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Summary
Summary
The Biology of Canceris a textbook for undergraduate and graduate biology students as well as medical students studying the molecular and cellular bases of cancer. The book presents the principles of cancer biology in an organized, cogent, and in-depth manner. The clarity of writing and the lucid full-color art program make the book accessible and engaging. The information unfolds through the presentation of key experiments which give readers a sense of discovery and provides insights into the conceptual foundation underlying modern cancer biology.
The Biology of Cancersynthesizes the findings of three decades of recent cancer research and proposes a conceptual framework from which to teach about these discoveries. It provides the necessary structure, organization, and content for a course on cancer biology for advanced undergraduates and beginning doctoral students. The book is comprehensive and offers many pedagogical features to assist teaching and learning. The book includes many recent and topical references, and is intended to empower the student to move directly into the primary research literature.
The text is up-to-date and provides current information on topics such as tumor stem cells and recently introduced chemotherapeutics. State-of-the-art techniques are discussed throughout. Modern biomedical research is explored, helping readers to hone their analytical abilities and to assimilate and think clearly about complex biological processes. The Biology of Cancerprovides insights into many aspects of immunology, developmental biology, and neurobiology.
The exceptional full-color art program contains many images published for the first time. The book is extensively illustrated with schematic drawings, micrographs, computer-generated models and graphs. The pieces were chosen to support and clarify the concepts, as well as to supply additional interest.
Besides its value as a textbook, The Biology of Cancerwill be a useful reference for individuals working in biomedical laboratories, and for clinical professionals.
Author Notes
Dr. Robert A. Weinbergis a founding member of the Whitehead Institute for Biomedical Research and the Daniel K. Ludwig Professor for Cancer Research at the Massachusetts Institute of Technology (MIT). He is an internationally recognized authority on the genetic basis of human cancer.
Dr. Weinberg and his colleagues isolated the first human cancer-causing gene, the ras oncogene, and the first known tumor suppressor gene, Rb, the retinoblastoma gene. The principal goal of his research program is to determine how oncogenes, their normal counterparts (proto-oncogenes), and tumor suppressor genes fit together in the complex circuitry that controls cell growth. More recently, his group has succeeded in creating the first genetically defined human cancer cells. He is particularly interested in applying this knowledge to improve the diagnosis and treatment of breast cancer.
Dr. Weinberg is the author or editor of five books and more than 325 articles. His three most recent books, intended for a lay audience, are "One Renegade Cell", "Racing to the Beginning of the Road: The Search for the Origin of Cancer" and "Genes and the Biology of Cancer," co-authored with Dr. Harold E. Varmus, former Director of the National Institutes of Health. He is an elected Member of the U.S. National Academy of Sciences and Fellow of the American Academy of Arts and Sciences.
Among Dr. Weinberg's many honors and awards are the Discover Magazine 1982 Scientist of the Year, the National Academy of Sciences/U.S. Steel Foundation Award in Molecular Biology, the Sloan Prize of the General Motors Cancer Research Foundation, the Bristol-Myers Award for Distinguished Achievement in Cancer Research, the Harvey Prize from the American Society for Technion Israel Institute of Technology, the Gairdner Foundation International Award, the Keio Medical Foundation Prize, the 1997 National Medal of Science, the City of Medicine Award and the 2004 Wolf Foundation Prize and the Prince of Asturias Science Prize. He has served on scientific advisory boards for the Institute of Molecular Pathology in Vienna, Austria, the Weizmann Institute in Rehovot, Israel, and the Massachusetts General Hospital in Boston.
Born in Pittsburgh in 1942, Dr. Weinberg received his BS (1964) and PhD (1969) degrees in Biology from MIT. He did postdoctoral research at the Weizmann Institute and the Salk Institute in La Jolla, California, and then returned to MIT in 1972. In 1982, he was appointed Professor of Biology at MIT and also became one of the five original Members of the Whitehead Institute. He has been an American Cancer Society Research Professor at Whitehead and MIT since 1985.
Table of Contents
| Preface |
| Chapter 1 The Biology and Genetics of Cells and Organisms |
| 1.1 Mendel establishes the basic rules of genetics |
| 1.2 Mendelian genetics helps to explain Darwinian evolution |
| 1.3 Mendelian genetics governs how both genes and chromosomes behave |
| 1.4 Chromosomes are altered in most types of cancer cells |
| 1.5 Mutations causing cancer occur in both the germ-line and the soma |
| 1.6 Genotype embodied in DNA sequences creates phenotype through proteins |
| 1.7 Gene expression patterns also control phenotype |
| 1.8 Transcription factors control gene expression |
| 1.9 Metazoa are formed from components conserved over vast evolutionary time periods |
| 1.10 Gene cloning techniques revolutionized the study of normal and malignant cells |
| Chapter 2 The Nature of Cancer |
| 2.1 Tumors are complex tissues |
| 2.2 Tumors arise from many specialized cell types throughout the body |
| 2.3 Some types of tumors do not fit into the major classifications |
| 2.4 Cancers seem to develop progressively |
| 2.5 Tumors are monoclonal growths |
| 2.6 Cancers occur with vastly different frequencies in different human populations |
| 2.7 The risks of cancers often seem to be increased by assignable influences including lifestyle |
| 2.8 Specific chemical agents can induce cancer 2.9 Both physical and chemical carcinogens act as mutagens |
| 2.10 Mutagens may be responsible for some human cancers |
| 2.11 Synopsis and prospects Essential Concepts Additional Reading |
| Chapter 3 Tumor viruses |
| 3.1 Peyton Rous discovers a chicken sarcoma virus |
| 3.2 Rous sarcoma virus is discovered to transform infected cells in culture |
| 3.3 The continued presence of RSV is needed to maintain transformation |
| 3.4 Viruses containing DNA molecules are also able to induce cancer |
| 3.5 Tumor viruses induce multiple changes in cell phenotype including acquisition of tumorigenicity |
| 3.6 Tumor virus genomes persist in virus-transformed cells by becoming part of host cell DNA |
| 3.7 Retroviral genomes become integrated into the chromosomes of infected cells |
| 3.8 A version of the src gene carried by RSV is also present in uninfected cells |
| 3.9 RSV exploits a kidnapped cellular gene to transform cells |
| 3.10 The vertebrate genome carries a large group of proto-oncogenes |
| 3.11 Slowly transforming retroviruses activate proto-oncogenes by inserting their genomes adjacent to these cellular genes |
| 3.12 Some retroviruses naturally carry oncogenes |
| 3.13 Synopsis and prospects Essential Concepts Additional Reading |
| Chapter 4 Cellular oncogenes |
| 4.1 Can cancers be triggered by the activation of endogenous retroviruses? |
| 4.2 Transfection of DNA provides a strategy for detecting nonviral oncogenes |
| 4.3 Oncogenes discovered in human tumor cell lines are related to those carried by transforming retroviruses |
| 4.4 Proto-oncogenes can be activated by genetic changes affecting either protein expression or structure |
| 4.5 Variations on a theme: the myc oncogene can arise via at least three additional distinct mechanisms |
| 4.6 A diverse array of structural changes in proteins can also lead to oncogene activation |
| 4.7 Synopsis and prospects Essential Concepts Additional Reading |
| Chapter 5 Growth factors and their receptors |
| 5.1 Normal metazoan cells control each other's lives |
| 5.2 The Src protein functions as a tyrosine kinase |
| 5.3 The EGF receptor functions as a tyrosine kinase |
| 5.4 An altered growth factor receptor can function as an oncoprotein |
| 5.5 A growth factor gene can become an oncogene: the case of sis |
| 5.6. Transphosphorylation underlies the operations of receptor tyrosine kinases |
| 5.7 Yet other types of receptors enable mammalian cells to communicate with their environment |
| 5.8 Integrin receptors sense association between the cell and the extracellular matrix |
| 5.9 The Ras protein, an apparent component of the downstream signaling cascade, functions as |
