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The Biology of Cancer, 2e

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Efnisyfirlit

  • Copyright page
  • Dedication
  • Preface
  • A Note to the Reader
  • Acknowledgments
  • Contents
  • List of Key Techniques
  • Detailed 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 Histone modification and transcription factors control gene expression
    • 1.9 Heritable gene expression is controlled through additional mechanisms
    • 1.10 Unconventional RNA molecules also affect the expression of genes
    • 1.11 Metazoa are formed from components conserved over vast evolutionary time periods
    • 1.12 Gene cloning techniques revolutionized the study of normal and malignant cells
    • Additional reading
  • Chapter 2 The Nature of Cancer
    • 2.1 Tumors arise from normal 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 Cancer cells exhibit an altered energy metabolism
    • 2.7 Cancers occur with vastly different frequencies in different human populations
    • 2.8 The risks of cancers often seem to be increased by assignable influences including lifestyle
    • 2.9 Specific chemical agents can induce cancer
    • 2.10 Both physical and chemical carcinogens act as mutagens
    • 2.11 Mutagens may be responsible for some human cancers
    • 2.12 Synopsis and prospects
    • Key concepts
    • Thought questions
    • 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
    • 3.12 Some retroviruses naturally carry oncogenes
    • 3.13 Synopsis and prospects
    • Key concepts
    • Thought questions
    • 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 retr
    • 4.4 Proto-oncogenes can be activated by genetic changes affecting either protein expression or struc
    • 4.5 Variations on a theme: the myc oncogene can arise via at least three additional distinct mechani
    • 4.6 A diverse array of structural changes in proteins can also lead to oncogene activation
    • 4.7 Synopsis and prospects
    • Key concepts
    • Thought questions
    • Additional reading
  • Chapter 5 Growth Factors, Receptors, and Cancer
    • 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 Nuclear receptors sense the presence of low–molecular–weight lipophilic ligands
    • 5.9 Integrin receptors sense association between the cell and the extracellular matrix
    • 5.10 The Ras protein, an apparent component of the downstream signaling cascade, functions as a G pr
    • 5.11 Synopsis and prospects
    • Key concepts
    • Thought questions
    • 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 signa
    • 6.4 SH2 and SH3 groups explain how growth factor receptors activate Ras and acquire signaling specif
    • 6.5 Ras-regulated signaling pathways: A cascade of kinases forms one of three important signaling pa
    • 6.6 Ras-regulated signaling pathways: a second downstream pathway controls inositol lipids and the A
    • 6.7 Ras-regulated signaling pathways: a third downstream pathway acts through Ral, a distant cousin
    • 6.8 The Jak–STAT pathway allows signals to be transmitted from the plasma membrane directly to the
    • 6.9 Cell adhesion receptors emit signals that converge with those released by growth factor receptor
    • 6.10 The Wnt–ß-catenin pathway contributes to cell proliferation
    • 6.11 G-protein–coupled receptors can also drive normal and neoplastic proliferation
    • 6.12 Four additional “dual-address” signaling pathways contribute in various ways to normal and
    • 6.13 Well-designed signaling circuits require both negative and positive feedback controls
    • 6.14 Synopsis and prospects
    • Key concepts
    • Thought questions
    • 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 in tumors
    • 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
    • Key concepts
    • Thought questions
    • Additional reading
  • Chapter 8 pRb and Control of the Cell Cycle Clock
    • 8.1 Cell growth and division is coordinated by a complex array of regulators
    • 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 blocks advance 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 protein governs decisions to proliferate or differentiate
    • 8.10 TGF-ß prevents phosphorylation of pRb and thereby blocks cell cycle progression
    • 8.11 pRb function and the controls 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
    • Key concepts
    • Thought questions
    • 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 lifetimes
    • 9.5 A variety of signals cause p53 induction
    • 9.6 DNA damage and deregulated growth signals cause p53 stabilization
    • 9.7 Mdm2 destroys its own creator
    • 9.8 ARF and p53-mediated apoptosis protect against cancer by monitoring intracellular signaling
    • 9.9 p53 functions as a transcription factor that halts cell cycle advance in response to DNA damage
    • 9.10 p53 often ushers in the apoptotic death program
    • 9.11 p53 inactivation provides advantage to incipient cancer cells at a number of steps in tumor pro
    • 9.12 Inherited mutant alleles affecting the p53 pathway predispose one to a variety of tumors
    • 9.13 Apoptosis is a complex program that often depends on mitochondria
    • 9.14 Both intrinsic and extrinsic apoptotic programs can lead to cell death
    • 9.15 Cancer cells invent numerous ways to inactivate some or all of the apoptotic machinery
    • 9.16 Necrosis and autophagy: two additional forks in the road of tumor progression
    • 9.17 Synopsis and prospects
    • Key concepts
    • Thought questions
    • Additional reading
  • Chapter 10 Eternal Life: Cell Immortalization and Tumorigenesis
    • 10.1 Normal cell populations register the number of cell generations separating them from their ance
    • 10.2 Cancer cells need to become immortal in order to form tumors
    • 10.3 Cell-physiologic stresses impose a limitation on replication
    • 10.4 The proliferation of cultured cells is also limited by the telomeres of their chromosomes
    • 10.5 Telomeres are complex molecular structures that are not easily replicated
    • 10.6 Incipient cancer cells can escape crisis by expressing telomerase
    • 10.7 Telomerase plays a key role in the proliferation of human cancer cells
    • 10.8 Some immortalized cells can maintain telomeres without telomerase
    • 10.9 Telomeres play different roles in the cells of laboratory mice and in human cells
    • 10.10 Telomerase-negative mice show both decreased and increased cancer susceptibility
    • 10.11 The mechanisms underlying cancer pathogenesis in telomerase-negative mice may also operate dur
    • 10.12 Synopsis and prospects
    • Key concepts
    • Thought questions
    • Additional reading
  • Chapter 11 Multi-Step Tumorigenesis
    • 11.1 Most human cancers develop over many decades of time
    • 11.2 Histopathology provides evidence of multi-step tumor formation
    • 11.3 Cells accumulate genetic and epigenetic alterations as tumor progression proceeds
    • 11.4 Multi-step tumor progression helps to explain familial polyposis and field cancerization
    • 11.5 Cancer development seems to follow the rules of Darwinian evolution
    • 11.6 Tumor stem cells further complicate the Darwinian model of clonal succession and tumor progress
    • 11.7 A linear path of clonal succession oversimplifies the reality of cancer: intra-tumor heterogene
    • 11.8 The Darwinian model of tumor development is difficult to validate experimentally
    • 11.9 Multiple lines of evidence reveal that normal cells are resistant to transformation by a single
    • 11.10 Transformation usually requires collaboration between two or more mutant genes
    • 11.11 Transgenic mice provide models of oncogene collaboration and multi-step cell transformation
    • 11.12 Human cells are constructed to be highly resistant to immortalization and transformation
    • 11.13 Nonmutagenic agents, including those favoring cell proliferation, make important contributions
    • 11.14 Toxic and mitogenic agents can act as human tumor promoters
    • 11.15 Chronic inflammation often serves to promote tumor progression in mice and humans
    • 11.16 Inflammation-dependent tumor promotion operates through defined signaling pathways
    • 11.17 Tumor promotion is likely to be a critical determinant of the rate of tumor progression in man
    • 11.18 Synopsis and prospects
    • Key concepts
    • Thought questions
    • Additional reading
  • Chapter 12 Maintenance of Genomic Integrity and the Development of Cancer
    • 12.1 Tissues are organized to minimize the progressive accumulation of mutations
    • 12.2 Stem cells may or may not be targets of the mutagenesis that leads to cancer
    • 12.3 Apoptosis, drug pumps, and DNA replication mechanisms offer tissues a way to minimize the accum
    • 12.4 Cell genomes are threatened by errors made during DNA replication
    • 12.5 Cell genomes are under constant attack from endogenous biochemical processes
    • 12.6 Cell genomes are under occasional attack from exogenous mutagens and their metabolites
    • 12.7 Cells deploy a variety of defenses to protect DNA molecules from attack by mutagens
    • 12.8 Repair enzymes fix DNA that has been altered by mutagens
    • 12.9 Inherited defects in nucleotide-excision repair, base-excision repair, and mismatch repair lead
    • 12.10 A variety of other DNA repair defects confer increased cancer susceptibility through poorly un
    • 12.11 The karyotype of cancer cells is often changed through alterations in chromosome structure
    • 12.12 The karyotype of cancer cells is often changed through alterations in chromosome number
    • 12.13 Synopsis and prospects
    • Key concepts
    • Thought questions
    • Additional reading
  • Chapter 13 Dialogue Replaces Monologue: Heterotypic Interactions and the Biology of Angiogenesis
    • 13.1 Normal and neoplastic epithelial tissues are formed from interdependent cell types
    • 13.2 The cells forming cancer cell lines develop without heterotypic interactions and deviate from t
    • 13.3 Tumors resemble wounded tissues that do not heal
    • 13.4 Experiments directly demonstrate that stromal cells are active contributors to tumorigenesis
    • 13.5 Macrophages and myeloid cells play important roles in activating the tumor-associated stroma
    • 13.6 Endothelial cells and the vessels that they form ensure tumors adequate access to the circulati
    • 13.7 Tripping the angiogenic switch is essential for tumor expansion
    • 13.8 The angiogenic switch initiates a highly complex process
    • 13.9 Angiogenesis is normally suppressed by physiologic inhibitors
    • 13.10 Anti-angiogenesis therapies can be employed to treat cancer
    • 13.11 Synopsis and prospects
    • Key concepts
    • Thought questions
    • Additional reading
  • Chapter 14 Moving Out: Invasion and Metastasis
    • 14.1 Travel of cancer cells from a primary tumor to a site of potential metastasis depends on a ser
    • 14.2 Colonization represents the most complex and challenging step of the invasion–metastasis casc
    • 14.3 The epithelial–mesenchymal transition and associated loss of E-cadherin expression enable car
    • 14.4 Epithelial–mesenchymal transitions are often induced by contextual signals
    • 14.5 Stromal cells contribute to the induction of invasiveness
    • 14.6 EMTs are programmed by transcription factors that orchestrate key steps of embryogenesis
    • 14.7 EMT-inducing transcription factors also enable entrance into the stem cell state
    • 14.8 EMT-inducing TFs help drive malignant progression
    • 14.9 Extracellular proteases play key roles in invasiveness
    • 14.10 Small Ras-like GTPases control cellular processes such as adhesion, cell shape, and cell motil
    • 14.11 Metastasizing cells can use lymphatic vessels to disperse from the primary tumor
    • 14.12 A variety of factors govern the organ sites in which disseminated cancer cells form metastases
    • 14.13 Metastasis to bone requires the subversion of osteoblasts and osteoclasts
    • 14.14 Metastasis suppressor genes contribute to regulating the metastatic phenotype
    • 14.15 Occult micrometastases threaten the long-term survival of cancer patients
    • 14.16 Synopsis and prospects
    • Key concepts
    • Thought questions
    • Additional reading
  • Chapter 15 Crowd Control: Tumor Immunology and Immunotherapy
    • 15.1 The immune system functions to destroy foreign invaders and abnormal cells in the body’s tiss
    • 15.2 The adaptive immune response leads to antibody production
    • 15.3 Another adaptive immune response leads to the formation of cytotoxic cells
    • 15.4 The innate immune response does not require prior sensitization
    • 15.5 The need to distinguish self from non-self results in immune tolerance
    • 15.6 Regulatory T cells are able to suppress major components of the adaptive immune response
    • 15.7 The immunosurveillance theory is born and then suffers major setbacks
    • 15.8 Use of genetically altered mice leads to a resurrection of the immunosurveillance theory
    • 15.9 The human immune system plays a critical role in warding off various types of human cancer
    • 15.10 Subtle differences between normal and neoplastic tissues may allow the immune system to distin
    • 15.11 Tumor transplantation antigens often provoke potent immune responses
    • 15.12 Tumor-associated transplantation antigens may also evoke anti-tumor immunity
    • 15.13 Cancer cells can evade immune detection by suppressing cell-surface display of tumor antigens
    • 15.14 Cancer cells protect themselves from destruction by NK cells and macrophages
    • 15.15 Tumor cells launch counterattacks on immunocytes
    • 15.16 Cancer cells become intrinsically resistant to various forms of killing used by the immune sys
    • 15.17 Cancer cells attract regulatory T cells to fend off attacks by other lymphocytes
    • 15.18 Passive immunization with monoclonal antibodies can be used to kill breast cancer cells
    • 15.19 Passive immunization with antibody can also be used to treat B-cell tumors
    • 15.20 Transfer of foreign immunocytes can lead to cures of certain hematopoietic malignancies
    • 15.21 Patients’ immune systems can be mobilized to attack their tumors
    • 15.22 Synopsis and prospects
    • Key concepts
    • Thought questions
    • Additional reading
  • Chapter 16 The Rational Treatment of Cancer
    • 16.1 The development and clinical use of effective therapies will depend on accurate diagnosis of di
    • 16.2 Surgery, radiotherapy, and chemotherapy are the major pillars on which current cancer therapies
    • 16.3 Differentiation, apoptosis, and cell cycle checkpoints can be exploited to kill cancer cells
    • 16.4 Functional considerations dictate that only a subset of the defective proteins in cancer cells
    • 16.5 The biochemistry of proteins also determines whether they are attractive targets for interventi
    • 16.6 Pharmaceutical chemists can generate and explore
    • 16.7 Drug candidates must be tested on cell models as an initial measurement of their utility in who
    • 16.8 Studies of a drug’s action in laboratory animals are an essential part of pre-clinical testin
    • 16.9 Promising candidate drugs are subjected to rigorous clinical tests in Phase I trials in humans
    • 16.10 Phase II and III trials provide credible indications of clinical efficacy
    • 16.11 Tumors often develop resistance to initially effective therapy
    • 16.12 Gleevec paved the way for the development of many other highly targeted compounds
    • 16.13 EGF receptor antagonists may be useful for treating a wide variety of tumor types
    • 16.14 Proteasome inhibitors yield unexpected therapeutic benefit
    • 16.15 A sheep teratogen may be useful as a highly potent anti-cancer drug
    • 16.16 mTOR, a master regulator of cell physiology, represents an attractive target for anti-cancer t
    • 16.17 B-Raf discoveries have led to inroads into the melanoma problem
    • 16.18 Synopsis and prospects: challenges and opportunities on the road ahead
    • Key concepts
    • Thought questions
    • Additional reading
  • Abbreviations
  • Glossary
  • Index

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Vörumerki: Norton
Vörunúmer: 9781317963462
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The Biology of Cancer, 2e

Vörumerki: Norton
Vörunúmer: 9781317963462
Rafræn bók. Uppl. sendar á netfangið þitt eftir kaup
9.990 kr.
Fá vöru senda með tölvupósti
9.990 kr.