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Tumors can be induced by a variety of physical and chemical carcinogens. The resulting tumor cells are usually abnormal in their morphology and behavior and transmit their abnormalities to their daughter tumor cells. Most theories of the pathogenesis of tumors suggest that carcinogens in some way cause alterations either of the genomes or of inheritable patterns of gene expression in normal cells, which then cause morphological and behavioral changes. This volume presents a collection of articles aimed at the question by what genetic or epigenetic mechanisms carcinogens can cause morphological abnormalities of tumor cells. It includes reviews of cellular targets of known carcinogens, and presents varying viewpoints of how morphological abnormalities and the actions of carcinogens might be related. The volume will be of interest to all those who are involved in cancer research or in the prevention, diagnosis or management of tumors in humans or animals.
This volume began with an invitation from the publishers to edit a volume of EXS on Cancer. This invitation undoubtedly derived from my articles in Cellular and Molecular Life Sciences in 2002 and 2003 on the relationships between the morphology, aetiology and pathogenesis of tumours, especially in relation to genetic instability. After many years of teaching the theories of c- cer in undergraduate medical school courses, it seemed to me that the variably chaotic histopathologic features of tumours parallel in some way, the variably unstable genomes of tumour cells, which were being discovered in the 1990s. Thus the title of the volume has come to include morphology, carcinogenesis and genetic instability. The invitation came while I was working with Herrn Dr. med. Hubertus Jersmann (MD Düsseldorf, PhD, now Senior Lecturer in Medicine of the University of Adelaide) and Professor Brian Coghlan (Emeritus Professor of German, the University of Adelaide), on the work of the nineteenth century cancer pathologists, especially David Paul von Hansemann (1858–1920). With the delivery of the manuscripts from the authors of the chapters, it became obvious that a background chapter for the volume could include some of the material which we had “uncovered” together. Because of this, chapter 1 is authored by the three of us, and the “new” material figures prominently.
Genome Stability: From Virus to Human Application, Second Edition, a volume in the Translational Epigenetics series, explores how various species maintain genome stability and genome diversification in response to environmental factors. Here, across thirty-eight chapters, leading researchers provide a deep analysis of genome stability in DNA/RNA viruses, prokaryotes, single cell eukaryotes, lower multicellular eukaryotes, and mammals, examining how epigenetic factors contribute to genome stability and how these species pass memories of encounters to progeny. Topics also include major DNA repair mechanisms, the role of chromatin in genome stability, human diseases associated with genome instability, and genome stability in response to aging. This second edition has been fully revised to address evolving research trends, including CRISPRs/Cas9 genome editing; conventional versus transgenic genome instability; breeding and genetic diseases associated with abnormal DNA repair; RNA and extrachromosomal DNA; cloning, stem cells, and embryo development; programmed genome instability; and conserved and divergent features of repair. This volume is an essential resource for geneticists, epigeneticists, and molecular biologists who are looking to gain a deeper understanding of this rapidly expanding field, and can also be of great use to advanced students who are looking to gain additional expertise in genome stability. - A deep analysis of genome stability research from various kingdoms, including epigenetics and transgenerational effects - Provides comprehensive coverage of mechanisms utilized by different organisms to maintain genomic stability - Contains applications of genome instability research and outcomes for human disease - Features all-new chapters on evolving areas of genome stability research, including CRISPRs/Cas9 genome editing, RNA and extrachromosomal DNA, programmed genome instability, and conserved and divergent features of repair
but also the possibility of intervention in specific stages. In Human behavior, including stress and other factors, plays an important role in neoplasia, although too little is known addition, variables which affect cancer development as well on the reasons for such development. Carcinogens, which as some endogenous factors can be better delineated help initiate the neoplastic process, may be either synthetic through such investigations. The topics of this volume encompass premalignant non or naturally-occurring. Cancer causation may be ascribed to invasive lesions, species-specific aspects of carcinogenicity, certain chemicals, physical agents, radioactive materials, viruses, parasites, the genetic make-up of the organism, and radiation, viruses, a quantum theory of carinogenesis, onco bacteria. Humans, eumetazoan animals and vascular plants genes, and selected environmental carcinogens. are susceptible to the first six groups of cancer causes, whe reas the last group, bacteria, seems to affect only vascular plants. Neoplastic development may begin with impairment ofJmdy defenses by a toxic material (carcinogen) which acts as an initiator, followed by promotion and progression to an overt neoplastic state. Investigation of these processes Series Editor Volume Editor allows not only a better insight into the mechanism of action Hans E. Kaiser Elizabeth K. Weisburger vii ACKNOWLEDGEMENT Inspiration and encouragement for this wide ranging project on cancer distribution and dissemination from a comparative biological and clinical point of view, was given by my late friend E. H. Krokowski.
The book addresses controversies related to the origins of cancer and provides solutions to cancer management and prevention. It expands upon Otto Warburg's well-known theory that all cancer is a disease of energy metabolism. However, Warburg did not link his theory to the "hallmarks of cancer" and thus his theory was discredited. This book aims to provide evidence, through case studies, that cancer is primarily a metabolic disease requring metabolic solutions for its management and prevention. Support for this position is derived from critical assessment of current cancer theories. Brain cancer case studies are presented as a proof of principle for metabolic solutions to disease management, but similarities are drawn to other types of cancer, including breast and colon, due to the same cellular mutations that they demonstrate.
Telomerase, an enzyme that maintains telomeres and endows eukaryotic cells with immortality, was first discovered in tetrahymena in 1985. In 1990s, it was proven that this enzyme also plays a key role in the infinite proliferation of human cancer cells. Now telomere and telomerase are widely accepted as important factors involved in cancer biology, and as promising diagnostic tools and therapeutic targets. Recently, role of telomerase in “cancer stem cells” has become another attractive story. Until now, there are several good books on telomere and telomerase focusing on biology in ciliates, yeasts, and mouse or basic sciences in human, providing basic scientists or students with updated knowledge.
This book provides the first comprehensive and systematic survey of present knowledge about radiation carcinogenesis. World experts review in detail current information on such topics as the incidence of various forms of cancer in irradiated populations, the carcinogenic effects of ionizing radiation in laboratory animals, theoretical mechanisms of radiation carcinogenesis, and the implications of the data for assessing the risks of human cancer. In view of recent controversy about the carcinogenic hazards of low-level exposure to radiation and other carcinogens, this book is a timely contribution toward our understanding of the carcinogenic risks of low-level radiation.