The Pathobiology of Neoplasia
(Sprache: Englisch)
This book is directed primarily to advanced graduate and medical students, postdoctoral trainees, and established investigators having basic research interests in neoplasia. Its content is based in part on the lecture outlines and selected histopathology...
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Klappentext zu „The Pathobiology of Neoplasia “
This book is directed primarily to advanced graduate and medical students, postdoctoral trainees, and established investigators having basic research interests in neoplasia. Its content is based in part on the lecture outlines and selected histopathology laboratory components of an advanced course entitled The Pathobiology of Experimental Animal and Human Neoplasia, developed by me for the Experimental Pathology Curriculum of the Department of Pathology at the Medical College of Virginia. In this regard, an effort has been made to integrate pathology with carcinogenesis, genetics, biochemistry, and cellular and molecular biology in order to present a comprehensive and current view of the neoplastic process. For focus, emphasis is mainly being placed on the neoplastic cells themselves, and not on associated host-mediated responses. It ishoped that this book will accomplish its purpose of providing students and researchers who already possess strong but diverse basic science backgrounds with unifying concepts in tumor pathobiology, so as to stimulate new research aimed at furthering our understanding of neoplastic disease. I wish to express my appreciation and heartfelt thanks to the authors, whose individual ranges of expertise and research experience clearly bring to their respective chapters unique perspectives that easily transcend any redundancy that may be present. In addition, I am grateful to Drs. George Vennart, Saul Kay, and Fred Meier, and to Ms. Connie Wilkerson of the Department of Pathology at MCV, for their helpful comments and their review of some of the material.
Inhaltsverzeichnis zu „The Pathobiology of Neoplasia “
Introduction: Chronology of Significant Events in the Study of Neoplasia.- 1. Classification of Neoplasms.- 1. Introduction.- 2. Non-Neoplastic Adaptive Growth Changes.- 2.1. Atrophy.- 2.2. Hypertrophy.- 2.3. Hyperplasia.- 2.4. Metaplasia.- 2.5. Dysplasia.- 3. Preneoplastic Lesions and Malformations.- 4. Anaplasia and Differentiation in Neoplasms.- 5. Pathobiologic Characteristics of Benign and Malignant Neoplasms.- 6. Nomenclature of Neoplasms.- 7. Grading and Staging of Malignant Neoplasms.- References.- 2. Chemical Carcinogenesis in Experimental Animals and Humans.- 1. Background.- 2. Metabolism of Chemical Carcinogens.- 2.1. Aromatic Compounds.- 2.2. Aliphatic Compounds.- 2.3. Miscellaneous.- 3. Classification of Chemical Carcinogens.- 3.1. Direct-Acting versus Indirect-Acting Carcinogens.- 3.2. Genotoxic versus Epigenetic Carcinogens.- 3.3. Initiators and Promoters.- 4. Structure-Activity Relationships.- 5. Relevance to Humans.- References.- 3. DNA Adducts and Carcinogenesis.- 1. General Considerations.- 2. DNA Adduct Determination and Quantitation.- 3. DNA Adducts from Specific Classes of Carcinogens.- 3.1. N-Nitrosamines.- 3.2. Aflatoxins.- 3.3. Aromatic Amines.- 3.4. Polycyclic Aromatic Hydrocarbons.- 4. Conclusions.- References.- 4. Oncogenic Viruses.- 1. Introduction.- 1.1. Purpose.- 1.2. Overview and Historic Events.- 1.3. Classification.- 2. Host Cells, Tumor Viruses, and Their Interactions.- 2.1. Host Cells.- 2.2. Tumor Viruses.- 2.3. Interactions: Proto-Oncogenes and Retro-Oncogenes.- 3. Common Pathways of Cell Transformation and Neoplasia: Unifying Features of Viral Oncogenesis.- 3.1. Virus-Induced Transformation.- 3.2. Unifying Features of Viral Carcinogenesis.- 4. Pathobiology of Oncogenic Viruses and Experimental Animal Models of Virus-Induced Human Neoplasia.- 4.1. DNA Tumor Viruses.- 4.2. RNA Tumor Viruses.- 5. Immunologic Aspects of Virus-Induced Neoplasia.- 5.1. Virus-Associated Antigens.- 5.2. Effector Mechanisms of Virus-Induced Tumor
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Immunity.- 6. Concluding Remarks.- References.- 5. Radiation Carcinogenesis.- 1. Introduction.- 1.1. Historic Perspective.- 1.2. Ionizing Radiation and Its Interaction with Matter.- 2. Radiation Carcinogenesis in Vivo.- 2.1. The Human Experience.- 2.2. Radiation Carcinogenesis in Animal Models.- 3. Pathology of Radiation Carcinogenesis in Vivo.- 3.1. Incidence and Morphology.- 3.2. Relative Tissue Sensitivity.- 3.3. Latency.- 4. Radiation Transformation in Vitro.- 4.1. Experimental Techniques.- 4.2. Properties of Transformed Cells.- 5. Factors Influencing Radiation Carcinogenesis or Transformation.- 5.1. Physical Factors.- 5.2. Host/Environmental Factors.- 6. Pathogenesis of Radiation Carcinogenesis.- 6.1. Multistep Process: Initiation and Promotion.- 6.2. DNA as a Critical Target.- 6.3. Oncogenes in Radiation Carcinogenesis.- 7. Conclusion.- References.- 6. The Multistage Concept of Carcinogenesis.- 1. Types of Tumorigenic Enhancement.- 2. Multistage Skin Tumorigenesis.- 3. Multistage Tumorigenesis in Nonepidermal Systems.- 3.1. Bladder.- 3.2. Liver.- 3.3. Respiratory Tract.- 3.4. Intestine.- 3.5. Mammary Gland.- 3.6. Other Nonepidermal Systems.- 4. Multistage Models of Neoplasia in Cell-Culture Systems.- 4.1. Measurement of Multistage Development of Cell Transformation.- 4.2. Measurement of Promoter-Induced Changes in Intercellular Relationships.- 4.3. Measurement of Promoter-Induced Changes in Membrane Function.- 4.4. Measurement of Changes in Cellular Differentiation.- 5. Conclusions.- References.- 7. Organ and Species Specificity in Chemical Carcinogenesis and Tumor Promotion.- 1. Introduction.- 2. Organ and Species Specificity Attributable to Metabolism.- 3. Biologic Effects of Alkylating Agents.- 3.1. Direct-Acting Compounds.- 3.2. Metabolism-Dependent Compounds.- 3.3. Molecular Targets of Alkylating Agents.- 4. Organ and Species Specificity in Tumor Promotion.- 4.1. Promotion in Squamous Epithelia.- 4.2. Promotion in Nonsquamous Epithelia.- 4.3. Dietary Factors That Promote Carcinogenesis.- References.- 8. DNA Repair Mechanisms and Carcinogenesis.- 1. Introduction.- 2. Damage to DNA.- 3. DNA Repair Systems.- 3.1. Direct Repair of Damage.- 3.2. Excision Repair.- 4. Relationship of DNA Repair to Carcinogenesis.- 4.1. Causes of Incomplete DNA Repair.- 4.2. Mechanisms for Tolerating Unrepaired DNA Damage.- 5. Summary.- References.- 9. Preneoplasia and Precancerous Lesions.- 1. Introduction.- 2. Preneoplastic and Precancerous Lesions in Experimental Animals.- 2.1. Squamous Cell Papilloma as a Precancerous Lesion in Mouse Skin Carcinogenesis.- 2.2. Precursor Lesions Associated with Hepatocarcinogenesis in the Rat.- 3. Preneoplastic and Precancerous Lesions in Humans.- 3.1. Cervical Dysplasia and Carcinoma in Situ of the Uterine Cervix.- 3.2. Adenomatous Polyps of the Colon and Rectum.- 3.3. Dysplastic Nevi.- 3.4. Liver Cell Dysplasia and Adenomatous Hyperplastic Liver Nodules.- 3.5. Other Examples of Putative Epithelial Cell Preneoplasia.- 4. Conclusions.- References.- 10. Tumor Progression and the Clonal Evolution of Neoplasia.- 1 Introduction.- 2. Structural Variation in Tumors.- 3. Foulds' General Principles of Tumor Progression.- 4. Clonal Origins of Neoplasms in Humans and Experimental Animals.- 5. Mechanisms of Tumor Progression.- 5.1. Aneuploidy and Tumor Progression.- 5.2. Oncogenes and Tumor Progression.- 6. Conclusions.- References.- 11. Cytogenetics and Human Neoplasia.- 1. Introduction.- 2. Chromosomal Symbols, Abbreviations, and Nomenclature.- 3. Computer Data Management.- 4. Constitutional versus Acquired Chromosomal Abnormalities in Cancer.- 4.1. Constitutional Chromosomal Abnormalities.- 4.2. Acquired Chromosomal Abnormalities.- 5. Cytogenetic Dissection of a Translocation between Chromosomes 9 and 22: The Philadelphia Translocation.- 5.1. The Philadelphia Translocation Occurs in Multiple Types of Leukemia and Related Disorders.- 5.2. Biology of Cell Lineages.- 5.3. Molecular Dissection of the Ph Translocation.- 6. Cytogenetic Dissection of the Acute Nonlymphocytic Leukemias.- 6.1. The French-American-British Classification of ANLL.- 6.2. Primary Chromosomal Rearrangements and Numerical Changes.- 6.3. Cytogenetic Dissection: A New Perspective on ANLL.- 7. Cytogenetic Dissection of ALL.- 8. Other Hematologic Conditions.- 9. Comments on Chromosomal Changes in Hematologic Disorders.- 10. Chromosomal Changes in CLL and Lymphoma.- 11. Cytogenetics of Solid Tumors.- References.- 12. Genetics of Susceptibility to Mouse Skin Tumor Promotion.- 1. Introduction.- 1.1. Multistage Carcinogenesis in Mouse Skin.- 1.2. Morphologic and Biochemical Effects of Tumor Promoters in Mouse Skin.- 2. Genetic Differences in Response to Skin Tumor Promoters.- 2.1. Species Differences.- 2.2. Strain Differences.- 2.3. Inheritance of Susceptibility to Phorbol Ester Skin Tumor Promotion.- 3. Morphologic Changes in Mouse Skin Potentially Important in Determining Genetic Differences in Response to Phorbol Esters.- 3.1. Hyperplasia.- 3.2. Dark Basal Keratinocytes.- 3.3. Inflammation.- 4. Biochemical and Molecular Changes Potentially Important in Determining Genetic Differences in Response to Phorbol Esters.- 4.1. Receptor-Mediated Events.- 4.2. Phorbol Ester Metabolism.- 4.3. Other Mechanisms.- 5. Genetic Differences in Response to Stage-Specific Promoters in Mouse Skin.- 5.1. Two-Stage Promotion.- 5.2. Genetic Differences in Response to Stage-Specific Promoters.- 6. Genetic Differences in Response to Other Classes of Tumor-Promoting Agents.- 6.1. Characteristics of the Response of Mouse Skin to Different Classes of Tumor Promoters.- 6.2. Genetic Differences in Response to Different Classes of Promoters.- 7. Use of Genetic Differences to Develop Models for Studying Mechanisms of Tumor Promotion.- 8. Concluding Remarks.- References.- 13. Oncogenes.- 1. Introduction.- 2. Retroviruses and Oncogenes.- 2.1. Acute and Chronic Transforming Retroviruses.- 2.2. Acute Transforming Retroviruses and Viral Oncogenes.- 3. Cellular Proto-Oncogenes.- 3.1. Conservation among Species.- 3.2. Cellular Proto-Oncogenes as Control Elements in Normal Cell Growth and Differentiation.- 4. Tumor Formation and Mechanisms of Activation of Cellular Proto-Oncogenes.- 4.1. Overview of Mechanisms of Activation.- 4.2. Activation of Cellular Proto-Oncogenes by Retroviral Insertion.- 4.3. Mutations Activating Proto-Oncogenes.- 4.4. Amplification of Proto-Oncogenes.- 4.5. Chromosomal Translocations in the Activation of Cellular Proto-Oncogenes.- 5. Cooperation among Activated Oncogenes in Cell Transformation.- 6. Summary.- References.- 14. Activation of Oncogenes by Chemical Carcinogens.- 1. Introduction.- 2. Activation of Proto-Oncogenes by Gene Amplification and Chromosomal Translocation.- 3. Detection of Oncogenes by Gene Transfer (DNA Transfection Assay).- 4. Activation of Proto-Oncogenes by Carcinogens.- 5. Oncogene Activation in Long-Term Rodent Carcinogenic Studies.- 6. Tissue- and Carcinogen-Specific Activation of Proto-Oncogenes.- 7. Extrapolation from Rodents to Humans.- References.- 15. Alterations in Biochemical Control Mechanisms of Neoplastic Cells.- 1. Introduction.- 2. Alterations of Membrane Transport in Neoplasia.- 2.1. Acceleration of Amino Acid Uptake by Transformed Cells-Relationship to (Na+/K+)ATPase Activity.- 2.2. Alterations in (Na+/K+)ATPase in Neoplasia.- 3. Alterations in Metabolic Pathways in Transformed Cells-Enhanced Glycolysis.- 3.1. (Na+1K+)ATPase as a Major Contributor of ADP and Pi Rate-Limiting Factors for Glycolysis.- 3.2. Role of Transforming Growth Factors in Increased Glycolysis of Transformed Cells.- 3.3. Metabolic Alterations Induced by Specific Oncogenes.- 4. Cytoskeletal Alterations in Transformed Cells.- 5. Alterations in Mitochondrial Citric Acid Cycle.- 6. Alterations in Proto-Oncogenes in Neoplasia.- 6.1. The ras Oncogene, G Proteins, and Transforming Growth Factors.- 6.2. The myc Oncogene in Burkitt Lymphomas and Murine Plasmacytomas.- 7. Conclusions.- References.- 16. Membrane Alterations in Neoplasia.- 1. Introduction.- 2. Ultrastructural Membrane Pathology of Neoplasia.- 2.1. Endomembranes.- 2.2. Lysosomes and Endocytic Compartments.- 2.3. Mitochondria and Peroxisomes.- 2.4. Plasma Membrane.- 3. Functional Alterations of Endomembranes and the Plasma Membrane in Neoplasia.- 3.1 Endoplasmic Reticulum.- 3.2. Golgi Apparatus.- 3.3. Membrane Dynamics and Membrane Recycling.- 3.4. Role of Endomembranes in Oncogene Expression.- 3.5. Plasma Membranes.- 3.6. Intercellular Communication.- 4. The Cytoskeleton in Cell Transformation and Malignant Neoplasia.- 5. Membranes and Carcinogenesis.- 5.1. Endoplasmic Reticulum and Carcinogen Activation.- 5.2. Peroxisomes and Carcinogenesis.- 5.3. Lipid Peroxidation and Carcinogenesis.- 5.4. Lysosomes and Carcinogenesis.- 6. Conclusions.- References.- 17. Growth Factors and Neoplasia.- 1. Introduction.- 2. Epidermal Growth Factor.- 3. Transforming Growth Factor-?.- 4. Platelet-Derived Growth Factor.- 5. Bombesin.- 6. Fibroblast Growth Factor(s).- 7. Interleukin-2.- 8. Insulinlike Growth Factors: IGFs and Somatomedins.- 9. Nerve Growth Factor.- 10. Macrophage Colony-Stimulating Factor-1.- 11. Transforming Growth Factor-ß.- 12. Other Growth Factors.- 13. Second Messengers Mediating Growth Factor Effects.- References.- 18. Biochemical Mechanisms of Action of the Phorbol Ester Class of Tumor Promoters.- 1. Introduction.- 2. Effects of Phorbol Esters.- 3. Receptors for Phorbol Esters.- 3.1. Identification of Receptors.- 3.2. Similarities between Phorbol Ester Receptors and Protein Kinase C.- 3.3. Evidence That Protein Kinase C Is the Major Phorbol Ester Receptor.- 4. Characterization of Protein Kinase C in Vitro.- 4.1. Domains.- 4.2. Molecular Cloning.- 4.3. Substrate Specificity.- 4.4. Activators of Protein Kinase C.- 4.5. Inhibitors of Protein Kinase C.- 5. Regulation of Phorbol Ester Receptor/Protein Kinase C in Vivo.- 5.1. Translocation and Proteolytic Processing.- 5.2. Modulation of the Affinity of Receptors for Phorbol Esters.- 5.3. Modulation of the Number of Receptors.- 6. Feedback of Protein Kinase C on Other Pathways.- 6.1. Signal Transduction.- 6.2. Phosphatidylinositol Turnover.- 6.3. Cellular Responses to Growth Factors.- 6.4. Activation of Oncogenes.- 7. Concluding Remarks.- References.- 19. Biochemical Marker Alterations in Hepatic Preneoplasia Neoplasia.- 1. Introduction.- 1.1. Relationship of Markers to Different Stages in Neoplasia.- 1.2. Approaches to Evaluation of Markers.- 2. Marker Alterations in Preneoplastic and Neoplastic Liver Lesions.- 2.1. Two-Dimensional Polyacrylamide Gel Electrophoresis.- 2.2. Known Markers of Hepatocarcinogenesis.- 2.3. New Markers for Hepatocarcinogenesis.- 2.4. Specific Markers for the Neoplastic Stage.- 3. Concluding Comments.- References.- 20. Oncogene Activation and Expression during Carcinogenesis in Liver and Pancreas.- 1. Introduction.- 1.1. Activated Oncogenes versus Proto-Oncogenes.- 1.2. Proto-Oncogene Activation by Chemical Carcinogens and Ionizing Radiation.- 2. Multistage Carcinogenesis in Liver and Pancreas.- 2.1. Initiation and Promotion in Liver.- 2.2. Initiation and Promotion in Pancreas.- 3. Proto-oncogene Activation in Liver and Pancreatic Neoplasms.- 3.1. Transforming Genes Associated with Human Liver and Pancreatic Neoplasms.- 3.2. Transforming Genes in Spontaneous and Chemically Induced Liver and Pancreatic Neoplasms.- 4. Modulation of Proto-Oncogene Expression during Liver and Pancreatic Growth.- 4.1. Growth in the Liver.- 4.2. Growth in the Pancreas.- 5. Concluding Remarks.- References.- 21. Oncodevelopmental Expression and Neoplasia.- 1 Introduction.- 2. Oncodevelopmental Antigens, Proteins, and Enzymes in Malignant Neoplasms.- 3. Concepts of Stem Cells, Blocked and Partially Blocked Ontogeny, and Retrodifferentiation in Neoplastic Cell Development.- 4. Expression of Developmental Genes during Various Non-Neoplastic Conditions and in Cell Culture.- 5. Possible Mechanisms for Developmental Gene Expression in Neoplastic and Non-Neoplastic Cells of the Adult Organism.- References.- 22. Expression of Differentiated Function in Neoplasms.- 1. Embryos, Stem Cells, and Cancer Cells.- 1.1. Similarities between Normal Cells and Cancer Cells.- 1.2. Historic Considerations.- 2. Differentiated Cell Progeny Obtained from Tumor Cells.- 2.1. A Plant Tumor.- 2.2. Fish Pigment Cell Neoplasm.- 2.3. Amphibian Tumor: The Lucké Renal Adenocarcinoma.- 2.4. Neuroblastomas.- 2.5. Rhabdomyosarcoma.- 2.6. Teratocarcinomas.- 2.7. Squamous Cell Carcinoma.- 2.8. Myeloid Leukemia.- 2.9. Murine Erythroleukemia.- 2.10. Other Tumors That Differentiate.- 3. Primary Induction in the Vertebrate Embryo Compared with the Induction of Cancer Cell Differentiation.- References.- 23. Ectopic Hormone Production and Neoplasia.- 1. Introduction.- 2. ACTH, POMC-Derived Peptides, CRH.- 3. Vasopressin.- 4. Human Chorionic Gonadotropin.- 5. Parathormone (PTH) and Other Hypercalcemia-Inducing Factors.- 6. Insulinlike Hypoglycemic Factors.- 7. Growth Hormone-Releasing Factor.- 8. Other Ectopically Produced Hormones.- 8.1. Calcitonin.- 8.2. Prolactin.- 8.3. Gastrin-Releasing Peptide.- 8.4. Vasointestinal Peptide.- 8.5. Erythropoietin.- 9. Conclusion.- References.- 24. Metaplastic Transformation of Pancreatic Cells to Hepatocytes.- 1. Introduction.- 2. Animal Models.- 2.1. Hamster.- 2.2. Rat.- 2.3. Human.- 3. Characterization of the Metaplastic Cells in Pancreas.- 4. Cells of Origin.- 4.1. Hamster.- 4.2. Rat.- 5. Other Examples of Metaplasia in Gut Entoderm-Derived Tissues.- 5.1. Rat.- 5.2. Rainbow Trout.- 5.3. Human.- 6. Possible Genetic and Developmental Mechanisms Involved in Metaplasia.- 6.1. Gene Regulation of Determination.- 6.2. Role of Gene Switching in Cell Specialization.- 6.3. DNA Methylation and Gene Expression.- 7. Summary.- References.- 25. Crown Gall Neoplasms.- 1. Introduction.- 2. Pathology.- 2.1. Symptoms.- 2.2. Pathogen.- 2.3. Development of Disease.- 2.4. Genetic Organization.- 3. The Infectious Process.- 3.1. Recognition and Attachment.- 3.2. DNA Transfer.- 4. Differentiation of Crown Gall Cells.- 4.1. Phytohormone Synthesis and Differentiation.- 4.2. Opine Synthesis and Utilization.- 4.3. Reversal of the Tumorous State in Crown Gall.- 5. Summary and Conclusions.- References.- 26. Angiogenesis: Factors and Mechanisms.- 1. Tumor Vasculature.- 1.1. Background.- 1.2. Differences between Normal and Tumor Vessels.- 1.3. Relationship between Vascularization and Tumor Growth.- 1.4. Role for Growth Factors.- 2. Angiogenesis Factors.- 2.1. Introduction.- 2.2. Non-Heparin-Binding Factors: Low-Molecular-Weight Factors.- 2.3. Non-Heparin-Binding Factors: Polypeptide Factors.- 2.4. Heparin-Binding Growth Factors.- 3. Regulation of Angiogenesis.- 3.1. Actions of Angiogenesis Factors.- 3.2. Control of Availability of Angiogenic Factors.- 3.3. Role of Ischemia in Angiogenesis.- 3.4. Storage of FGF.- 4. Summary.- References.- 27 Tumor Invasion and Metastases: Biochemical Mechanisms.- 1. Multistep Cascade of Metastases.- 2. Organ Tropism for Metastases.- 3. Tumor Cell Interaction with the Extracellular Matrix.- 4. Three-Step Theory of Invasion.- 5. Tumor Cell Motility Factors.- 6. Isolation and Characterization of a Human Melanoma Autocrine Motility Factor.- 7. Transduction of the Chemical Signal in the Motile Response of Tumor Cells.- 8. Laminin Receptors.- 9. Effect of Anti-Laminin Receptor Antisera on Laminin-Mediated Haptotaxis.- 10. In Vivo Expression of Laminin Receptor in Human Tumors Correlates with Their Invasive and Migratory Capacities.- 11. RGD Recognition Receptors.- 12. Tumor Cell Proteinases.- 13. Molecular Genetics of Metastases.- 14. Conclusions.- References.- 28. Phenotypic Heterogeneity and Metastasis.- 1. Introduction.- 2. Pathogenesis of Metastasis (Mechanisms).- 2.1. Invasion.- 2.2. Lymphatic-Hematogenous Spread.- 3. Biologic Heterogeneity of a Metastatic Tumor.- 3.1. Metastatic Heterogeneity of Tumor Cells in Primary Neoplasms.- 3.2. Origin of Cellular Diversity in Malignant Neoplasms.- 3.3. Instability of Heterogeneous Tumor Populations.- 3.4. Origin of Biologic Heterogeneity in Metastases.- 3.5. Development of Intralesional Heterogeneity within Metastases.- 4. The Challenge of Biologic Heterogeneity of Neoplasms.- 4.1. Effect of Tumor Cell Heterogeneity on Chemotherapy.- 4.2. Antigenic and Immunogenic Heterogeneity.- 5. Summary.- References.
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Bibliographische Angaben
- 2012, Softcover reprint of the original 1st ed. 1989, XXII, 583 Seiten, Maße: 17 x 24,4 cm, Kartoniert (TB), Englisch
- Herausgegeben: A. E. Sirica
- Verlag: Springer, Berlin
- ISBN-10: 1468455257
- ISBN-13: 9781468455250
Sprache:
Englisch
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