Table of contents for Neoplasms : principles of development and diversity / Jules J. Berman.

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Table of Contents
Introduction: What You Will Learn By Reading this Book
Why is cancer such a difficult disease to understand?
Is cancer one disease or many diseases?
Part I. Speciation
Chapter 1. What Properties are Shared by All Cancers? 
1.1 Background
1.2 Are there any properties of neoplasms that are not found in normal cells?
1.3 Persistent growth in normal cells
1.4 Invasion by normal cells
1.5 Metastasis in normal cells
1.6 Is there a common temporal sequence leading to the development of cancer?
1.7 Why is it important to treat cancer early?
1.8 Cancer morphology
1.9 General rules for naming neoplasms
1.10 What is a cytologic diagnosis?
1.11 Morphology of malignant cells
1.12 Cancerous atypia and reactive atypia
1.13 How can you distinguish reactive atypia from cancerous atypia?
1.14 Dysplastic cells, and how they differ from cancer cells
1.15 Nuclear atypia in cancer cells
1.16 Why are the nuclei of malignant cells different from the nuclei of normal cells?
1.17 Tumor monoclonality
1.18 Monoclonal proliferative lesions
1.19 Clonal expansion in paroxysmal nocturnal hemoglobinuria
1.20 Clonal expansions that may not lead to cancer
1.21 Polyclonal expansions that may lead to monoclonal cancer
1.22 Tumor growth regulation and tumor autonomy
1.23 Limits on tumor autonomy
Chapter 1 summary
Chapter 2. Carcinogenesis 
2.1 Background
2.2 Oncogenes and tumor suppressor genes
2.3 The narrow range of tissue-specificity of oncogenes
2.4 Are there tumors that have multiple activated oncogenes?
2.5 Do tumor suppressor genes cause cancer?
2.6 Can genetic alterations in cancer cells be mediated (and reversed) through epigenetic modifications?
2.7 Tumor initiation
2.8 Tumor latency
2.9 Tumor dormancy
2.10 Spontaneous regression of latent tumors
2.11 Are tumor latency and tumor dormancy related phenomena?
2.12 Chemical carcinogenesis
2.13 Why do chemical carcinogens need to be activated by cells in our bodies before they can cause cancer?
2.14 Do we know which chemicals are likely to cause cancer in humans?
2.15 Naturally occurring carcinogens
2.16 Do viruses cause cancer?
2.17 Are there tumors that arise spontaneously, without initiation, and without any contribution from an external carcinogen?
2.18 Cancer regression
2.19 The inherited syndromes that cause cancers
2.20 Minimal number of events necessary for tumor development
2.21 Fast and slow carcinogenesis
2.22 Iatrogenic insertional carcinogenesis
2.23 Can cancer be reversed by modifying a single oncogene?
Chapter 2 summary
Chapter 3. The Mystery of Tumor Diversity and of Type-Specific Tumor Uniformity
3.1 Background
3.2 Tumor heterogeneity
3.3 How are clonality, progression, and heterogeneity related?
3.4 The complexity of cancers
3.5 Tumor diversity and the disconnect between genotype and phenotype
3.6 Animal speciation and tumor speciation
3.7 Benign tumors
3.8 Are there benign oncogenes?
Chapter 3 summary
Chapter 4. The Range of Neoplastic Phenotypes
4.1 Background
4.2 Neoplastic lesions
4.3 Do benign tumor cells develop into malignant tumor cells over time?
4.4 How do we know when a lesion is a neoplasm?
4.5 Borderline tumors
4.6 Precancers
4.7 Concensus definition of precancers
4.8 The difference between a precancerous condition and a precancer?
4.9 What is the difference between a benign tumor and a precancer?
4.10 Is there a difference between precancer genes and cancer genes?
4.11 Is there value in treating precancers?
4.12 Hamartomas and choristomas
4.13 Are hamartomas types of neoplasms?
4.14 Hamartoma syndromes
4.15 Is there a pure hamartoma syndrome?
Chapter 4 summary
Chapter 5. What Can We Learn About Human Neoplasms by Studying Animals, Plants, Fish and Insects?
5.1 Background
5.2 Neoplasia in plants
5.3 Neoplasia in insects
5.4 Neoplasia in the amphibia
5.5 Carcinogenesis in fish
5.6 Zebrafish
5.7 Neoplasia in mammals
5.8 Oncogenes in the animal kingdom
5.9 Tumor suppressor genes in the animal kingdom
5.10 Why don't whales develop more tumors than mice?
5.11 Evolutionary mimicry and evolutionary convergence
5.12 Goodbye to the apudoma
5.13 Are animal tumors good models for human tumors?
5.14 What kinds of questions can best be answered in animal systems?
5.15 Is cancer directly transmissible from organism to organism?
5.16 Transmission of virally-induced cancers
5.17 What can we learn from the differences between animal and human tumors?
5.18 The hepatopancreas of arthropods, gastropods and fish
Chapter 5 summary
Chapter 6. What Does Classification of All Animals Tell Us About the Classification of All Neoplasms?
6.1 Background
6.2 What is speciation and how does it relate to evolution, taxonomy and classification?
6.3 How does animal classification relate to the classification of neoplasms?
6.4 What is the most common impediment to classifying a species?
6.5 The sui generis taxon
6.6 The classification of organisms is not strictly cladistic
Chapter 6 summary
Chapter 7. Classification of Neoplasms
7.1 Background
7.2 The challenge of classifying neoplasms
7.3 Discrimination methods
7.4 Formal principles of biological classification
7.5 Current status of tumor classification
Chapter 7 summary
Chapter 8. Classification by Morphology (What the Tumor Looks Like)
8.1 Background
8.2 Epithelial and non-epithelial tumors
8.3 Tumor variants
8.4 Determining histogenesis
8.5 Morphology and the invention of rare tumors
8.6 What is a rare tumor?
8.7 Why are rare tumors important?
8.8 The importance of uncommon variants of common tumors
8.9 Example case: gastrointestinal stromal tumor
8.10 What do rare tumors have in common with uncommon variants of common tumors?
8.11 What can we learn from uncommon variants of common tumors?
8.12 Can we understand common, sporadic tumors by studying rare, inherited tumors?
8.13 Will we learn how to prevent common tumors by studying the rare tumors?
8.14 Why are we likely to prevent and cure rare tumors before we cure common tumors?
8.15 Are sporadic tumors always characterized by the same mutation that is present in the germline of patients who develop the same type of tumor as part of an inherited condition?
Chapter 8 summary
Chapter 9. Classification by Cause
9.1 Background
9.2 Determining the cause of a cancer
9.3 Carcinogen exposure and type of cancer
9.4 How does sunlight produce melanomas in locations that are not exposed to sunlight?
9.5 Are the steps in chemical carcinogenesis class-dependent?
9.6 If liver is the most powerful activator of chemical carcinogens, why are liver tumors less frequent than tumors in lung, colon, skin and other epithelial tissues?
9.7 Variations in tumor progression
9.8 Clastogens and leukemias
9.9 Why do chromosome breakage syndromes often cause leukemias and seldom cause carcinomas?
9.10 Myeloproliferative disorders, myelodysplasias and preleukemic conditions
9.11 What are the chief differences between myelodysplasias and myeloproliferative disorders?
9.12 What are the features shared among tumors produced by a particular carcinogen?
9.13 Do some carcinogens cause only benign tumors and others cause only malignant tumors?
9.14 Tumors caused by viruses
9.15 Immune surveillance and the role of immunosuppression in carcinogenesis
9.16 Why do the tumors that occur in some tumor inheritance syndromes cross multiple cell lineages?
Chapter 9 summary
Chapter 10. Classification by Topography (Where the Tumor is Located)
10.1 Background
10.2 The range of tumors occurring in a single organ
10.3 Subsets of anatomic classifications
Chapter 10 summary
Chapter 11. Classification by the Age at Which the Cancer Occurs
11.1 Background
11.2 What tumors occur in infants and children?
11.3 The pnet tumors
11.4 What are the ews family of tumors?
11.5 Leukemias
11.6 Transplacental carcinogenesis
11.7 There are only a few known human transplacental carcinogens
11.8 Why are congenital and childhood tumors extremely rare?
11.9 Why does transplacental carcinogenesis seldom produce tumors of primitive cells?
11.10 Why are the early-stage embryos resistant to carcinogenesis?
11.11 Congenital tumors
11.12 Why do pediatric tumors respond so well to chemotherapeutic agents, and adult tumors respond so poorly?
11.13 Why can we infer that most tumors occurring in adults have a long latency?
11.14 What do we learn from age at diagnosis and synchronous appearance of tumors in germline mutation syndromes?
Chapter 11 summary
Chapter 12. Classification by Function and Common Pathways
12.1 Background
12.2 Endocrine neoplasia
12.3 Pathways
Chapter 12 summary
Chapter 13. Molecular Classification of Neoplasms
13.1 Background
13.2 Fundamental properties are not always good classifiers
13.3 Limitations of a molecular classification of neoplasms
13.4 A genetic classification for the major categories of human tumors
13.5 Complexities in the genetic approach to cancer classification
13.6 Proteomic classification of cancer
13.7 Epigenomic classification of cancer
13.8 Is a human tumor genome project feasible?
Chapter 13 summary
Chapter 14. Classification by Developmental Lineage is Best
14.1 Background
14.2 Lineage can be determined with certainty
14.3 Developmental lineage pathways are often preserved in tumors
14.4 Are there examples known tumors of unknown or ambiguous lineage?
14.5 Are there tumors that arise through transdifferentation?
Chapter 14 summary
Chapter 15. The Six Major Classes of Neoplasms
15.1 Background
15.2 Class endoderm/ectoderm neoplasms
15.3 Class mesoderm neoplasms
15.4 Class neuroectoderm neoplasms
15.5 Class neural crest neoplasms
15.6 Class germ cell (includes teratomatous) neoplasms
15.7 Class trophectoderm (cells of extra-embryonic origin) neoplasms
15.8 Primitive tumors are somatic neoplasms that occur in different classes and that are unrelated to germ cell tumors
15.9 Organs with multiple anlagen
15.10 Rhabdoid tumor: the neoplasm that breaks all the rules
Chapter 15 summary
Chapter 16. Ectodermal and Endodermal Neoplasms
16.1 Background
16.2 Properties of class endoderm/ectoderm
16.3 Neoplasms that are too numerous to count
16.4 Tumors of class endoderm/ectoderm in childhood
16.5 Why are the major embryonic layers of ectoderm and endoderm combined in the developmental classification?
16.6 The differences between endoderm and ectoderm
16.7 Polyphyly and the strange origin of transitional cells
16.8 Squamous cell carcinomas
16.9 Adenocarcinoma
16.10 Endodermal and ectodermal tumors that do not seem to follow the rules
16.11 The genetic causes of endoderm/ectoderm tumors
16.12 Can a single gene alteration characterize a tumor of class endoderm/ectoderm?
Chapter 16 summary
Chapter 17. Mesodermal Neoplasms
17.1 Background
17.2 The mesenchyme
17.3 Coelomic tissues
17.4 The sub-coelomic mesodermal tissues
17.5 Generalizations about mesodermal tumors
17.6 Why do soft tissue tumors have simple genetic markers?
17.7 Why do tumors of mesodermal origin occur infrequently?
17.8 Leukemias and lymphomas
17.9 Helicobacter-induced pre-lymphoma
Chapter 17 summary
Chapter 18. Tumors of Neuroextoderm (Brain and Central Nervous System)
18.1 Background
18.2 The types of neuroectodermal tumors
18.3 Pnet tumors do not belong in class neuroectoderm
18.4 The so-called blastomas of neuroectodermal origin (glioblastoma, ependymoblastoma, medulloblastoma, retinoblastoma, and pineoblastoma)
18.5 Glioblastoma
18.6 Ependymoblastoma
18.7 Medulloblastoma
18.8 Retinoblastoma and pineoblastoma
18.9 Phakomatoses
Chapter 18 summary
Chapter 19. Neural Crest Tumors
19.1 Background
19.2 The neural crest in human development
19.3 Tumors of the peripheral nervous system
19.4 Melanocytic lesions
19.5 Odontogenic tumors
19.6 Ameloblastomas
19.7 Endocrine tumors of neural crest origin
19.8 Cladistics and the neural crest-derived mesenchymal tumors
19.9 Meningiomas
19.10 Triton tumors
Chapter 19 summary
Chapter 20. Tumors of Class Germ Cell and Class Trophectoderm
20.1 Background
20.2 Definitions
20.3 Diverse nature of germ cell tumors
20.4 Embryonic stem cell tumors
20.5 Germ cell tumors are not equivalent to stem cell tumors
20.6 What is the stem cell theory of cancer?
20.7 Tumors of class trophectoderm (gestational trophoblastic tumors)
20.8 Complete and partial hydatidiform moles
20.9 Why does paternal disomy lead to hydatidiform moles?
20.10 The totipotent fascination of the 129 mouse
Chapter 20 summary
Chapter 21. Specialized Cancer Nomenclatures and the Developmental Lineage Classification and Taxonomy of Neoplasms
21.1 Background
21.2 Nomenclatures, taxonomies, classifications
21.3 Inconsistent meanings within standardized medical nomenclatures
21.4 Incompleteness in standard nomenclatures
21.5 Striving for completeness
21.6 Informatics support within the developmental classification of neoplasms
21.7 Coding medical information
21.8 Re-coding data
Chapter 21 summary
Chapter 22. Cancer Ontologies
22.1 Background
22.2 Introduction to ontologies
22.3 Ontologies and complexity
22.4 The national cancer institute's thesaurus
Chapter 22 summary
Chapter 23. Class-Dependent Cancer Prevention, Diagnosis and Treatment
23.1 Background
23.2 The malignancy detector
23.3 Why are there so few tumors that we can now cure?
23.4 First priority: drugs that induce precancer regression
23.5 Second priority: cancer prevention
23.6 Third priority: treatments for tumors of primitive cells (almost all of which are tumors of childhood)
23.7 Fourth priority: vaccines against oncogenic viruses
23.8 Fifth priority: epigenomic drugs for germ cell tumors
23.9 Sixth priority: treatments for tumors of mesoderm, neuroectoderm and neural crest
23.10 Seventh priority: non-surgical treatment for benign neoplasms
23.11 Eighth priority: new diagnostic and predictive markers for cancers
23.12 Ninth priority: use experience obtained from items 3, 6, 7, and 8 to develop targeted drug treatments for endoderm/ectoderm tumors
Chapter 23 summary
Chapter 24. Finding Neoplasms: Suggestions for Cancer Researchers
24.1 Background
24.2 What do pathologists do?
24.3 Times are changing
24.4 Who owns the tissues and the reports that are archived within pathology departments?
24.5 What role will computers play in cancer treatment?
24.6 Pathologists and non-pathologists
Chapter 24 summary
Chapter 25. Principles
25.1 Background
25.2 Principles of neoplasms
Chapter 25 summary
List of Figures and Attribution of Sources
Author Biography

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