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Biology of Cancer - With CD and Poster

Biology of Cancer - With CD and Poster - 07 edition

ISBN13: 978-0815340768

Cover of Biology of Cancer - With CD and Poster 07 (ISBN 978-0815340768)
ISBN13: 978-0815340768
ISBN10: 0815340761
Cover type: Paperback
Edition/Copyright: 07
Publisher: Garland Publishing
Published: 2007
International: No

List price: $154.00

Biology of Cancer - With CD and Poster - 07 edition

ISBN13: 978-0815340768

Robert A. Weinberg

ISBN13: 978-0815340768
ISBN10: 0815340761
Cover type: Paperback
Edition/Copyright: 07
Publisher: Garland Publishing

Published: 2007
International: No

The Biology of Cancer is a new 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-colour 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 Cancer synthesizes 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 tumour 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 Cancer provides insights into many aspects of immunology, developmental biology, and neurobiology.

The exceptional full-colour 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 Cancer will be a useful reference for individuals working in biomedical laboratories, and for clinical professionals.

Table of Contents

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 a G protein
5.10 Synopsis and Prospects
Essential Concepts
Additional Reading

Chapter 6. Cytoplasmic Signaling Circuitry Programs Many of the Traits of Cancer

6.1 A signaling pathway reaches from the cell surface into the nucleus
6.2 The Ras protein stands in the middle of a complex signaling cascade
6.3 Tyrosine phosphorylation controls the location and thereby the actions of many cytoplasmic signaling proteins
6.4 SH2 groups explain how growth factor receptors activate Ras and acquire signaling specificity
6.5 A cascade of kinases forms one of three important signaling pathways downstream of Ras
6.6 A second pathway downstream of Ras controls inositol lipids and the Akt/PKB kinase
6.7 A third Ras-regulated pathway acts through the Ral, a distant cousin of Ras
6.8 The Jak-STAT pathway allows signals to be transmitted from the plasma membrane directly to the nucleus
6.9 Cell adhesion receptors emit signals that converge with those released by growth factor receptors
6.10 The Wnt-b-catenin pathway contributes to cell proliferation
6.11 G-protein coupled receptors can also drive normal and neoplastic proliferation
6.12 Four other signaling pathways contribute in different fashions to normal and neoplastic proliferation
6.13 Synopsis and prospects
Essential Concepts
Additional reading

Chapter 7. Tumor suppressor genes

7.1 Cell fusion experiments indicate that the cancer phenotype is recessive
7.2 The recessive nature of the cancer cell phenotype requires a genetic explanation
7.3 The retinoblastoma tumor provides a solution to the genetic puzzle of tumor suppressor genes
7.4 Incipient cancer cells invent ways to eliminate wild-type copies of tumor suppressor genes
7.5 The Rb gene often undergoes loss-of-heterozygosity
7.6 Loss-of-heterozygosity events can be used to find tumor suppressor genes
7.7 Many familial cancers can be explained by inheritance of mutant tumor suppressor genes
7. 8 Promoter methylation represents an important mechanism for inactivating tumor suppressor genes
7.9 Tumor suppressor genes and proteins function in diverse ways
7.10 The NF1 protein acts as a negative regulator of Ras signaling
7.11 Apc facilitates egress of cells from colonic crypts
7.12 Von Hippel-Lindau disease: pVHL modulates the hypoxic response
7.13 Synopsis and Prospects
Essential Concepts
Additional reading

Chapter 8. pRb and Control of the Cell Cycle Clock

8.1 External signals influence a cell's decision to enter into the active cell cycle
8.2 Cells make decisions about growth and quiescence during a specific period in the G1 phase
8.3 Cyclins and cyclin-dependent kinases constitute the core components of the cell cycle clock
8.4 Cyclin-Cdk complexes are also regulated by Cdk inhibitors
8.5 Viral oncoproteins reveal how pRb controls the transition through the cell cycle
8.6 pRb is deployed by the cell cycle clock to serve as a guardian of the restriction point gate
8.7 E2F transcription factors enable pRb to implement growth-versus-quiescence decisions
8.8 A variety of mitogenic signaling pathways control the phosphorylation state of pRb
8.9 The Myc oncoprotein perturbs the decision to phosphorylate pRb and thereby deregulates control of cell cycle progression
8.10 TGF-b prevents phosphorylation of pRb and thereby blocks cell cycle progression
8.11 pRb function and the process of differentiation are closely linked
8.12 Control of pRb function is perturbed in most if not all human cancers
8.13 Synopsis and Prospects
Essential Concepts
Additional reading

Chapter 9. p53 and Apoptosis: Master Guardian and Executioner

9.1 Papovaviruses lead to the discovery of p53
9.2 p53 is discovered to be a tumor suppressor gene
9.3 Mutant versions of p53 interfere with normal p53 function
9.4 p53 protein molecules usually have short lifetime