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E-Book

E-Book, Englisch, Band 12, 314 Seiten

Reihe: Cancer Growth and Progression

Coppola Mechanisms of Oncogenesis

An update on Tumorigenesis
1. Auflage 2010
ISBN: 978-90-481-3725-1
Verlag: Springer Netherlands
Format: PDF
Kopierschutz: 1 - PDF Watermark

An update on Tumorigenesis

E-Book, Englisch, Band 12, 314 Seiten

Reihe: Cancer Growth and Progression

ISBN: 978-90-481-3725-1
Verlag: Springer Netherlands
Format: PDF
Kopierschutz: 1 - PDF Watermark





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1;Preface;5
2;Contents;7
3;Contributors;9
4;1 Cytokines and Stressors: Implications for Cancer Immunotherapy;13
4.1;1.1 Introduction;13
4.2;1.2 Stressor Effects on Neurochemical Processes;14
4.2.1;1.2.1 Hypothalamic-Pituitary-Adrenal Effects of Stressors;14
4.2.2;1.2.2 Central Neurochemical Effects of Stressors;15
4.3;1.3 Cytokine Contribution to the Stress Response and Mood States;16
4.3.1;1.3.1 Neurochemical Consequences of Cytokine Treatment;16
4.3.2;1.3.2 Behavioral Effects of Cytokines;17
4.3.3;1.3.3 Cytokines and Mood States;17
4.4;1.4 Immunological Consequences of Stressor Exposure;18
4.5;1.5 Stress and Cytokine Production;19
4.5.1;1.5.1 Stressors Influence Th1 and Th2 Derived Cytokines;19
4.5.1.1;1.5.1.1 Impact on Interferon-;19
4.5.1.2;1.5.1.2 Impact on Interleukin-4;19
4.5.1.3;1.5.1.3 Impact on Interleukin-10 and Interleukin-2;20
4.5.1.4;1.5.1.4 Impact on Interleukin-5;21
4.5.1.5;1.5.1.5 Impact on Interleukin-6;21
4.5.1.6;1.5.1.6 Impact on Interleukin-1 and Tumor Necrosis Factor-;22
4.6;1.6 Cytokines and Depression;23
4.7;1.7 Conclusion;24
4.8;References;24
5;2 The Role of Oncogene Activation in Tumor Progression;31
5.1;2.1 Introduction;31
5.2;2.2 The Epidermal Growth Factor Receptor Family;31
5.3;2.3 Mechanisms of EGFR Dysregulation;32
5.4;2.4 The EGFR Receptor Signal Pathway;32
5.5;2.5 EGFR-Targeted Therapy in Human Cancers;33
5.6;2.6 Role of the EGFR Family Member ErbB2/HER2 in Breast Cancer;33
5.7;2.7 The c-Met Receptor;34
5.8;2.8 The c-MET-HGF/SF Signal Pathway: Role in Malignant Progression;35
5.9;2.9 The Ras Oncogene;36
5.10;2.10 Mechanisms of Ras Dysregulation;36
5.11;2.11 Ras Mediated Signaling Cascade: Implications in Malignant Progression;37
5.12;2.12 Ras in Human Cancers and Targeted Ras Therapies;37
5.13;2.13 The Src Kinase Family;38
5.14;2.14 Src Dysregulation;38
5.15;2.15 The Src Signaling PathwayImplications in Malignant Progression;39
5.16;2.16 The c-Myc Oncogene;40
5.17;2.17 Mechanisms of c-Myc Dysregulation;40
5.18;2.18 The Role of c-myc in Oncogenesis and Malignant Transformation;40
5.19;2.19 Conclusion;41
5.20;References;41
6;3 Carcinogenic Effects of Ionising Radiation;54
6.1;3.1 Introduction;54
6.2;3.2 Historical Highlights;55
6.2.1;3.2.1 Early Radiologists;55
6.2.2;3.2.2 Radium Dial Painters;55
6.2.3;3.2.3 Underground Hard-Rock Miners;55
6.2.4;3.2.4 Medically Irradiated Patients;55
6.2.5;3.2.5 Marshall Islanders Exposed to Radioactive Fallout;56
6.2.6;3.2.6 Experimental Radiation Carcinogenesis ;56
6.3;3.3 Sources, and Levels of Ionising Radiation in the Environment;56
6.4;3.4 Carcinogenic Effects on Specific Tissues;58
6.4.1;3.4.1 Skin;58
6.4.2;3.4.2 Hematopoietic and Lymphoid Tissues;58
6.4.3;3.4.3 Thyroid Gland;59
6.4.4;3.4.4 Other Endocrine Glands;59
6.4.5;3.4.5 Breast;60
6.4.6;3.4.6 Respiratory Tract;60
6.4.7;3.4.7 Gastrointestinal Tract;61
6.4.8;3.4.8 Skeleton;62
6.4.9;3.4.9 Genital Organs;63
6.4.10;3.4.10 Kidney and Urinary Bladder;63
6.4.11;3.4.11 Central Nervous System;64
6.4.12;3.4.12 Cancers, All Sites Combined;64
6.5;3.5 Mechanisms and DoseIncidence Relationships;64
6.5.1;3.5.1 Effects of Radiation at the Cellular and Subcellular Levels;64
6.5.2;3.5.2 In Vitro Neoplastic Transformation;65
6.5.3;3.5.3 Carcinogenesis In Vivo;66
6.6;3.6 Modifying Effects of Other Physical and Chemical Agents;67
6.7;3.7 Assessment of the Carcinogenic Risks of Low-Level Irradiation;67
6.8;References;69
7;4 Chemical Carcinogenesis Role of Chloroform 0 Further Studies;73
7.1;4.1 Introduction;73
7.2;4.2 Short-Term Studies;73
7.3;4.3 Carcinogenicity Studies;74
7.4;4.4 Mechanistic and Interactive Effects;74
7.5;4.5 Risk;75
7.6;4.6 Conclusion;75
7.7;4.7 Addendum;75
7.8;References;76
8;5 Use of Organ Explant and Cell Culture in Cancer Research;80
8.1;5.1 Introduction to Tissue Culture and References;80
8.2;5.2 Standard Definitions and Uses of Tissue Culture;81
8.3;5.3 Gene-Expression Profiling;83
8.4;5.4 Laser Capture Microdissection;83
8.5;5.5 Molecular Imaging;84
8.5.1;5.5.1 In Vitro Mouse Models;85
8.5.2;5.5.2 Magnetic Resonance Imaging;85
8.5.3;5.5.3 Fluorescence Imaging;85
8.5.4;5.5.4 Intravital Microscopy;86
8.5.5;5.5.5 Other Imaging Methods;86
8.5.6;5.5.6 Met-HGF/SF: A System Studied Through Molecular Imaging;87
8.6;5.6 Quantitative Analysis;88
8.6.1;5.6.1 Advantages of Quantitative Analysis;88
8.6.2;5.6.2 Methods of Quantitative Analysis;89
8.7;5.7 Conclusion;91
8.8;References;92
9;6 Chromosomal Abnormalities in Selected Hematopoietic Malignancies Detected by Conventional and Molecular Cytogenetics: Diagnostic and Prognostic Significance;97
9.1;6.1 Introduction;97
9.2;6.2 Technological Advances in Cancer Cytogenetics;97
9.2.1;6.2.1 Harvesting of Cells for Cancer Cytogenetics;98
9.2.2;6.2.2 Conventional Cytogenetic Banding Techniques in Cancer Cytogenetics;98
9.2.3;6.2.3 Molecular Cytogenetic Techniques in Cancer Cytogenetics;98
9.3;6.3 Numerical and Structural Chromosomal Abnormalities;99
9.4;6.4 The Classification of Hematopoietic Malignancies;100
9.5;6.5 Cytogenetic Abnormalities in Selected Hematopoietic Malignancies;100
9.5.1;6.5.1 The Philadelphia Chromosome in Chronic Myelocytic Leukemia;100
9.5.2;6.5.2 Chromosomal Abnormalities in Chronic Lymphocytic Leukemia (CLL);103
9.5.3;6.5.3 T(8;14) in Burkitt Lymphoma/Leukemia;104
9.5.4;6.5.4 Recurrent Cytogenetic Abnormalities in Acute Myeloid Leukemia (AML);105
9.5.4.1;6.5.4.1 AML with t(8;21)(q22;q22);105
9.5.4.2;6.5.4.2 AML with t(15;17)(q22;q12) and Variants;105
9.5.4.3;6.5.4.3 AML with inv(16)(p13.1q22) or t(16;16)(p13.1;q22);106
9.5.4.4;6.5.4.4 AML with 11q23 (MLL) Abnormalities;106
9.5.5;6.5.5 Recurrent Cytogenetic Abnormalities in Acute Lymphoblastic Leukemia (ALL);107
9.5.6;6.5.6 Structural Changes in ALL;107
9.5.6.1;6.5.6.1 t(12;21)(p13.3;q22);107
9.5.6.2;6.5.6.2 CBFA2 (AML1/RUNX1) Amplification;108
9.5.6.3;6.5.6.3 11q23/MLL Gene Rearrangement and t(4;11) in ALL;108
9.5.6.4;6.5.6.4 T(1;19)(q23;p13.3);109
9.5.6.5;6.5.6.5 t(17;19)(q22;p13.3) and inv(19)(p13.3q13.4);110
9.5.7;6.5.7 Numerical Chromosomal Abnormalities in ALL;111
9.5.7.1;6.5.7.1 Near-Tetraploidy and Near-Triploidy in ALL;111
9.5.7.2;6.5.7.2 Hyperdiploidy (>50 Chromosomes);111
9.5.7.3;6.5.7.3 Hyperdiploidy (47--50 Chromosomes);111
9.5.7.4;6.5.7.4 Hypodiploidy and Near-Haploidy;111
9.5.8;6.5.8 Selected Recurrent Cytogenetic Abnormalities in Myelodysplastic Syndrome (MDS);112
9.5.8.1;6.5.8.1 Cytogenetic Features and Classification Criteria;112
9.5.8.2;6.5.8.2 Chromosome 5 Abnormality;113
9.5.8.3;6.5.8.3 Chromosome 7 Abnormality;113
9.5.8.4;6.5.8.4 Therapy-Related MDS (t-MDS);114
9.5.9;6.5.9 Myeloproliferative Diseases;114
9.5.9.1;6.5.9.1 MPDs Other than CML;114
9.6;6.6 Conclusion;115
9.7;References;116
10;7 Mechanisms of Cancer Growth and Progression in Lymphoma;122
10.1;7.1 Introduction;122
10.2;7.2 B Cell Development;122
10.2.1;7.2.1 Early B Cell Maturation: Production of B Cell Receptor (BCR);123
10.2.2;7.2.2 Late B Cell Maturation: Production of High Affinity Immunoglobulin;123
10.3;7.3 Cellular Origin of B Cell Lymphomas;124
10.3.1;7.3.1 Naïve (Circulating) B Cells;126
10.3.2;7.3.2 Germinal Center B Cells;126
10.3.3;7.3.3 Memory B Cells (Post-germinal Center Cells);127
10.3.4;7.3.4 Molecular Profiling Supports Differentiation Stages for Neoplastic B Cells;127
10.4;7.4 Transforming Events in Lymphomagenesis;128
10.4.1;7.4.1 Genomic DNA Modification: Point Mutations and Translocations;128
10.4.2;7.4.2 Transforming Viruses;130
10.5;7.5 Role of Antigen Receptor, Microenvironment and Antigenic Stimulation in B-Cell Lymphomas;131
10.5.1;7.5.1 Chronic Infection and Lymphoma;131
10.5.2;7.5.2 Lymphoma and Immunologic Disorders;131
10.6;7.6 Functional Consequences of Genetic Lesions in Lymphomagenesis;132
10.6.1;7.6.1 Blocking Apoptosis;132
10.6.2;7.6.2 Enhancing Cell Growth and Proliferation;132
10.6.3;7.6.3 Blocking Differentiation;132
10.7;7.7 Conclusion;133
10.8;References;133
11;8 Pediatric Cancer Mechanisms of Cancer Growth and Progression;136
11.1;8.1 Introduction;136
11.2;8.2 Teratomas;137
11.3;8.3 Malignant Tumors;137
11.4;8.4 Incidence;137
11.5;8.5 Etiology;137
11.6;8.6 Environmental Factors;137
11.7;8.7 Mechanisms in Carcinogenesis;138
11.8;8.8 Chromosme Translocations;138
11.9;8.9 Genomic Imprinting;139
11.10;8.10 Proto-oncogenes and Oncogenes;139
11.11;8.11 Anti-oncogenes;139
11.12;8.12 Controlling Gene Expression;140
11.13;8.13 DNA Methylation;141
11.14;8.14 Zinc-Fingers;142
11.15;8.15 Proteomics;142
11.16;8.16 Differentiation (Epigenetic Control of Gene Expression);142
11.17;8.17 Loss of Imprinting and Cancer;142
11.18;8.18 Cell Proliferation: Proto-oncogenes and Anti-oncogenes;143
11.19;8.19 Intercellular Signaling in Development: Sonic Hedgehog (SHH);143
11.20;8.20 Examples: Sequential Gene Expression in Growth and Neoplasia;144
11.20.1;8.20.1 Wilms Tumor;144
11.20.2;8.20.2 Beckwith-Wiedemann Syndrome;145
11.20.2.1;8.20.2.1 IGF2;145
11.20.2.2;8.20.2.2 H19;147
11.20.2.3;8.20.2.3 CDKN1C;147
11.20.2.4;8.20.2.4 KCNQ1;147
11.20.2.5;8.20.2.5 KCNQ1OT1;147
11.20.2.6;8.20.2.6 Other Imprinted Genes;147
11.21;8.21 Defects of Differentiation and CNS Tumor Syndromes;147
11.21.1;8.21.1 Neurofibromatosis Type 1 (NF1);147
11.21.2;8.21.2 Neurofibromatosis Type 2 (NF2);147
11.21.3;8.21.3 Tuberous Sclerosis (TS);148
11.21.4;8.21.4 Von Hippel-Lindau Disease (VHL);148
11.21.5;8.21.5 Turcot Syndrome;148
11.21.6;8.21.6 Gorlin Syndrome (Nevoid Basal Cell Carcinoma Syndrome -- NBCC);148
11.21.7;8.21.7 Cowden Syndrome;148
11.21.8;8.21.8 Li-Fraumeni Syndrome (LFS);148
11.22;8.22 Similarities Between the Embryo and Cancer;149
11.23;References;150
12;9 Carcinogenetic Pathway of Malignant Melanoma;155
12.1;9.1 Introduction;155
12.2;9.2 The Role of Photocarcinogenesis in Melanoma;156
12.3;9.3 Tumorigenesis of Melanoma;157
12.3.1;9.3.1 p16 (INK4A);157
12.3.2;9.3.2 p53 (TP53);158
12.3.3;9.3.3 c-KIT;158
12.3.4;9.3.4 EGFR;159
12.3.5;9.3.5 Cyclin D1;159
12.3.6;9.3.6 Telomerase;160
12.3.7;9.3.7 RAS;160
12.4;9.4 Conclusion;161
12.5;References;161
13;10 Ewing Sarcoma: Molecular Characterization and Potential Molecular Therapeutic Targets;164
13.1;10.1 Introduction;164
13.2;10.2 Etiology and Pathogenesis;164
13.3;10.3 Tissue Diagnosis;165
13.4;10.4 Prognostic Factors;166
13.5;10.5 Treatment and Clinical Outcomes;166
13.6;10.6 Approaches to Identify Molecular Targets;167
13.7;10.7 Other Therapeutic Alternatives;168
13.7.1;10.7.1 Dendritic Cell Immunotherapy;168
13.7.2;10.7.2 siRNA Targets Against the EWS-FLI1 Oncogene;168
13.8;10.8 Future Directions;169
13.9;References;169
14;11 Molecular Mechanisms of Central Nervous System Metastasis;172
14.1;11.1 Introduction;172
14.2;11.2 The Metastatic Process;172
14.3;11.3 Molecular Mechanisms;173
14.4;11.4 Hedgehog Signaling Pathway;173
14.5;11.5 Transforming Growth Factor-;174
14.6;11.6 Angiopoietin Pathway;174
14.7;11.7 Matrix Interactions;175
14.8;11.8 VEGF Pathway;175
14.9;11.9 Other Molecular Pathways;176
14.10;11.10 Endogenous Inhibitors;177
14.11;11.11 Conclusions;177
14.12;References;177
15;12 Carcinogenesis of Human Papillomavirus in Head and Neck Squamous Cell Carcinoma;183
15.1;12.1 Introduction;183
15.2;12.2 Squamous Cell Carcinoma;183
15.3;12.3 Squamous Epithelium;183
15.4;12.4 Carcinogeneis of Head and Neck Squamous Cell Carcinoma;184
15.4.1;12.4.1 Human Papillomavirus (HPV);184
15.4.2;12.4.2 Role of HPV in Head and Neck Squamous Cell Carcinoma Carcinogenesis;184
15.4.2.1;12.4.2.1 Epidemiology Analysis;185
15.4.2.2;12.4.2.2 Laboratory Analysis;185
15.4.2.3;12.4.2.3 Clinical Analysis;185
15.5;12.5 HPV Testing Methods;187
15.6;12.6 Conclusion;188
15.7;References;188
16;13 Postmenopausal Hormone Replacement Therapy and Breast Cancer 0 Clinicopathologic Associations and Molecular Mechanisms;191
16.1;13.1 Introduction;191
16.2;13.2 Endogenous Sex Steroid Hormones and Breast Carcinogenesis;191
16.3;13.3 Long Term Use of Postmenopausal Combined Hormone Replacement Therapy (HRT) Is Associated with an Increased Risk of Breast Cancer;192
16.4;13.4 Association of HRT Use with Histologic Features and Prognosis of Breast Cancers;194
16.5;13.5 Initiation of New Breast Cancers Versus Promotion of Pre-existing Tumors;196
16.6;13.6 The Effect of HRT on the Proliferation of Breast Cancers;197
16.7;13.7 Effect of HRT on Hormone Receptor and Gene Expression Profile in Breast Cancers;199
16.8;13.8 Chemo-/Hormonal Prevention;200
16.9;References;200
17;14 Carcinogenesis of Lung Cancer;207
17.1;14.1 Incidence and Epidemiology;207
17.2;14.2 Cancer Risk in Smoking;207
17.3;14.3 Etiology and Pathogenesis;208
17.4;14.4 Histology of Lung Adenocarcinoma, Pneumocyte Hyperplasia and Emphysema;209
17.5;14.5 Cytology of Lung Adenocarcinoma;211
17.6;14.6 Molecular Pathways;211
17.6.1;14.6.1 Chromosomal Changes;212
17.6.2;14.6.2 Tumor Suppressor Oncogenes;212
17.6.3;14.6.3 Proliferation Markers;214
17.7;14.7 Conclusion;215
17.8;References;215
18;15 Genesis of Barrett0s Neoplasia: Current Concepts;217
18.1;15.1 Introduction;217
18.2;15.2 Etiology and Pathogenesis;217
18.3;15.3 Cancer Risk in Barretts Esophagus;217
18.4;15.4 Pathology of Barretts Esophagus and of Barretts Esophagus Associated Neoplasia;218
18.5;15.5 Differential Diagnosis of Barretts Esophagus;220
18.6;15.6 Cytology and Barretts-Associated Neoplasia;221
18.7;15.7 Molecular Pathways of Neoplastic Progression;221
18.8;15.8 Cell Cycle and DNA Ploidy;221
18.9;15.9 Proliferation Markers and Adhesion Molecules;221
18.10;15.10 Tumor Suppressor Genes;222
18.11;15.11 Death-Inducing Signaling Molecules;222
18.12;15.12 Angiogenic Markers;223
18.13;15.13 Other Molecular Markers;223
18.14;15.14 Omics of Barretts Neoplasia;224
18.15;15.15 Conclusion;225
18.16;References;225
19;16 Genesis of Pancreatic Ductal Neoplasia;229
19.1;16.1 Introduction;229
19.2;16.2 Epidemiology and Etiology;230
19.3;16.3 Hereditary Pancreatic Carcinoma;230
19.4;16.4 Pancreatic Ductal Adenocarcinoma Precursor Lesions;230
19.5;16.5 Genetic and Molecular Alterations in Pancreatic Carcinoma;232
19.5.1;16.5.1 Telomeres;232
19.5.2;16.5.2 Tumor Suppressor Genes;232
19.5.3;16.5.3 Oncogenes;232
19.5.4;16.5.4 BRCA 2 and Fanconi Anemia Pathway Genes: Caretaker Genes;233
19.5.5;16.5.5 Gene Overexpression;233
19.6;16.6 Epigenetic Changes;233
19.7;16.7 Alterations in Core Signaling Pathways;233
19.7.1;16.7.1 Developmental Signaling Pathways;234
19.8;16.8 Altered Protein Expression;234
19.8.1;16.8.1 Cyclooxygenase 2 (COX-2);234
19.8.2;16.8.2 Matrix Metalloproteinase 7 (MMP-7, Matrilysin);234
19.8.3;16.8.3 Mucins;235
19.8.4;16.8.4 Cell Cycle Regulation Proteins;235
19.9;16.9 Gene Expression Profiling;235
19.10;16.10 miRNA Analysis;235
19.11;16.11 Progression Pathway in PanINs;235
19.12;16.12 Mouse Models of Pancreatic Cancer;236
19.13;16.13 Pancreatic Cancer Cell of Origin;237
19.14;16.14 Conclusion;237
19.15;References;237
20;17 Recent Advances in the Pathogenesis of Pancreatic Endocrine Neoplasms;241
20.1;17.1 Introduction;241
20.2;17.2 Categorization and Classification;242
20.3;17.3 Composition and Development of the Normal Pancreas;243
20.4;17.4 Formation and Regulation of Endocrine Cell Mass;243
20.4.1;17.4.1 Beta-Cell Neogenesis;243
20.4.2;17.4.2 Beta-Cell Replication;245
20.4.3;17.4.3 Beta-Cell Hypertrophy;245
20.4.4;17.4.4 Apoptosis in Beta Cells;245
20.5;17.5 Regulators of Pancreatic Endocrine Cell Mass;246
20.6;17.6 Pathways of Pathogenesis in Multiple Endocrine Neoplasia Syndromes;248
20.7;17.7 Multiple Endocrine Neoplasia Type 1;248
20.7.1;17.7.1 MEN1 Gene;249
20.7.2;17.7.2 MEN-1 Tumorigenesis: A Two-Step Inactivation;249
20.7.3;17.7.3 First Step;249
20.7.4;17.7.4 Second Step;250
20.7.5;17.7.5 Loss of Heterozygosity at 11q13;250
20.7.6;17.7.6 Events Following Inactivation of MEN1 Gene;250
20.8;17.8 Von Hippel-Lindau Syndrome;251
20.9;17.9 Neurofibromatosis Type 1;251
20.10;17.10 Tuberous Sclerosis;251
20.11;17.11 Findings of Molecular Genetic Analyses;252
20.11.1;17.11.1 Comparative Genomic Hybridization;254
20.11.2;17.11.2 Specific Chromosomal Aberrations;254
20.11.3;17.11.3 Cell Cycle Regulators;258
20.11.4;17.11.4 Gene Expression Profiling;260
20.12;17.12 Additional Evidence in Support of Pancreatic Endocrine Tumorigenesis;260
20.13;17.13 Summary;262
20.14;References;263
21;18 Mechanisms of Carcinogenesis in Colorectal Cancer;273
21.1;18.1 Introduction;273
21.2;18.2 Chromosomal Instability and Microsatellite Instability Pathways;274
21.3;18.3 APC and -Catenin;274
21.4;18.4 K-ras and p53;274
21.5;18.5 DCC;275
21.6;18.6 DNA Mismatch Repair (MMR) Genes;275
21.7;18.7 TGF Pathway;276
21.8;18.8 MicroRNAs;277
21.9;18.9 Conclusion Remarks;277
21.10;References;278
22;19 Carcinogenetic Pathway of Superficial Low-Grade Urothelial Carcinoma;282
22.1;19.1 Introduction;282
22.2;19.2 Chromosomal Aberrations;283
22.3;19.3 Activation of Tyrosine Kinase Receptor and Pathway;283
22.3.1;19.3.1 Fibroblastic Growth Factor Receptor 3 (FGFR3);284
22.3.2;19.3.2 Phosphatidylinositol 3 Kinase p110 (PI3KCA);284
22.3.3;19.3.3 Ras;284
22.3.4;19.3.4 Other Tyrosine Kinase Receptors;285
22.4;19.4 Conclusion;285
22.5;References;285
23;20 Carcinogenetic Pathway of Urothelial Carcinoma;288
23.1;20.1 Introduction;288
23.2;20.2 p53 Cell Cycle Regulation Pathway;289
23.3;20.3 Ras-MAPK Signal Transduction Pathway;291
23.4;20.4 Retinoblastoma Pathway;291
23.5;20.5 Combined Effects of p53, p21 and Rb;293
23.6;20.6 Angiogenesis;293
23.7;20.7 DNA Methylation;294
23.8;20.8 Conclusion;294
23.9;References;294
24;21 Mechanisms of Carcinogenesis in Prostate Cancer;297
24.1;21.1 Introduction;297
24.1.1;21.1.1 Prostate Cancer Subtypes;297
24.1.1.1;21.1.1.1 Hereditary (Genetic Material Damage): Familial, Racial;297
24.1.1.2;21.1.1.2 Sporadic (Genetic Material Damage): Diet, Age, Occupation;298
24.2;21.2 Genetics;298
24.2.1;21.2.1 RNASEL;298
24.2.2;21.2.2 MSR1;298
24.3;21.3 Inflammation and Prostate Cancer;299
24.3.1;21.3.1 Proliferative Inflammatory Atrophy (PIA);299
24.3.2;21.3.2 GSTP1 (p Class Gluthatione S-Transferase Gene);299
24.3.3;21.3.3 NKX3.1;300
24.3.4;21.3.4 Additional Genes;300
24.3.4.1;21.3.4.1 OOG1;300
24.3.4.2;21.3.4.2 CHECK2;300
24.3.4.3;21.3.4.3 BRCA2;300
24.4;21.4 Cyclooxygenase 2(COX-2) Pathway and Pc Relation;300
24.5;21.5 Hormonal Related Theories of Prostate Carcinogenesis;301
24.5.1;21.5.1 Androgen Receptor Gene (AR);301
24.5.2;21.5.2 Cytochrome P-450c17 (CYP17) Gene;301
24.5.3;21.5.3 5-Alpha-Reductase Type II (SRD5A2) Gene;302
24.5.4;21.5.4 Estrogens and Prostate Cancer;302
24.6;21.6 Conclusion;303
24.7;References;303
25;22 HPV in Cervical Carcinoma;307
25.1;22.1 Introduction;307
25.2;22.2 Human Papillomavirus (HPV);307
25.3;22.3 Detection of HPV and Cervical Lesions;308
25.3.1;22.3.1 Papanicolaou (PAP) Smear;308
25.3.2;22.3.2 Immunohistochemistry;308
25.3.3;22.3.3 In Situ Hybridization (ISH) Assays;309
25.4;22.4 Dysplasia and the Progression to Carcinoma;310
25.5;22.5 Prevention and Therapy;311
25.6;References;311
25.7;Index;313



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