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The overall aim of this book is to give scientists in academia and industry a comprehensive overview of the field of DNA damage and DNA repair and related human diseases.
The DNA of all organisms is constantly being damaged by endogenous and exogenous sources. Oxygen metabolism generates reactive species that can damage DNA, proteins and other organic compounds in living cells. Exogenous sources include ionizing and ultraviolet radiations, carcinogenic compounds and environmental toxins among others. The discovery of multiple DNA lesions and DNA repair mechanisms showed the involvement of DNA damage and DNA repair in the pathogenesis of many human diseases, most notably cancer. These books provide a comprehensive overview of the interdisciplinary area of DNA damage and DNA repair, and their relevance to disease pathology. Edited by recognised leaders in the field, this two-volume set is an appealing resource to a variety of readers including chemists, chemical biologists, geneticists, cancer researchers and drug discovery scientists.
Continuing the tradition of presenting information on DNA damage and repair, this 3rd volume provides the latest reviews by leading researchers. They illuminate key aspects of DNA repair in mammalian systems and its relationship to human disease.
Cutting edge reviews by leading researchers illuminate key aspects of DNA repair in mammalian systems and its relationship to human genetic disease and cancer. Major topics include UV and X-Ray repair, repair of chemical damage, recombinational repair, mismatch repair, transcription-repair coupling, and the role of DNA repair in disease prevention. Extensive up-to-date references and rigorous peer-review of each chapter make this volume definitive and bring it to the active frontiers of research.
Since this book is geared to be used by varied groups of readers such as advanced students and instructors in the fields of biology and medicine, scientists and more importantly clinicians, it is considered important to provide brief accounts of the basics of DNA damage, repair, mutagenesis and cancer. The purpose of this book is to present an updated detailed account of some important additional diseases of DNA repair. It has not been possible to cover all the DNA repair deficient diseases in this volume, hence diseases such as Bloom’s syndrome, Werner’s syndrome, Nijmegen breakage syndrome, ataxia telangiectasia‐like disorder, RA D 50 deficiency, RIDDLE syndrome and others will be presented in a forthcoming volume.
An essential resource for all scientists researching cellular responses to DNA damage. • Introduces important new material reflective of the major changes and developments that have occurred in the field over the last decade. • Discussed the field within a strong historical framework, and all aspects of biological responses to DNA damage are detailed. • Provides information on covering sources and consequences of DNA damage; correcting altered bases in DNA: DNA repair; DNA damage tolerance and mutagenesis; regulatory responses to DNA damage in eukaryotes; and disease states associated with defective biological responses to DNA damage.
Jac A. Nickoloff and Merl F. Hoekstra update and expand their two earlier acclaimed volumes (Vol. I: DNA Repair in Prokaryotes and Lower Eukaryotes and Vol. II: DNA Repair in Higher Eurkaryotes) with cutting-edge reviews by leading authorities of primary experimental findings about DNA repair processes in cancer biology. The reviews cover a wide range of topics from viruses and prokaryotes to higher eukaryotes, and include several new topics, among them the role of recombination in replication of damaged DNA, X-ray crystallographic analysis of DNA repair protein structures, DNA repair proteins and teleomere function, and the roles of BRCA1 and BRCA2 in DNA repair. Authoritative and up-to-date, DNA Damage and Repair, Vol. III: Advances from Phage to Humans surveys the rapidly moving research in DNA damage and repair, and explains the important functional relationships among different DNA repair pathways and the relationship between DNA repair pathways, cancer etiology, and cancer therapies.
This book is based on the papers presented at the conference on "Mecha nisms of DNA Damage and Repair: Implications for Carcinogenesis and Risk Assessment," held at the National Bureau of Standards on June 2-7, 1985, This volume deals with mechanisms of DNA damage and repair at the molecular level; consequences of unrepaired or misrepaired damage, with major emphasis on carcinogenesis; drugs which bind selectively to altered and potentially damaging DNA sequences; and potential utilization of DNA damage as an endpoint for assessing risks of UV light, ionizing radiations, chemicals, drugs, and hazardous agents in foods. Because the induction of mutations by radiation and genotoxic chemicals has been observed to follow one-hit kinetics in some instances, it is generally assumed that any level of exposure to a DNA-damaging agent may increase the risk of genetic disease or cancer in an exposed population. At the same time, however, there is evidence that although the DNA of living cells is continually damaged by natural background radiation, free radicals, and other naturally occurring processes, most of the damage is normally repaired.
The ?eld of cellular responses to DNA damage has attained widespread recognition and interest in recent years commensurate with its fundamental role in the ma- tenance of genomic stability. These responses, which are essential to preventing cellular death or malignant transformation, are organized into a sophisticated s- tem designated the “DNA damage response”. This system operates in all living organisms to maintain genomic stability in the face of constant attacks on the DNA from a variety of endogenous by-products of normal metabolism, as well as exogenous agents such as radiation and toxic chemicals in the environment. The response repairs DNA damage via an intricate cellular signal transduction network that coordinates with various processes such as regulation of DNA replication, tr- scriptional responses, and temporary cell cycle arrest to allow the repair to take place. Defects in this system result in severe genetic disorders involving tissue degeneration, sensitivity to speci?c damaging agents, immunode?ciency, genomic instability, cancer predisposition and premature aging. The ?nding that many of the crucial players involved in DNA damage response are structurally and functionally conserved in different species spurred discoveries of new players through similar analyses in yeast and mammals. We now understand the chain of events that leads to instantaneous activation of the massive cellular responses to DNA lesions. This book summarizes several new concepts in this rapidly evolving ?eld, and the advances in our understanding of the complex network of processes that respond to DNA damage.