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Genetic alterations in cancer, in addition to being the fundamental drivers of tumorigenesis, can give rise to a variety of metabolic adaptations that allow cancer cells to survive and proliferate in diverse tumor microenvironments. This metabolic flexibility is different from normal cellular metabolic processes and leads to heterogeneity in cancer metabolism within the same cancer type or even within the same tumor. In this book, we delve into the complexity and diversity of cancer metabolism, and highlight how understanding the heterogeneity of cancer metabolism is fundamental to the development of effective metabolism-based therapeutic strategies. Deciphering how cancer cells utilize various nutrient resources will enable clinicians and researchers to pair specific chemotherapeutic agents with patients who are most likely to respond with positive outcomes, allowing for more cost-effective and personalized cancer therapeutic strategies.
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.
Rapid progress has been made in our understanding of the molecular mechanisms of cell growth and oncogenesis during the past decade. This book comprises recent results on the regulation of cell growth in normal and neoplastic tissues by growth factors including hormones, and by the activation and inactivation of oncogenes and tumor suppressor genes, respectively. Special attention has been given to the presentation of the frequently neglected close correlation between changes in signal transduction and metabolism pathways during oncogenesis.
An overview of the current systems biology-based knowledge and the experimental approaches for deciphering the biological basis of cancer.
The scientific basis, inference assumptions, regulatory uses, and research needs in risk assessment are considered in this two-part volume. The first part, Use of Maximum Tolerated Dose in Animal Bioassays for Carcinogenicity, focuses on whether the maximum tolerated dose should continue to be used in carcinogenesis bioassays. The committee considers several options for modifying current bioassay procedures. The second part, Two-Stage Models of Carcinogenesis, stems from efforts to identify improved means of cancer risk assessment that have resulted in the development of a mathematical dose-response model based on a paradigm for the biologic phenomena thought to be associated with carcinogenesis.
This comprehensive account of the human herpesviruses provides an encyclopedic overview of their basic virology and clinical manifestations. This group of viruses includes human simplex type 1 and 2, Epstein–Barr virus, Kaposi's Sarcoma-associated herpesvirus, cytomegalovirus, HHV6A, 6B and 7, and varicella-zoster virus. The viral diseases and cancers they cause are significant and often recurrent. Their prevalence in the developed world accounts for a major burden of disease, and as a result there is a great deal of research into the pathophysiology of infection and immunobiology. Another important area covered within this volume concerns antiviral therapy and the development of vaccines. All these aspects are covered in depth, both scientifically and in terms of clinical guidelines for patient care. The text is illustrated generously throughout and is fully referenced to the latest research and developments.
Telomerase, an enzyme that maintains telomeres and endows eukaryotic cells with immortality, was first discovered in tetrahymena in 1985. In 1990s, it was proven that this enzyme also plays a key role in the infinite proliferation of human cancer cells. Now telomere and telomerase are widely accepted as important factors involved in cancer biology, and as promising diagnostic tools and therapeutic targets. Recently, role of telomerase in “cancer stem cells” has become another attractive story. Until now, there are several good books on telomere and telomerase focusing on biology in ciliates, yeasts, and mouse or basic sciences in human, providing basic scientists or students with updated knowledge.
"Yet another cell and molecular biology book? At the very least, you would think that if I was going to write a textbook, I should write one in an area that really needs one instead of a subject that already has multiple excellent and definitive books. So, why write this book, then? First, it's a course that I have enjoyed teaching for many years, so I am very familiar with what a student really needs to take away from this class within the time constraints of a semester. Second, because it is a course that many students take, there is a greater opportunity to make an impact on more students' pocketbooks than if I were to start off writing a book for a highly specialized upper- level course. And finally, it was fun to research and write, and can be revised easily for inclusion as part of our next textbook, High School Biology."--Open Textbook Library.