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Volume 100 compiles information on tumor sites and mechanisms of carcinogenesis. About half of the agents classified in Group 1 were last reviewed more than 20 years ago, before mechanistic studies became prominent in evaluations of carcinogenicity. In addition, more recent epidemiological studies and animal cancer bioassays have demonstrated that many cancer hazards reported in earlier studies were later observed in other organs or through different exposure scenarios. Much can be learned by updating the assessments of agents that are known to cause cancer in humans. Accordingly, IARC has selected A Review of Human Carcinogensto be the topic for Volume 100. It is hoped that this volume, by compiling the knowledge accumulated through several decades of cancer research, will stimulate cancer prevention activities worldwide, and will be a valued resource for future research to identify other agents suspected of causing cancer in humans. Volume 100 was developed by six separate Working Groups: Pharmaceuticals; Biological agents; Metals, particles, and fibres; Radiation; Personal habits and household exposures; Chemical agents and related occupations. Because the scope of Volume 100 is so broad, its Monographs are focused on key information. Each Monograph presents a description of a carcinogenic agent and how people are exposed, critical overviews of the epidemiological studies and animal cancer bioassays, and a concise review of the agent's toxicokinetics, plausible mechanisms of carcinogenesis, and potentially susceptible populations, and life-stages. Details of the design and results of individual epidemiological studies and animal cancer bioassays are summarized in tables. Short tables that highlight key results are printed in Volume 100, and more extensive tables that include all studies appear on the Monographs programe website (http://monographs.iarc.fr/). For a few well-established associations (for example, tobacco smoke and human lung cancer), it was impractical to include all studies, even in the website tables. In those instances, the rationale for inclusion or exclusion of sets of studies is given.
Despite increasing knowledge of human nutrition, the dietary contribution to cancer remains a troubling question. Carcinogens and Anticarcinogens assembles the best available information on the magnitude of potential cancer riskâ€"and potential anticarcinogenic effectâ€"from naturally occurring chemicals compared with risk from synthetic chemical constituents. The committee draws important conclusions about diet and cancer, including the carcinogenic role of excess calories and fat, the anticarcinogenic benefit of fiber and other substances, and the impact of food additive regulation. The book offers recommendations for epidemiological and diet research. Carcinogens and Anticarcinogens provides a readable overview of issues and addresses critical questions: Does diet contribute to an appreciable proportion of human cancer? Are there significant interactions between carcinogens and anticarcinogens in the diet? The volume discusses the mechanisms of carcinogenic and anticarcinogenic properties and considers whether techniques used to evaluate the carcinogenic potential of synthetics can be used with naturally occurring chemicals. The committee provides criteria for prioritizing the vast number of substances that need to be tested. Carcinogens and Anticarcinogens clarifies the issues and sets the direction for further investigations into diet and cancer. This volume will be of interest to anyone involved in food and health issues: policymakers, regulators, researchers, nutrition professionals, and health advocates.
This work presents a summary of research evidence on links between work, health and disability. Across two sections it summarizes updated knowledge on adverse effects of distinct occupational hazards, and it covers concerns with employment opportunities or restrictions. The handbook delivers an overview of material and psychosocial factors as occupational hazards on working people’s physical or mental health that may result in functional impairment and disability. This knowledge can be instrumental in strengthening efforts of professionals and other stakeholders to promote health-conducive working conditions and prevent work-related disability risks. It also covers concerns with employment opportunities or restrictions of persons with physical or mental health problems and disability. This field of interdisciplinary research has grown with a broad range of solid new findings that can have favorable impact on work disability prevention and the practice of medical and vocational rehabilitation. Prominent experts discuss this evidence for major manifestations of physical and mental health problems and disabilities. As a further innovative feature, this handbook integrates biomedical, psychological, and sociological knowledge on major aspects of the links between work, health and disability. It is therefore of interest to students and professionals in related disciplines, as well as for stakeholders involved in the prevention of work disability and rehabilitation into paid work. In times of an increasingly aging work force with elevated risks of reduced health and work functioning, this knowledge can contribute to turning the threats associated with disability into opportunities. This handbook supports the overall aim of enabling persons with (chronic) health problems and disability to participate in work and social life.
This volume will provide a contemporary account of advances in chemical carcinogenesis. It will promote the view that it is chemical alteration of the DNA that is a route cause of many cancers. The multi-stage model of chemical carcinogenesis, exposure to major classes of human carcinogens and their mode-of-action will be a focal point. The balance between metabolic activation to form biological reactive intermediates and their detoxification, ensuing DNA-lesions and their repair will be profiled. It will describe the chemical changes that occur in DNA that result from endogenous insults including epigenetic changes that lead to gene silencing. It will describe major mechanisms of mutagenesis, affects on tumor suppressor genes and proto-oncogenes, and how cell-cycle check points can be by-passed by the "stealth-like" properties of chemical carcinogens. Environmental agents that can promote tumor formation will be discussed. The monograph will have wide appeal as a knowledge base for graduate students, post-doctoral fellows and faculty interested in this aspect of cancer causation and research.
Though overall cancer incidence and mortality have continued to decline in recent years, cancer continues to devastate the lives of far too many Americans. In 2009 alone, 1.5 million American men, women, and children were diagnosed with cancer, and 562,000 died from the disease. There is a growing body of evidence linking environmental exposures to cancer. The Pres. Cancer Panel dedicated its 2008¿2009 activities to examining the impact of environmental factors on cancer risk. The Panel considered industrial, occupational, and agricultural exposures as well as exposures related to medical practice, military activities, modern lifestyles, and natural sources. This report presents the Panel¿s recommend. to mitigate or eliminate these barriers. Illus.
"This publication represents the views and expert opinions of an IARC Working Group on the Evaluation of Carcinogenic Risk to Humans, which met in Lyon, 8-15 October 2013."
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.
Infections must be thought as one of the most important, if not the most important, risk factors for cancer development in humans. Approximately 15-20% of all cases of cancer around the world are caused by viruses. The establishment of a causal relationship between the presence of specific infective agents and certain types of human cancer represents a key step in the development of novel therapeutic and preventive strategies. In this book, Professor zur Hausen (Nobel Prize in Physiology/Medicine 2008) provides a thorough and comprehensive overview on carcinogenic infective agents -- viruses, bacteria, parasites and protozoons -- as well as their corresponding transforming capacities and mechanisms. The result is an invaluable and instructive reference for all oncologists, microbiologists and molecular biologists working in the area of infections and cancer. The author was among the first scientists to reveal the cervical cancer-inducing mechanisms of human papilloma viruses and isolated HPV16 and HPV18, and, as early as 1976, published the hypothesis that wart viruses play a role in the development of this type of cancer.