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Tumor progression is driven by mutations that confer growth advantages to different subpopulations of cancer cells. As a tumor grows, these subpopulations expand, accumulate new mutations, and are subjected to selective pressures from the environment, including anticancer interventions. This process, termed clonal evolution, can lead to the emergence of therapy-resistant tumors and poses a major challenge for cancer eradication efforts. Written and edited by experts in the field, this collection from Cold Spring Harbor Perspectives in Medicine examines cancer progression as an evolutionary process and explores how this way of looking at cancer may lead to more effective strategies for managing and treating it. The contributors review efforts to characterize the subclonal architecture and dynamics of tumors, understand the roles of chromosomal instability, driver mutations, and mutation order, and determine how cancer cells respond to selective pressures imposed by anticancer agents, immune cells, and other components of the tumor microenvironment. They compare cancer evolution to organismal evolution and describe how ecological theories and mathematical models are being used to understand the complex dynamics between a tumor and its microenvironment during cancer progression. The authors also discuss improved methods to monitor tumor evolution (e.g., liquid biopsies) and the development of more effective strategies for managing and treating cancers (e.g., immunotherapies). This volume will therefore serve as a vital reference for all cancer biologists as well as anyone seeking to improve clinical outcomes for patients with cancer.
The onset of cancer presents one of the most fundamental problems in modern biology. In Dynamics of Cancer, Steven Frank produces the first comprehensive analysis of how particular genetic and environmental causes influence the age of onset. The book provides a unique conceptual and historical framework for understanding the causes of cancer and other diseases that increase with age. Using a novel quantitative framework of reliability and multistage breakdown, Frank unifies molecular, demographic, and evolutionary levels of analysis. He interprets a wide variety of observations on the age of cancer onset, the genetic and environmental causes of disease, and the organization of tissues with regard to stem cell biology and somatic mutation. Frank uses new quantitative methods to tackle some of the classic problems in cancer biology and aging: how the rate of increase in the incidence of lung cancer declines after individuals quit smoking, the distinction between the dosage of a chemical carcinogen and the time of exposure, and the role of inherited genetic variation in familial patterns of cancer. This is the only book that presents a full analysis of the age of cancer onset. It is a superb teaching tool and a rich source of ideas for new and experienced researchers. For cancer biologists, population geneticists, evolutionary biologists, and demographers interested in aging, this book provides new insight into disease progression, the inheritance of predisposition to disease, and the evolutionary processes that have shaped organismal design.
Cancer is characterized by heterogeneous cells with capacity for self renewal, and selective pressures in the microenvironment which constantly change the cell population. This "descent with modification" is consistent with Darwin's definition of evolution, and accordingly, cancer progression can be captured from an evolutionary angle. However, there is also a clear difference between cancer progression and biological evolution. First, contrary to the evolution of complex organisms, cancer originates from cells of multicellular organisms that escape their constraints and behave like unicellular organisms. Therefore, from the beginning, cancer cells have complex genomes that contain abundant genetic materials which they can use to change their phenotype by dynamic rearrangements and modifications. Secondly, epigenetic effects promote cancer evolution in contrast to the evolution of life. Some tumors develop with minimal genetic alterations, and cell plasticity contributes to both initiation and progression in various tumors. However, an evolutionary theory that encompasses these characteristics of cancer remains to be developed.
Molecular and Cellular Changes in the Cancer Cell,the latest volume in the Progress in Molecular Biology and Translational Science series, includes a comprehensive summary of the evidence accumulated thus far on the molecular and cellular regulation of the various adaptations taking place in response to exercise. This volume examines some of the latest advances, highlighting some of the most important molecular and cellular alterations and environmental influences that collectively cause a normal cell to become cancerous. Special emphasis is given to changes that take place at the molecular and cellular level. Comprehensive and up-to-date survey of current knowledge on the cancer cell Includes the latest advances and the most important molecular and cellular alterations and environmental influences collectively causing cells to become cancerous Written by leading experts in the field
The book shows how mathematical and computational models can be used to study cancer biology. It introduces the concept of mathematical modeling and then applies it to a variety of topics in cancer biology. These include aspects of cancer initiation and progression, such as the somatic evolution of cells, genetic instability, and angiogenesis. The book also discusses the use of mathematical models for the analysis of therapeutic approaches such as chemotherapy, immunotherapy, and the use of oncolytic viruses.
Every day, 1500 Americans die of cancer, and yet for most of us this deadly disease remains mysterious. Why is it so common? Why are there so many different causes? Why does treatment so often fail? What, ultimately, is cancer? In this fascinating new book, a leading cancer researcher offers general readers clear and convincing answers to these and many other questions. Mel Greaves places cancer in its evolutionary context, arguing that we can best answer the big questions about cancer by looking through a Darwinian lens. Drawing on both ancient and more modern evolutionary legacies, he shows how human development has changed the rules of evolutionary games, trapping us in a nature-nurture mismatch. Compelling examples, from the King of Naples intestinal tumor in the 15th century, through the epidemic of scrotal skin cancer in 18th-century chimney sweeps, to the current surge of cases of prostate cancer illustrate his thesis. He also shows why the old paradigms of infectious diseases or genetic disorders have proved fruitless when trying to explain this complex and elusive disease. And finally, he looks at the implications for research, prevention, and treatment of cancer that an evolutionary perspective provides. Drawing on the most recent research, this is the first book to put cancer in its evolutionary framework. At a time when Darwinian perspectives on everything from language acquisition to economics are providing new breakthroughs in understanding, medicine seems to have much to gain from the insights provided by evolutionary biology. Written in an exceptionally lucid and entertaining style, this book will be of broad interest to all those who wish to know more about this dread disease.
The book aims to provide an introduction to mathematical models that describe the dynamics of tumor growth and the evolution of tumor cells. It can be used as a textbook for advanced undergraduate or graduate courses, and also serves as a reference book for researchers. The book has a strong evolutionary component and reflects the viewpoint that cancer can be understood rationally through a combination of mathematical and biological tools. It can be used both by mathematicians and biologists. Mathematically, the book starts with relatively simple ordinary differential equation models, and subsequently explores more complex stochastic and spatial models. Biologically, the book starts with explorations of the basic dynamics of tumor growth, including competitive interactions among cells, and subsequently moves on to the evolutionary dynamics of cancer cells, including scenarios of cancer initiation, progression, and treatment. The book finishes with a discussion of advanced topics, which describe how some of the mathematical concepts can be used to gain insights into a variety of questions, such as epigenetics, telomeres, gene therapy, and social interactions of cancer cells.
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.
Composed of contributions from an international team of leading researchers, this book pulls together the most recent research results in the field of cancer modeling to provide readers with the most advanced mathematical models of cancer and their applications.Topics included in the book cover oncogenetic trees, stochastic multistage models of carcinogenesis, effects of ionizing radiation on cell cycle and genomic instability, induction of DNA damage by ionizing radiation and its repair, epigenetic cancer models, bystander effects of radiation, multiple pathway models of human colon cancer, and stochastic models of metastasis. The book also provides some important applications of cancer models to the assessment of cancer risk associated with various hazardous environmental agents, to cancer screening by MRI, and to drug resistance in cancer chemotherapy. An updated statistical design and analysis of xenograft experiments as well as a statistical analysis of cancer occult clinical data are also provided.The book will serve as a useful source of reference for researchers in biomathematics, biostatistics and bioinformatics; for clinical investigators and medical doctors employing quantitative methods to develop procedures for cancer diagnosis, prevention, control and treatment; and for graduate students.