are epigenetic features of cancer, which are independent of changes in the DNA sequence. Despite the knowledge that these epigenetic alterations disrupt essential pathways that protect cells from uncontrolled growth, how these modifications collectively coordinate cancer gene expression programs remains poorly understood. In this dissertation, I utilize molecular and informatic approaches to define and characterize the genome-wide epigenetic patterns of two important human cancer cell models. I further explore the dynamic alterations of chromatin structure and its interplay with gene regulation in response to therapeutic agents. In the first part of this dissertation, pancreatic ductal adenocarcinoma (PDAC) cell models were used to characterize genome-wide patterns of chromatin structure. The effects of histone acetyltransferase (HAT) inhibitors on chromatin structure patterns were investigated to understand how these potential therapeutics influence the epigenome and gene regulation. Accordingly, HAT inhibitors globally target histone modifications and also impacted specific gene pathways and regulatory domains such as super-enhancers. Overall, the results from this study uncover potential roles for specific epigenomic domains in PDAC cells and demonstrate epigenomic plasticity to HAT inhibitors. In the second part of this dissertation, I investigate the dynamic changes of chromatin structure in response to estrogen signaling over a time-course using Estrogen Receptor (ER) positive breast cancer cell models. Accordingly, I generated genome-wide chromatin contact maps, ER, CTCF and regulatory histone modification profiles and compared and integrated these profiles to determine the temporal patterns of regulatory chromatin compartments. The results reveal that the majority of alterations occur in regions that correspond to active chromatin states, and that dynamic chromatin is linked to genes associated with specific cancer growth and metabolic signaling pathways. To distinguish ER-regulated processes in tamoxifen-sensitive and in tamoxifen-resistant (TAMR) cell models, we determined the corresponding chromatin and gene expression profiles using ER-positive TAMR cancer cell derivatives. Comparison of the patterns revealed characteristic features of estrogen responsiveness and show a global reprogramming of chromatin structure in breast cancer cells with acquired tamoxifen resistance. Taken together, this dissertation reveals novel insight into dynamic epigenomic alterations that occur with extrinsic stimuli and provides insight into mechanisms underlying the therapeutic responses in cancer cells.
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Books on the topic "Epigenomics and epigenetics"

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Spillane, Charles, and Peter McKeown, eds. Plant Epigenetics and Epigenomics. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0179-2.

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Spillane, Charles, and Peter C. McKeown, eds. Plant Epigenetics and Epigenomics. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-773-0.

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Epigenomics, from chromatin biology to therapeutics. Cambridge: Cambridge University Press, 2012.

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Craig, Jeffrey, and Nicholas C. Wong. Epigenetics: A reference manual. Norfolk: Caister Academic Press, 2011.

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Jirtle, Randy L. Environmental Epigenomics in Health and Disease: Epigenetics and Disease Origins. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013.

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Epigenetics, environment, and genes. Toronto: Apple Academic Press, 2013.

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The epigenetics revolution: How modern biology is rewriting our understanding of genetics, disease, and inheritance. New York: Columbia University Press, 2012.

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Payne, Christopher J., ed. Epigenetics and Epigenomics. InTech, 2014. http://dx.doi.org/10.5772/57037.

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Epigenetics. Garland Science, 2013.

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Armstrong, Lyle. Epigenetics. CRC Press LLC, 2020.

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Book chapters on the topic "Epigenomics and epigenetics"

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Tian, Xiuchun cindy. "Bovine Epigenetics and Epigenomics." In Bovine Genomics, 144–68. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118301739.ch11.

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Qiu, Chuan, Fangtang Yu, Hong-Wen Deng, and Hui Shen. "Clinical Epigenetics and Epigenomics." In Translational Bioinformatics, 269–93. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-017-7543-4_10.

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Dong, Nian, Lin Shi, Chengshui Chen, Wenhuan Ma, and Xiangdong Wang. "Clinical Epigenetics and Epigenomics." In Translational Bioinformatics, 115–32. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-017-7543-4_5.

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Skinner, Michael K. "Environmental Epigenetics and Epigenetic Transgenerational Inheritance." In Environmental Epigenomics in Health and Disease, 245–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-23380-7_11.

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Lempiäinen, Harri, Raphaëlle Luisier, Arne Müller, Philippe Marc, David Heard, Federico Bolognani, Pierre Moulin, et al. "Epigenomics - Impact for Drug Safety Sciences." In Toxicology and Epigenetics, 365–85. Chichester, UK: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781118349045.ch19.

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Umashankar, V., and S. Gurunathan. "Databases and Tools for Computational Epigenomics." In Toxicology and Epigenetics, 595–614. Chichester, UK: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781118349045.ch30.

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Yadav, Chandra Bhan, Garima Pandey, Mehanathan Muthamilarasan, and Manoj Prasad. "Epigenetics and Epigenomics of Plants." In Plant Genetics and Molecular Biology, 237–61. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/10_2017_51.

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Carmona, F. Javier, and Manel Esteller. "Human Cancer Epigenetics." In Environmental Epigenomics in Health and Disease, 269–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36827-1_13.

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Hawkins, R. David, and Bing Ren. "Epigenetics of Pluripotency." In Environmental Epigenomics in Health and Disease, 207–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-23380-7_9.

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Sartor, Maureen A., Dana C. Dolinoy, Laura S. Rozek, and Gilbert S. Omenn. "Bioinformatics for High-Throughput Toxico-Epigenomics Studies." In Toxicology and Epigenetics, 569–88. Chichester, UK: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781118349045.ch28.

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Conference papers on the topic "Epigenomics and epigenetics"

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Tomar, Tushar, Nicolette G. Alkema, Gert Jan Meersma, Tim De Meyer, Wim van Criekinge, Harry G. Klip, Ate GJ van der Zee, Steven de Jong, and G. Bea A. Wisman. "Abstract B19: Genome-wide integrated epigenomics identifies FZD-X as novel modulator for platinum sensitivity in high-grade serous ovarian cancer." In Abstracts: AACR Special Conference: Chromatin and Epigenetics in Cancer; September 24-27, 2015; Atlanta, GA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.chromepi15-b19.

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Chung, Chan, Stefan Sweha, Drew Pratt, Benita Tamrazi, Pooja Panwalkar, Adam Banda, Jill Bayliss, et al. "Abstract PR02: Integrated metabolic and epigenomic reprograming by H3K27M mutations in diffuse intrinsic pontine gliomas." In Abstracts: AACR Special Virtual Conference on Epigenetics and Metabolism; October 15-16, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.epimetab20-pr02.

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Mitra, Sheetal A., Anirban P. Mitra, Jonathan D. Buckley, William A. May, Philipp Kapranov, Robert A. Arceci, and Timothy J. Triche. "Abstract PR04: Genomic and epigenomic interactions of an Ewing sarcoma-specific long noncoding RNA." In Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-pr04.

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Labbé, David P., Giorgia Zadra, Ericka M. Ebot, Charles Y. Lin, Jaime M. Reyes, Stefano Cacciatore, Maura Cotter, et al. "Abstract A10: High-fat diet enhances MYC-driven prostate cancer through epigenomic and metabolomic rewiring." In Abstracts: AACR Special Conference: Chromatin and Epigenetics in Cancer; September 24-27, 2015; Atlanta, GA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.chromepi15-a10.

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Yan Zhang, Jangzhong Su, Di Yu, Qiong Wu, and Haidan Yan. "EpiDiff: Entropy-based quantitative identification of differential epigenetic modification regions from epigenomes." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6609585.

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Vaz, Michelle, Stephen Y. Hwang, Ashwini Patil, Hariharan Easwaran, and Stephen B. Baylin. "Abstract B18: Chronic cigarette smoke exposure of bronchial epithelial cells induces progressive epigenomic changes leading to early steps of transformation." In Abstracts: AACR Special Conference: Chromatin and Epigenetics in Cancer; September 24-27, 2015; Atlanta, GA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.chromepi15-b18.

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Mills, Jamie N., and Stephen P. Ethier. "Abstract 2405: The 8p11 amplicon oncogenes ASH2L and NSD3 alter the epigenomic landscape and provide the foundation for novel application of epigenetic therapy in luminal B breast cancers." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2405.

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