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This book describes the changing role of pathology in aiding reproducible and accurate patient selection for predictive cancer therapy. Particular attention is given to the clinical application of cutting-edge cancer biomarkers to accurately select patients for targeted cancer therapy and how artificial intelligence can improve the precision of treatments. The advent and basis of predictive cancer care, the role of pathologists in translational cancer research, the analysis of cancer samples, the management of biopsy results, and the accuracy of biopsy results are also discussed. Precision Cancer Medicine: Role of the Pathologist details how pathologists can use the latest biomarkers and apply artificial intelligence technology in cancer diagnosis and management. It is also relevant to oncologists and medical practitioners involved in cancer management seeking an up-to-date resource on the topic.

Cancer: Oxidative Stress and Dietary Antioxidants, Second Edition, covers the science of oxidative stress in cancer and the potentially therapeutic usage of natural antioxidants in the diet or food matrix. The processes within the science of oxidative stress are described in concert with other processes, such as apoptosis, cell signaling, and receptor-mediated responses. This approach recognizes that diseases are often multifactorial and that oxidative stress is a single component. Other sections cover new organ site tumors—skin and liver cancer, the role of polymorphisms, cytochrome p450s, COX gene, fatty acids, apoptosis, T cells and mitochondria, prevention/protection with anthocyanins, esculetin, nanoparticles, and more. This book is a valuable resource for cancer researchers, oncologists, nutritionists and other members of the biomedical field who are interested in enhancing treatment outcome, improving the quality of life of patients, and developing new treatments in the fight against cancer. - Encompasses updated, revised and state-of-the-art information to advance cancer research - Bridges the gaps between nutrition, oxidative stress, and cancer, presenting a holistic approach for health care and research - Contains wide applicability to cancer research, from prevention to novel therapeutics

Cancer is a collection of diseases that can affect basically every organ of our body, all of which have in common uncontrolled cellular growth. The cells forming our body have the potential to grow in the context of wound healing or for the constant replacement of cells in our blood, skin or intestine. Behind every newly diagnosed malignant tumor in adulthood there is an individual history of probably 20 or more years of tumorigenesis. Therefore, malignant tumor formation often takes time making cancer in most cases to an aging-related disease that we seem not to be able to evade. However, tumorigenesis is dependent on multiple environmental influences, many of which we have under control by lifestyle decisions, such as retaining from smoking, selecting healthy food and being physically active. Thus, cancer preventive interventions are the most effective way to fight against cancer. This textbook wants not only to describe basic mechanisms leading to cancer but also to provide the readers with a more holistic view including cancer surveaillance mechanisms of the immune system. We will place these insights in the context of the personal consequences of everyone's lifestyle decisions. The content of the book is linked to the lecture course in “Cancer Biology”, which is given by Prof. Carlberg since 2005 at the University of Eastern Finland in Kuopio. Moreover, biological processes explained in this book will be set into a clinical context using the experience of Dr. Velleuer in the daily care in oncology. This book also relates to the textbooks “Mechanisms of Gene Regulation: How Science Works” (ISBN 978-3-030-52321-3), “Human Epigenetics: How Science Works” (ISBN 978-3-030-22907-8) and “Nutrigenomics: How Science Works” (ISBN 978-3-030-36948-4), the studying of which may be interesting to readers who like to get more detailed information.

Human Papillomavirus: Proving and Using a Viral Cause for Cancer presents a steady and massive accumulation of evidence about the role of HPV and prevention of HPV-induced cancer, along with the role and personal commitment of many scientists of different backgrounds in establishing global relevance. This exercise involved years of personal commitment to proving or disproving an idea that aroused initial skepticism, and that still has difficult implications for some. It remains one of the big successes of medicine that exploited both established medical science dating back to the nineteenth century and new molecular genetic science during a time of transition in medicine. - Presents a comprehensive, up-to-date review of the role of HPV in cancer from those involved in its study - Includes the way evidence on the role and utility of HPV based prevention has been accumulated over almost 40 years - Gives a series of vignettes of individual scientists involved in the development of the science of HPV and cancer at different stages and their experiences and reasons for involvement

Why do we get cancer? Is it our modern diets and unhealthy habits? Chemicals in the environment? An unwelcome genetic inheritance? Or is it just bad luck? The answer is all of these and none of them. We get cancer because we can't avoid it—it's a bug in the system of life itself. Cancer exists in nearly every animal and has afflicted humans as long as our species has walked the earth. In Rebel Cell: Cancer, Evolution, and the New Science of Life's Oldest Betrayal, Kat Arney reveals the secrets of our most formidable medical enemy, most notably the fact that it isn't so much a foreign invader as a double agent: cancer is hardwired into the fundamental processes of life. New evidence shows that this disease is the result of the same evolutionary changes that allowed us to thrive. Evolution helped us outsmart our environment, and it helps cancer outsmart its environment as well—alas, that environment is us. Explaining why'everything we know about cancer is wrong,'Arney, a geneticist and award-winning science writer, guides readers with her trademark wit and clarity through the latest research into the cellular mavericks that rebel against the rigid biological'society'of the body and make a leap towards anarchy. We need to be a lot smarter to defeat such a wily foe—smarter even than Darwin himself. In this new world, where we know that every cancer is unique and can evolve its way out of trouble, the old models of treatment have reached their limits. But we are starting to decipher cancer's secret evolutionary playbook, mapping the landscapes in which these rogue cells survive, thrive, or die, and using this knowledge to predict and confound cancer's next move. Rebel Cell is a story about life and death, hope and hubris, nature and nurture. It's about a new way of thinking about what this disease really is and the role it plays in human life. Above all, it's a story about where cancer came from, where it's going, and how we can stop it.

Renommierte Heidelberger Wissenschaftler haben in diesem Buch zusammengetragen, was heute über Krebserkrankungen und ihre Ursachen bekannt ist. Lediglich 5 bis 10% aller Krebserkrankungen werden durch vererbte Gendefekte verursacht. Epidemiologische und experimentelle Daten aus wissenschaftlichen Studien und Hochrechnungen zeigen, wie sehr das Erkrankungsrisiko durch die eigene moderne Lebensweise beeinflusst wird. Die Autoren haben sich zum Ziel gesetzt, diffusen Ängsten und gefährlichem Halbwissen wissenschaftlich valides Wissen entgegenzusetzen und diese Daten und Fakten verständlich und unterhaltsam zu präsentieren. Das Buch richtet sich an alle medizinisch Interessierten, Betroffene und Angehörige.

The questions we ask in this book about cancer are actually quite elementary. What is the origin of cancer? Does cancer arise in any cell in the body, or only in certain cells? Is cancer a genetic or a stem-cell disease? We illustrate that cancer is a multicellular rather than a unicellular process, a cellular rather than a genetic problem, and a stem-cell rather than a somatic-cell disease. We reveal that the incredible resemblance between a cancer cell and a stem cell suggests that they are intimately related. The uncanny ingenuity of a cancer cell is also innate in a stem cell. The recognition that cancer has a stem-cell origin indicates that a stem-cell theory of cancer may be the unified theory that we need to make sense of the torrents of new data and new insights into different facets of cancer, to see how they fit together into one picture, and to disarm the disease. A stem-cell theory of cancer can potentially accept, embrace, and integrate all of its genetic, epigenetic, proteomic, and metabolic aspects. Such a unified theory can account for all cancer hallmarks, including metastasis, heterogeneity, dormancy, and immune evasion. It predicts that multimodal therapy may be more beneficial than targeted therapy, and integrated medicine more effective than precision medicine for the management of all but the simplest tumors. It predicts that when we have the correct cancer theory, clinical progress will advance by monumental leaps rather than incremental steps. Indeed, I predict that successful clinical outcomes will ultimately provide irrefutable validation that cancer is a stem-cell disease. Therefore, the thesis of this book is actually quite simple. When we have a pertinent and correct theory of the origin of cancer, all ideas, observations, experiments, and treatments will begin to fall into place and make perfect sense. We would like to convince readers that a stem-cell theory is the elusive, long-sought unified theory, the theory of all theories, of cancer.

Popular understanding holds that genetic changes create cancer. James DeGregori uses evolutionary principles to propose a new way of thinking about cancer's occurrence. Cancer is as much a disease of evolution as it is of mutation, one in which mutated cells outcompete healthy cells in the ecosystem of the body's tissues. His theory ties cancer's progression, or lack thereof, to evolved strategies to maximize reproductive success.Through natural selection, humans evolved genetic programs to maintain bodily health for as long as necessary to increase the odds of passing on our genes—but not much longer. These mechanisms engender a tissue environment that favors normal stem cells over precancerous ones. Healthy tissues thwart cancer cells'ability to outcompete their precancerous rivals. But as our tissues age or accumulate damage from exposures such as smoking, normal stem cells find themselves less optimized to their ecosystem. Cancer-causing mutations can now help cells adapt to these altered tissue environments, and thus outcompete normal cells. Just as changes in a species'habitat favor the evolution of new species, changes in tissue environments favor the growth of cancerous cells.DeGregori's perspective goes far in explaining who gets cancer, when it appears, and why. While we cannot avoid mutations, it may be possible to sustain our tissues'natural and effective system of defense, even in the face of aging or harmful exposures. For those interested in learning how cancers arise within the human body, the insights in Adaptive Oncogenesis offer a compelling perspective.

The book Psychoneurocybernetic Conquest of Carcinogenesis and Cancers is written to be understood by the informed layman as well as by scientists. It should be of special interest to physicians, health-care givers and laymen who want to know about the latest knowledge concerning the true cause of all cancers and their prevention, diagnosis and modern therapy. It will surely inform and entertain anyone who cares about ethics in medicine or the funding of medical research, including references to original scientific and popular literature. According to general (not only medical) knowledge, based upon personal experiences in conservative, surgical, thermo- and radiotherapy of neoplasms over many years, the authors have presented the dissipative nature of cancer so that everyone could understand the neoplastic diseases, the modern rules of psycho-oncology and the primary significance of one's own lifestyle in the formation and progress of cancer along with importance of caring about the environment inhabited by people. They have summarized the public reactions to cancer and infertility in relation to the historic discovery of natural psychoneurocybernetic cause of cancer, mathematical interpretation of its cause, obstetrical prevention of human cancers and psycho-neuro-endocrine therapy of diseases, especially caused by baneful information.

Molecular Therapies of Cancer comprehensively covers the molecular mechanisms of anti-cancer drug actions in a comparably systematic fashion. While there is currently available a great deal of literature on anti-cancer drugs, books on the subject are often concoctions of invited review articles superficially connected to one another. There is a lack of comprehensive and systematic text on the topic of molecular therapies in cancer. A further deficit in the relevant literature is a progressive sub-specialization that typically limits textbooks on cancer drugs to cover either pharmacology or medicinal chemistry or signal transduction, rather than explaining molecular drug actions across all those areas; Molecular Therapies of Cancer fills this void. The book is divided into five sections: 1. Molecular Targeting of Cancer Cells; 2. Emerging and Alternative Treatment Modalities; 3. Molecular Targeting of Tumor-Host Interactions; 4. Anti-Cancer Drug Pharmacokinetics; and 5. Supportive Therapies.

An international team of accomplished researchers has been assembled to define the role that antioxidants and pro-oxidants play in cancer. Increasing scientific evidence points to the importance of antioxidants and pro-oxidants in both the etiology of cancer development and in cancer treatments. This book should prove useful for research scientists wanting a comprehensive review of the latest accomplishment in this area and for health care-providers who advise patients and the general public about dietary antioxidants and the safety and appropriate use of antioxidant supplements. Endogenous antioxidants systems that play key roles in modulating the in vivo effects of reactive oxygen species (ROS) are reviewed in detail. Many exogenous antioxidants such as vitamin E (tocopherols and tocotrienols), vitamin C, green tea polyphenols, beta-carotene and curcumin are individually discussed as well as their potential roles in alternative and complementary medicine approaches to cancer prevention and treatment. For public health professionals the question of whether or not antioxidants have a safe chemopreventive role is central: it is clearly much more effective to prevent cancer than deal with its consequences including the damaging side effects of many chemotherapeutics. A key theme explored throughout this book is the cancer-related events arising from oxidative stress and the over production of ROS. On the one hand, oxidative stress has been linked to DNA damage, mutations and an increased risk of cancer. Quite remarkably, cancer cells often exhibit a high level of intrinsic oxidative stress that is fundamental to the expression of many cancer phenotypes. The molecular mechanism whereby ROS modulate cell signaling pathways related to cancer phenotypes is, therefore, carefully reviewed. One chapter, based on original research, describes a novel methodology for measuring the cellular production of specific reactive oxygen species. A most important question is whether or not antioxidants can reduce the incidence of cancers or block the expression of cancer phenotypes. Oxidative stress in cancer cells is, however, a dual-edged sword and many cancer therapies rely on using an additional oxidative stressor to selectively drive cancer cells into programmed cell death. The high level of intrinsic oxidative stress expressed by many cancer cells has often been called the “Achilles'heal” of cancer. A second question is whether antioxidants could negatively interfere with pro-oxidant based cancer therapies. These two questions and related issues are addressed in this book. Pharmacologists with an interest in the rationale design of drugs and prodrugs for treating cancer by exploiting its high level of intrinsic oxidative stress will also benefit from this book since this issue is specifically addressed in a number of chapters. Issues related to antioxidants and pro-oxidants are also discussed in relationship to specific cancers such colorectal cancer, pancreatic cancer and prostate cancer.

This book from the International Agency for Research on Cancer, the specialized cancer agency of the World Health Organization, provides a unique global view of cancer, including cancer patterns, causes, and prevention. The World Cancer Report series is recognized as an authoritative source of global perspective and information on cancer. The first volume appeared in 2003 and the second in 2008. This third volume in the series encompasses both established knowledge and recent research achievement. World Cancer Report provides a professional, multidisciplinary assessment of all aspects of the geographical distribution, biology, etiology, prevention, and control of cancer, predicated on research. The concise nature of the text and the high graphic content (hundreds of colour maps, diagrams, and photographs) make the publication accessible to a broad readership. World Cancer Report is designed to provide non-specialist health professionals and policy-makers with a balanced understanding of cancer control and to provide established cancer professionals with insights about recent development. The book includes chapters in which distinguished scientists from around the world provide a broad overview of established knowledge and then emphasize research activity and progress. In addition, text boxes distributed throughout the book provide short, in-depth discussions of selected questions or topics. A new feature of this volume is the inclusion of Perspectives considering the future development of different aspects of cancer research, written by those whose record of outstanding achievement qualifies them as individuals having unique vision. Includes more than 60 chapters with contributions from more than 150 distinguished scientists from around the world, with information on:. Cancer Worldwide. Cancer Etiology. Cancer Biology. Cancer Prevention. Cancer by Organ Site. Cancer Control

The Epstein-Barr virus (EBV) was discovered in 1964. At the time, the very idea of a virus underlying a cancer was revolutionary. Cancer is, after all, not catching. Even now, the idea of a virus causing cancer surprises many people. But Epstein-Barr, named after its discoverers, Sir Anthony Epstein and Dr Yvonne Barr, is fascinating for other reasons too. Almost everyone carries it, yet it is only under certain circumstances that it produces disease. It has been associated with different, apparently unrelated, diseases in different populations: Burkitt's Lymphoma, producing tumours in the jaw, in African children; a nasal tumour in China; glandular fever in Europe and the USA; and the majority of cases of Hodgkin's Disease everywhere. This book tells the story of the discovery of the virus, and the recognition of its connection with these various diseases - an account that spans the world and involves some remarkable characters and individual stories.

This book would combine chapters written by the most qualified authors around the world whose research encompasses the effect of morphine or other opioids on tumor growth and metastasis. This includes clinicians involved in trials determining which type of post surgical pain management can minimize the risk of recurrence or metastasis, researchers working on animal models and studying the effect of morphine on tumors, and most importantly the mechanism for this effect, and lastly cell biologists. There is currently a lot of research going on trying to reconcile the pro- and anti-cancer aspects of opioids actions.

In addition to its metabolic and endocrinologic effects, obesity and adipose tissue have now been shown to be associated with low grade inflammation resulting in cellular and humoral inflammatory factors of which the latter may act by endocrine, paracrine and autocrine mechanisms. These inflammatory mediators have increasingly been suggested as contributing to the obesity link to carcinogenesis and cancer promotion. This volume of Energy Balance and Cancer will focus on recent developments and cutting edge research pointing to inflammation and inflammatory factors as key mediators of this linkage. The volume first provides information on inflammation as an important link between obesity and insulin resistance, which is in itself linked to promotion of cancer through hyperinsulinemia. The volume then covers some of the most important mechanisms by which obesity leads to inflammation, including the novel inflammasome concept, alterations in chromatin structure, circulating inflammatory factors, unique cellular interactions between adipocytes and macrophages and the direct link of dietary fat to inflammation and cancer. Overall, this volume will provide important insight to help understand how inflammation may help modulate the linkage between obesity and cancer and serve as a platform for developing future research in this area.

Catching Cancer introduces readers to the investigators who created a medical revolution—a new way of looking at cancer and its causes. Featuring interviews with notable scientists such as Harald zur Hausen, Barry Marshall, Robin Warren, and others, the book tells the story of their struggles, their frustrations, and finally the breakthroughs that helped form some of the most profound changes in the way we view cancer. Claudia Cornwall takes readers inside the lab to reveal the long and winding path to discoveries that have changed and continue to alter the course of medical approaches to one of the most confounding diseases mankind has known. She tells the stories of families who have benefited from this new knowledge, of the researchers who made the revolution happen, and the breakthroughs that continue to change our lives.For years, we've thought cancer was the result of lifestyle choices, environmental factors, or genetic mutations. But pioneering scientists have begun to change that picture. We now know that infections cause 20 percent of cancers, including liver, stomach, and cervical cancer, which together kill almost 1.8 million people every year. While the idea that you can catch cancer may sound unsettling, it is actually good news. It means antibiotics and vaccines can be used to combat this most dreaded disease. With this understanding, we have new methods of preventing cancer, and perhaps we may be able to look forward to a day when we will no more fear cancer than we do polio or rubella.

​Over the years of cancer investigation a lot of discoveries in this field were made, and many associations between various biological carcinogens and cancer were revealed. Some of them are credibly determined, thus these infectious agents (human papilloma virus, hepatitis B virus, hepatitis C virus, Epstein-Barr virus, human herpes virus 8, human T-cell lymphotropic virus 1, human immunodeficiency virus, Merkel cell polyomavirus, Helicobacter pylori, Opisthorchis viverrini, Clonorchis sinensis, Schistosoma haematobium) are recognized as carcinogens and probable carcinogens by International Agency for Research on Cancer (IARC). The problem is of large importance, since share of infectious agents-related cancer cases is steadily increasing, reaching 25% according to certain estimates. It is worth noting that many of cancer cases are caused by infectious agents other than «conventional ones» like HPV, EBV, HBV, HCV, H.pylori etc. In recent years, a number of significant breakthroughs in the field were performed, such as the discovery of the microbiota role in cancer causation.

In this book, the authors study the mutual interaction of cancer and its host body. The authors present the point of view that this interaction is mediated by human consciousness. Although the term cancer refers to undisciplined and uncontrollable cellular growth, a basal cell carcinoma of the skin is quite different from adenocarcinoma of the lung, prostate, or breast, brain tumors, lymphomas, leukemias, and other malignancies. These all differ markedly with respect to growth rates, metastatic tendencies, and sensitivity to neuroendocrine or immune system influences, particularly those that might be modulated by stress. There are critical concerns when it comes to determining exactly how long a cancer has been present. If a lump in the breast is found to be malignant, when did the cancer start? A month, six months, or years before clinical detection? Such information would be crucial to establish any temporal relationship with the antecedent.

The identification of occupational cancer risk factors and of carcinogens in the workplace is assuming increasing import­ ance in cancer epidemiology. This book, which contains the proceedings of a symposium held in Vancouver in June 1988, combines overviews by experts on substantive topics and methodologic issues of broad interest in occupational cancer epidemiology. Among the former are state of the art reviews emphasizing recent data and new and innovative analytic approaches. The substantive topics include discussion of cancer risks from exposure to complex organic mixtures, asbestos and man-made fibers, herbicides, radon, and electromagnetic fields. Risk assessment, exposure assessment, and analysis of occupa­ tional cohort studies are examples of the methodologic issues addressed. This book provides basic information and opens perspectives on new areas of research. In organizing our symposium we were greatly assisted by Betty Fata and Kim Rust of Venue West Conference Ltd. We appreciate the financial support received from the following: Cancer Control Agency of British Columbia Alcan Aluminium Ltd. National Health Research & Development Program Workers'Compensation Board of British Columbia Purdue Frederick Inc. Rhone-Poulenc Pharma Inc. London Drugs Ltd. Ciba-Geigy Canada Ltd. Bristol-Myers Pharmaceutical Group Schering Canada Inc. Hoffmann-La Roche Ltd. Sterling Drug Ltd. Parke-Davis Canada Inc. Beecham Laboratories Pfizer Canada Inc. Roussel Canada Inc.

This volume reviews our current knowledge concerning can­ Several chapters discuss the contributions of genetic asp­ cer growth and progression as it relates to the etiology of ects, metabolism, endocrine-related aspects and nutrition to human cancer. As emphasized in Volumes I-V of this series, cancer progression. Moreover, our current knowledge con­ neoplastic diseases are multistep maladies. There are many cerning urbanization factors, radiation, therapy-induced causes for the appearance of neoplastic diseases. Earlier neoplasms, environmentally induced neoplasms (e. g., chapters in the series have reviewed molecular and cellular mesotheliomas induced by asbestos) and malignant neo­ aspects of tumor initiation, promotion and progression to plasms in organ transplant recipients are summarized. the invasive and metastatic phenotype. Contributions to the The impact of AIDS on neoplasm development is re­ initiation and progression of neoplastic diseases are made by viewed from an epidemiologic perspective that explores mul­ natural features of the environment and by its contaminants tiple facets of immunity, infectious disease, sexual behavior and by nutritional factors. Neoplastic diseases show a dis­ and blood transfusion. Other chapters investigate the in­ tinct relationship to a variety of environmental stimuli and fluence of the host immune response in oncogenesis and the to diseases of a non-neoplastic nature. For example, familial relationship between atherosclerotic plaques and tumors.

The European School of Oncology came into existence to respond to a need for informa­ tion, education and training in the field of the diagnosis and treatment of cancer. There are two main reasons why such an initiative was considered necessary. Firstly, the teaching of oncology requires a rigorously multidisciplinary approach which is difficult for the Univer­ sities to put into practice since their system is mainly disciplinary orientated. Secondly, the rate of technological development that impinges on the diagnosis and treatment of cancer has been so rapid that it is not an easy task for medical faculties to adapt their curricula flexibly. With its residential courses for organ pathologies and the seminars on new techniques (laser, monoclonal antibodies, imaging techniques etc.) or on the principal therapeutic controversies (conservative or mutilating surgery, primary or adjuvant chemotherapy, radiotherapy alone or integrated), it is the ambition of the European School of Oncology to fill a cultural and scientific gap and, thereby, create a bridge between the University and Industry and between these two and daily medical practice. One of the more recent initiatives of ESO has been the institution of permanent study groups, also called task forces, where a limited number of leading experts are invited to meet once a year with the aim of defining the state of the art and possibly reaching a consensus on future developments in specific fields of oncology.

In the approach to the analysis of disease, including, of course, cancer, two major thrusts may be distinguished. These may be referred to, in shorthand, as agents and processes: the causative agents (chemical, microbial, physical, environmental, and psychosocial) and the organismic processes, initiated and furthered by the agents, culminating in observable pathology (at the macromolecular, cytological, histological, organ function, locomotor, and behavioral levels). The past 25 years, since the appearance of the first volume of the predecessor series (1) authored by the Editors of this present volume, have seen an impressive number of studies on chemicals (and other agents) as etiologic factors in the induction of cancer. The major emphasis has been on the discovery of many chemical carcinogens of widely different structures, their metabolism by various tissues and cells, and, in turn, their molecular-biochemical effects on the cells. This rapidly expanded body of information, as effectively covered in the predecessor volumes, is an excellent entree to the second half of the overall problem of chemical carcinogenesis, the processes. The active agents trigger a large array of molecular-biochemical alterations to which the target cells, target tissues, and target organisms respond in many select and common ways. This second major aspect of the induction of cancer by chemicals (and by other agents)- the sequence of cellular and tissue changes clearly relevant to cancer-remains the challenge for the future.

In the late 1980s, the National Cancer Institute initiated an investigation of cancer risks in populations near 52 commercial nuclear power plants and 10 Department of Energy nuclear facilities (including research and nuclear weapons production facilities and one reprocessing plant) in the United States. The results of the NCI investigation were used a primary resource for communicating with the public about the cancer risks near the nuclear facilities. However, this study is now over 20 years old. The U.S. Nuclear Regulatory Commission requested that the National Academy of Sciences provide an updated assessment of cancer risks in populations near USNRC-licensed nuclear facilities that utilize or process uranium for the production of electricity. Analysis of Cancer Risks in Populations near Nuclear Facilities: Phase 1 focuses on identifying scientifically sound approaches for carrying out an assessment of cancer risks associated with living near a nuclear facility, judgments about the strengths and weaknesses of various statistical power, ability to assess potential confounding factors, possible biases, and required effort. The results from this Phase 1 study will be used to inform the design of cancer risk assessment, which will be carried out in Phase 2. This report is beneficial for the general public, communities near nuclear facilities, stakeholders, healthcare providers, policy makers, state and local officials, community leaders, and the media.

'May 14, 2011.'

Channing Der and colleagues provide an encyclopedic overview of the Rho GTPases, providing enough detail to make any reader well-versed in the Rho field. Finally, Sofia Merajver's laboratory provides an overview, which details the roles of the Rho proteins in cancer progression. She provides us with the history of the study of the Rho GTPases, their regulatory and effector proteins in cancer and gives us a benchmark of where the field is today. The second section of the book details the current knowledge of the Rho regu- tory proteins in cancer progression: aberrant expression and activation of these proteins leads to dysfunctional Rho signaling and a cancer phenotype. Gary Bokoch's laboratory has provided a detailed overview of the role of Rho guanine dissociation inhibitors (GDIs) in cancer. These molecules are involved in preventing the Rho protein from associating with the inner plasma membrane and exchanging GDP for GTP, and thus becoming active. Next, Tozu Kazasa's labo- tory has worked on the link between heterotrimeric G proteins and Rho activation via the RGS–RhoGEFs. This aspect of Rho activation is particularly interesting in that heterotrimeric G proteins and their associated G-protein-coupled receptors are attractive and attainable therapeutic targets. Dan Billadeau's laboratory has worked extensively on the Vav RhoGEFs, which are potent oncogenes in their own right.

Epigenetics refers to DNA and chromatin modifications that persist from one cell division to the next despite a lack of change in the underlying DNA sequence. It is an emergent field since its implication in physiological and disease processes is now widely accepted. The effects of epigenetics play an important role in development but can also arise stochastically with aging. Since their discovery in 1983, cancer-associated epigenetic changes have become accepted as playing a pivotal role in carcinogenesis, in conjunction with classical genomic mutations. Thus it is now well established that an epigenetic mechanism underlies the pathogenesis of cancer and there is evidence implicating epigenetic factors in the pathogenesis of idiopathic mental disorders such as schizophrenia, bipolar disorder and even autism. This new book gathers the latest research from around the globe in this field of study and related topics.

Treating Weapons Proliferation is a chilling exploration of the dynamics of weapons proliferation and nonproliferation. In an analogy with the disease of cancer, the book walks the reader through the history of the phenomenon with its growing complexities and changing dimensions.

Significance of Stem Cells to Tumor Development Cancer stem cells remain a controversial topic and the criteria that define cancer stem cells are continuing to evolve. A recent surge in stem cell research has ignited a field of discovery into many human diseases including diabetes, neuropathologies, and cancer. By replacing specific differentiated cells that have either been lost or died, stem cell therapy proves to be a very promising approach to the treatment of many debilitating diseases. Though stem cells may provide therapeutic benefit under certain conditions, they are also often implicated in the initiation, progression, and therapeutic resistance of malignant disease. This first edition of Stem Cells and Cancer is intended to give a current perspective on the role of stem cells in cancer and strategies for novel therapies directed toward tumor stem cells. The current cancer stem cell hypothesis is presented in several chapters with distinctions made between the hierarchical and stochastic models of tumor cell development.'Stemness,'self-renewal, pluripotency, clonality, and tumorigenicity are important concepts applied towards defining cancer stem cells. Signaling pathways such as Wnt, Sonic Hedgehog, Notch, and Bmi-1 that are involved in differentiation, proliferation, and survival are implicated in the malignant process. Additional chapters address the identification of cancer stem cell populations through the evaluation of molecular markers such as CD133, CD44, and CD24, for example, or by Hoescht dye exclusion to recognize ‘side populations.'Mesenchymal and hematopoietic stem cells are described as well as mouse models that are employed to elucidate the properties and functionality of stem cells in cancer and the stem cell niche. This book encompasses a wide variety of human cancers that include but are not limited to leukemia, gliomas, breast, and prostate cancers. Resistance to conventionaltherapies, genetic versus epigenetic changes that affect therapeutic response and strategies to prevent disease recurrence are challenges have been incorporated into this volume. Stem Cells and Cancer represents a compendium of cutting edge research by experts in the field and will be instrumental in the study of this intriguing line of investigation for many years to come. Rebecca Bagley is a senior scientist at Genzyme Corporation and has worked in the biotechnology industry for 20 years with degrees in biology from Wellesley College and Harvard University. Her expertise in drug development spans a wide range of approaches including immunotherapies, gene and protein therapies, and small molecule delivery with publications in journals such as Molecular Cancer Therapeutics, Cancer Research, and Microvascular Research. Her current research focuses on stem cells, tumor vasculature, and target validation. Dr. Beverly A. Teicher is Vice President of Oncology Research at Genzyme Corporation. Dr. Teicher completed a PhD in Bioorganic Chemistry at the Johns Hopkins University and postdoctoral training at Yale University School of Medicine. Dr. Teicher joined Dana-Farber Cancer Institute as an Assistant Professor of Pathology and rose to Associate Professor of Medicine and Radiation Therapy, Harvard Medical School at Dana-Farber Cancer Institute and Joint Center for Radiation Therapy. Dr. Teicher is an active member of the international scientific community having authored or co-authored more than 400 scientific publications. She has edited eight books, is senior editor for the journal Clinical Cancer Research and is series editor for the Cancer Drug Discovery and Development book series.

Being obese increases the risk of leukemia, non-Hodgkin lymphoma, multiple myeloma, breast, cervical, colorectal, esophageal, gallbladder, kidney, liver, ovarian, pancreatic, prostate, stomach, and uterine cancers. In addition, some studies show that obesity negatively affects a person's prognosis (chance of recovery). For example, obese men are more likely to be diagnosed with advanced prostate cancer, have a recurrence of prostate cancer, or die of prostate cancer than men who are not obese. This new volume presents significant recent research in the field from around the world.

'United Nations publication sales no. E.09.IX.5'(v.2)--t.p. verso.

Cancer is a primary cause of human mortality worldwide. Despite decades of basic and clinical research, the outcome for most cancer patients is still dismal. Some stumbling blocks to developing effective therapy include the heterogeneity of cancer tissues, the lack of knowledge about the critical molecular mechanisms in cancer tissues (which are typically aberrant compared with mechanisms in normal tissue), and the lack of good mechanism-based therapeutic approaches. The recent findings that most cancers contain a small fraction of self-renewing, differentiation-blocked stem cell-like cells (cancer stem cells) and that it is these cells—and not the major bulk of the tissue—that are the root cause for cancer initiation and metastasis have also highlighted the need to change our approach to cancer therapy. The objectives of this book, therefore, would be to impart up-to-date information about the role of stem cells in the development of normal and cancerous tissue, the mechanisms that differentiate normal from cancerous functions, and the use of these findings in developing mechanism-based therapies.

Description based on print version record.

The interdisciplinary work revealing varied roles in biological processes of chronic diseases has led to a new field of research concerning common molecular and clinical features of chronic diseases. Epidemiological literature suggests an association between the history of metabolic syndrome/diabetes mellitus type 2 and the risk of developing a variety of cancers. This book, at the forefront of experimental and clinical research, is the first to highlight the common molecular links between these two diseases. These tight links indicate a complex interdependency between both diseases on a cellular and hormonal basis, which is influenced by a variety of aspects (e.g. nutritional, social and neuro-immunological factors). Special attention has been given to the fundamental role of the switch from oxidative phosphorylation to glycolysis of cancer cells - the Warburg effect. Offering insights into the interdisciplinary approaches of tomorrow, this publication will encourage endocrinologists, oncologists, diabetologists, general practitioners, diabetic nurses and students of life sciences working separately on various aspects of diabetes and cancer to come together and combine therapies and strategies.

Heat shock proteins are emerging as important molecules in the development of cancer and as key targets in cancer therapy. These proteins enhance the growth of cancer cells and protect tumors from treatments such as drugs or surgery. However, new drugs have recently been developed particularly those targeting heat shock protein 90. As heat shock protein 90 functions to stabilize many of the oncogenes and growth promoting proteins in cancer cells, such drugs have broad specificity in many types of cancer cell and offer the possibility of evading the development of resistance through point mutation or use of compensatory pathways. Heat shock proteins have a further property that makes them tempting targets in cancer immunotherapy. These proteins have the ability to induce an inflammatory response when released in tumors and to carry tumor antigens to antigen presenting cells. They have thus become important components of anticancer vaccines. Overall, heat shock proteins are important new targets in molecular cancer therapy and can be approached in a number of contrasting approaches to therapy.

This book aims to provide a comprehensive review of the most up-to-date knowledge of the sources and molecular mechanisms of oxidative stress, and its role in disease and cancer. It also focuses on the novel agents and methods that can be employed to prevent oxidative stress and associated diseases.The authors first review the most recent data on the basic mechanisms of oxidative stress. The second section discusses oxidative stress leading to several diseases and cancers, and in the third section, the strategies employed in the prevention and treatment of oxidative stress-related diseases are discussed.

Title from eBook title screen (viewed Jan. 11, 2007)

Cancer research has reached a major turning point. The quality and quantity of information gathered about this disease in the past twenty years has revolutionized our understanding of its origins and behavior. No one is better qualified to comment on these dramatic leaps forward than molecular biologist Robert A. Weinberg, director of one of the leading cancer research centers in the world. In One Renegade Cell, Weinberg presents an accessible and state-of-the-art account of how the disease begins and how, one day, it will be cured. Weinberg tells how the roots of cancer were uncovered in 1909 and when the first cancer-causing virus was discovered. He then moves forward to the discovery of the role of chemical carcinogens and radiation in triggering cancer, and relates the remarkable story of the discoveries of oncogenes and tumor suppressor genes, the master controllers of normal and malignant cell proliferation. This book, which presumes little prior knowledge of biology, describes the revolution in biomedical research that has finally uncovered the forces driving malignant growth. Drawing on insights that simply were not available until recently, the discoveries presented in One Renegade Cell have already begun to profoundly alter the way that we diagnose and treat human cancers.