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.

This book offers a comprehensive update on mechanisms of tumorigenesis. The first portion discusses pediatric cancer, the influence of environmental factors and oncogene activity in tumorigenesis; the second portion is structured by organ site for easy access.

Oncogenes are mutated and/or overexpressed at high levels in tumor cells. Tumors of the lung, breast, pancreas, and colon may display specific oncogenetic features. These tumors have been largely associated with exposure to environmental carcinogens and a variety of biological agents, including viruses. These carcinogens can induce specific genetic and epigenetic alterations in these tissues, leading to aberrant functioning of oncogenes and tumor suppressor genes. On the microRNAs (miRNAs) there are significant modifiers of both transcription and translation of oncogenes in carcinogenesis. In the last 50 years, several oncogenes and microRNAs related to these oncogenes have been identified in different types of human cancers. It is now clear that high expression of oncogenes, DNA damage response, and regulation of the cell cycle are related to the circadian clock. This book will mainly focus on the expressions of different oncogenes in breast, colon, and lung cancers. Moreover, readers will gain qualified scientific knowledge of the alterations in miRNAs in different types of cancers and the effects of the circadian clock on the expression of oncogenes in carcinogenesis.

Popular understanding holds that genetic changes create cancer. James DeGregori uses evolutionary principles to propose a new way of thinking about cancerÕs 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 bodyÕs tissues. His theory ties cancerÕs 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 genesÑbut not much longer. These mechanisms engender a tissue environment that favors normal stem cells over precancerous ones. Healthy tissues thwart cancer cellsÕ 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 speciesÕ habitat favor the evolution of new species, changes in tissue environments favor the growth of cancerous cells. DeGregoriÕs 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 tissuesÕ 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.

Carcinogen-Driven Mouse Models of Oncogenesis, Volume 163 contains a series of protocols written by world-leading experts in the field. Each manuscript provides a detailed methodological description to drive carcinogen-mediated oncogenesis in mice. Chapters in this new release include Chemical carcinogenesis in mice as a model of human cancer: Pros and cons, MPA/DMBA-driven mammary carcinomas, Dimethylbenz(a)anthracene-Induced Mammary Tumorigenesis in mice, Urethane-induced lung carcinogenesis, Methylcholanthrene-induced fibrosarcomas, BBN-driven bladder carcinomas, Oral squamous cell carcinomas driven by 4NQO, Analyzing skin tumor development in mice by the DMBA/TPA model, and much more. Other sections cover DSS/AOM-driven colorectal carcinomas, Diethylnitrosamine-induced liver tumorigenesis in mice, Two-stage 3-methylcholanthrene and butylated hydroxytoluene-induced lung carcinogenesis in mice, Lung carcinomas induced by NNK and LPS, Pristane-induced mammary carcinomas, The 4-NQO mouse model: an update on a well-established in vivo model of oral carcinogenesis, and more. Provides protocols provided by renowned experts in the field Presents detailed descriptions of protocols, hence allowing appropriate reproduction of the models Includes author notes for each protocol, covering useful tips and troubleshooting

Oncogenes are mutated and/or overexpressed at high levels in tumor cells. Tumors of the lung, breast, pancreas, and colon may display specific oncogenetic features. These tumors have been largely associated with exposure to environmental carcinogens and a variety of biological agents, including viruses. These carcinogens can induce specific genetic and epigenetic alterations in these tissues, leading to aberrant functioning of oncogenes and tumor suppressor genes. On the microRNAs (miRNAs) there are significant modifiers of both transcription and translation of oncogenes in carcinogenesis. In the last 50 years, several oncogenes and microRNAs related to these oncogenes have been identified in different types of human cancers. It is now clear that high expression of oncogenes, DNA damage response, and regulation of the cell cycle are related to the circadian clock. This book will mainly focus on the expressions of different oncogenes in breast, colon, and lung cancers. Moreover, readers will gain qualified scientific knowledge of the alterations in miRNAs in different types of cancers and the effects of the circadian clock on the expression of oncogenes in carcinogenesis.

Medicine is grounded in the natural sciences, among which biology stands out with regard to the understanding of human physiology and conditions that cause dysfunction. Ironically though, evolutionary biology is a relatively disregarded field. One reason for this omission is that evolution is deemed a slow process. Indeed, macroanatomical features of our species have changed very little in the last 300,000 years. A more detailed look, however, reveals that novel ecological contingencies, partly in relation to cultural evolution, have brought about subtle changes pertaining to metabolism and immunology, including adaptations to dietary innovations, as well as adaptations to the exposure to novel pathogens. Rapid pathogen evolution and evolution of cancer cells cause major problems for the immune system to find adequate responses. In addition, many adaptations to past ecologies have turned into risk factors for somatic disease and psychological disorder in our modern worlds (i.e. mismatch), among which epidemics of autoimmune diseases, cardiovascular diseases, diabetes and obesity, as well as several forms of cancer stand out. In addition, depression, anxiety and other psychiatric conditions add to the list. The Oxford Handbook of Evolutionary Medicine is a compilation of cutting edge insights into the evolutionary history of ourselves as a species, and how and why our evolved design may convey vulnerability to disease. Written in a classic textbook style emphasising physiology and pathophysiology of all major organ systems, the Oxford Handbook of Evolutionary Medicine will be valuable for students as well as scholars in the fields of medicine, biology, anthropology and psychology.