Epigenetic alteration including DNA methylation, histone modification, nucleosome positioning and non-coding RNAs expression are involved in a complex network of regulating expression of oncogenes and tumor suppressor genes and constitute an important event of the multistep process of carcinogenesis.
Recent advances in the understanding of the epigenetic regulation and detailed information of these epigenetic changes in various cancers provide new avenues of advancements in diagnostics, prognostics, and therapies of this highly fatal disease.
Epigenetics of Cancer Prevention, Volume Ten is the first to look at epigenetics and chemoprevention together. Although there is numerous scientific data available on how epigenetics can lead to cancer and how chemoprevention can be beneficial in the treatment of, or improvement of quality of life, together they will set an advanced understanding for the reader in this upcoming field of chemoprevention influencing epigenetics.
This book discusses molecular epigenetic targets of natural products, such as green tea polyphenols, curcumin and resveratrol, and organ specific epigenetic targets related to diverse types of cancer, for example prostate, colorectal, breast, lung and skin cancers. Additionally, it encompasses a discussion on research methods and limitations to study epigenetics and epigenomics of chemopreventive drugs and personalized cancer treatment with phytochemicals.
The book is ideal for cancer researchers, health care professionals and all individuals who are interested in cancer prevention research and its clinical applications, especially in natural remedies. Lists natural agents, including nutraceuticals, and their effects on normal or tumor genome Addresses various epigenetic systems and mechanisms in the regulation and support of the mammalian genome Discusses how various parts of dietary phytochemicals can influence or modify epigenetic mechanisms in several types of cancer.
Epigenetic mechanisms are of paramount importance in cancer. Historically, epigenetic studies of cancer have focused on aberrant DNA methylation events. Far less is known about the role of histone modifications in epigenetic mechanisms of human cancers, and of disease in general. There are a number of reasons why histone modifications are especially important to investigate in the context of tumor formation. While DNA methylation contributes to stable gene silencing and formation of heterochromatin, histone modifications are associated with much more dynamic gene expression patterns.
Importantly, histone modifications are also informative of the activity states of distal regulatory elements. Therefore we can use these epigenetic marks to study important regions of the cancer genome that are key regulators of transcription with unprecedented resolution and accuracy. In this work, in-depth studies of epigenetic features of both promoters and distal enhancer elements are described, in each case enabled by distinct histone modifications that are chromatin "signatures" of promoter and enhancer elements, respectively.
We show that in colon cancer, the presence of the H3K4me3 active mark is associated with resistance to silencing associated with DNA methylation.
We further show evidence that in colon cancer, DNA hypermethylation is likely a relatively rare event at CpG-islands, and that most CpG-islands are probably silenced by alternative mechanisms, specifically the acquisition of repressive histone marks.
With respect to distal regulatory elements, enhancer elements are especially attractive candidates to study in cancer, a disease of widespread and heterogeneous aberrant transcription, because they are under normal circumstances drivers of cellular identity and associated global gene expression programs. We report the discovery of thousands of Variant Enhancer Loci, or VELs, which have gained or lost H3K4me1 at enhancer elements in colon cancer samples.
We show that VELs are tightly linked to the in vivo colon cancer transcriptome, and furthermore are enriched at colon cancer susceptibility SNPs. We propose that the model describing gene dysregulation in cancer be revised to now include epigenetic dysregulation at enhancer elements as an important mechanism in cancer-specific gene expression.
Epigenetics and Metabolomics, a new volume in the Translational Epigenetics series, offers a synthesized discussion of epigenetic control of metabolic activity, and systems-based approaches for better understanding these mechanisms. Over a dozen chapter authors provide an overview of epigenetics in translational medicine and metabolomics techniques, followed by analyses of epigenetic and metabolomic linkage mechanisms likely to result in effective identification of disease biomarkers, as well as new therapies targeting the removal of the inappropriate epigenetic alterations.
Epigenetic interventions in cancer, brain damage, and neuroendocrine disease, among other disorders, are discussed in-depth, with an emphasis on exploring next steps for clinical translation and personalized healthcare.
Offers a synthesized discussion of epigenetic regulation of metabolic activity and systems-based approaches to power new research Discusses epigenetic control of metabolic pathways and possible therapeutic targets for cancer, neurodegenerative, and neuroendocrine diseases, among others Provides guidance in epigenomics and metabolomic research methodology.
The exploding field of epigenetics is challenging the dogma of traditional Mendelian inheritance. Epigenetics plays an important role in shaping who we are and contributes to our prospects of health and disease. While early epigenetic research focused on plant and animal models and in vitro experiments, population-based epidemiologic studies increasingly incorporate epigenetic components. The relevance of epigenetic marks, such as DNA methylation, genomic imprinting, and histone modification for disease causation has yet to be fully explored.
This book covers the basic concepts of epigenetic epidemiology, discusses challenges in study design, analysis, and interpretation, epigenetic laboratory techniques, the influence of of age and environmental factors on shaping the epigenome, the role of epigenetics in the developmental origins hypothesis, and provides the state of the art on the epigenetic epidemiology of various health conditions including childhood syndromes, cancer, infectious diseases, inflammation and rheumatoid arthritis, asthma, autism and other neurodevelopmental disorders, psychiatric disorders, diabetes, obesity and metabolic disorders, and atherosclerosis.
Overall, this book illustrates the complexities of the regulation and deregulation of genes mediated through epigenetics in the development and progression of human malignancies. All the articles have been carefully chosen to represent several cancer systems with state of our knowledge on the role of epigenetic deregulation of microRNAs miRNAs and their target mRNAs along with epigenetic deregulation of mRNAs.
Therefore, understanding the role of epigenetics in the regulation of genes especially through deregulated expression of miRNAs as presented in this book will allow scientists to devise targeted therapeutic strategies for re-expression of the lost genes or down-regulate the genes that are over-expressed in order to eradicate cancer.
It is hoped that targeting epigenetics will not only target cancer cells but it will also target the tumor microenvironment more like the entire tumor environment such as the entire host for achieving better treatment outcomes for patients diagnosed with cancer which will lead to achieve the long-term objective for complete eradication of cancer. This book contains fifteen chapters which begins with the concept of systems and network biology for investigating the epigenetics of cancer followed by a series of articles on the role of miRNAs and their target genes in the biology of pancreatic cancer and other cancers such as breast, kidney, prostate and and colon.
Since it is becoming increasingly clear that cancer stem cells CSCs are important in the development and progression of cancer, and CSCs are important in therapeutic resistance, treatment failure and tumor recurrence, thus the importance of CSCs and epigenetics has been highlighted by a very timely article on epigenetic variations of stem cell markers in cancer including miRNAs.
Moreover, just targeting heterogeneous cancer cell populations may not be optimal to eradicate tumors and for which one must take a holistic approach for developing drugs that could also target the tumor microenvironment and tumor dormancy that are regulated through epigenetics. Keeping abreast with this thought process the concluding chapter provides a concept towards curative cancer therapy with maspin, which could be a unique window of opportunity to target tumor dormancy.
Therefore, it suggest that targeting the tumor dormancy and the tumor microenvironment using novel therapeutics specifically by targeting epigenetics would become the future of medicine. In a simplified form, epigenetics refers to heritable changes in phenotype that are not due to changes in the underlying DNA sequence. In this book, epigenetic mechanisms of regulation and dysregulation in health and disease are explored in great depth. Detailed chapters on epigenetic processes including DNA methylation and chromatin post-translational modifications including potential interventions with DNA methyltransferase inhibitors and histone deacetylase inhibitors are explored in initial chapters.
These provide a detailed overview and important background to the entire field. The book is then focussed on epigenetic mechanisms involved in various diseases including anti-inflammatory and autoimmune conditions.
Important accounts relating to the effects of epigenetics in metabolic syndrome, cardiovascular disease and asthma are the focus of subsequent chapters. The role of epigenetic dysregulation in malignancy is a current topic of interest and represents an intense field of research. A large component of this book is dedicated to the analysis of aberrant epigenetic processes in carcinogenesis and cancer progression.
Further, chapters are focused on emerging cancer prevention using nutritional components and anti-cancer therapies particularly with histone deacetylase inhibitors, which have already been approved for the treatment of cutaneous T-cell lymphoma. The emerging role of nanoparticle preparations, especially in the context of delivering potential epigenetic therapies to target cells in various diseases, is also explored in this book.
Overall, this book encompasses a wide range of topics related to epigenetic mechanisms in health and disease and would appeal to anyone with an interest in epigenetics, chromatin biology and emerging epigenetic interventions and therapies.
Epigenetic mechanisms including DNA methylation and histone modifications are essential in many cellular processes including gene expression, chromatin compaction, genetic imprinting, cell differentiation, and X-chromosome and retrotransposon inactivation. Disruption of epigenetic mechanisms through genetic or environmental factors results in development of many diseases, including cancer.
Benzo a pyrene BaP is an environmental pollutant found in air, diet, or unhealthy lifestyle choices such as smoking, and has been linked to carcinogenesis. BaP exposure-associated DNA damage and disruption of gene expression have been linked to carcinogenesis, but its effect on the epigenetic mechanisms leading to breast cancer is less understood.
Global genomic approaches for the analysis of environmentally-induced epigenetic changes could play an important role in elucidating the role of environmental mediation of epigenetics in pathogenesis. Related Books Hot Free as in Freedom 2. Great book, Epigenetics Revolution pdf is enough to raise the goose bumps alone. Add a review Your Rating: Your Comment:. Carey by M. Hot Fellside by M. The Harvester by Gene Stratton-Porter. Woods Runner by Gary Paulsen.
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