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E-Book

E-Book, Englisch, 384 Seiten

Chen / Lai Apoptosis in Carcinogenesis and Chemotherapy

Apoptosis in cancer
1. Auflage 2009
ISBN: 978-1-4020-9597-9
Verlag: Springer Netherlands
Format: PDF
Kopierschutz: 1 - PDF Watermark

Apoptosis in cancer

E-Book, Englisch, 384 Seiten

ISBN: 978-1-4020-9597-9
Verlag: Springer Netherlands
Format: PDF
Kopierschutz: 1 - PDF Watermark



Although research on carcinogenesis has focused more on cellular proliferation than on cell death, yet understanding the mechanism of apoptosis may have important implications for cancer therapy. This book brings together experts from around the world who will discuss the common cancers encountered in clinical practice in the laboratory setting. During the induction of these common cancers, the role of apoptosis in cellular and molecular changes is emphasized, critically highlighting possible anti-cancer strategies. For those who are interested in carcinogenesis and for those who are seeking new approaches to anti-cancer therapy, this book is an important reference. It serves not only as a reference of the current understanding of apoptosis in common cancers but also an important bridge between the laboratory and clinical practice. The editors and contributors are to be congratulated in bringing together an important pool of up-to-date knowledge to light and further our interest in this exciting and expanding ?eld. Arthur K. C. Li Emeritus Professor of Surgery The Chinese University of Hong Kong v Preface The role of apoptosis in cancer development and emerging treatment strategies has rapidly expanded over the past few years. The novel discovery in the apoptotic pa- ways and their relevant molecules provides us not only the knowledge how tumors develop but also the opportunity to design new therapeutic tools to prevent or inhibit the growth of tumors with minimal side-effects. Undoubtedly, understanding the events involved at a molecular level can permit the manipulation of apoptosis for therapeutic purposes.

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Weitere Infos & Material


1;Foreword;5
2;Preface;6
3;Contents;7
4;Contributors;9
5;Abbreviations;12
6;Apoptotic Signaling Pathway and Resistance to Apoptosis in Breast Cancer Stem Cells;20
6.1;Introduction;20
6.2;Apoptotic Signal Pathway;22
6.3;Mechanisms of Resistance to Apoptosis;24
6.4;Cancer Stem Cells;30
6.5;References;35
7;Anti-Cancer Strategy of Transitional Cell Carcinoma of Bladder Based on Induction of Different Types of Programmed Cell Deaths;43
7.1;Introduction;43
7.2;Different Types of Programmed Cell Deaths;45
7.3;Autophagy;46
7.4;Necrosis;47
7.5;The Relationship Between Apoptosis, Autophagy and Necrosis;48
7.6;Signaling Pathways to Death;48
7.7;Caspase-3;49
7.8;Bcl-2;49
7.9;Survivin;49
7.10;EGCG [(-) epigallocatechin-3-gallate];50
7.11;Curcumin;50
7.12;Silibinin;51
7.13;Vitamins;51
7.14;Epigenetic Modifiers;52
7.15;Arsenic Compound;53
7.16;Bacillus Calmette-Guerin (BCG);54
7.17;Beclin-1/ATG6;54
7.18;LC3/ATG8;55
7.19;mTOR;55
7.20;Calpains;56
7.21;Poly-ADP Ribose Polymerase (PARP);57
7.22;Therapeutic Strategies Based on Different Programmed Cell Deaths;57
7.23;Conclusions;60
7.24;References;60
8;Apoptosis in Carcinogenesis and Chemoherapy of the Uterine Cervix;69
8.1;Introduction;69
8.2;Cervical Cancer Carcinogenesis and Apoptosis;70
8.3;Cervical Cancer Therapy and Apoptosis;75
8.4;Concluding Remarks;85
8.5;References;85
9;Apoptosis in Colorectal Tumorigenesis and Chemotherapy;92
9.1;Introduction;92
9.2;Colorectal Tumorigenesis;96
9.3;Apoptosis in Colorectal Tumorigenesis;101
9.4;Factors Effecting Apoptosis in Colorectal Cancer;107
9.5;Apoptosis and Colorectal Cancer Chemotherapy;110
9.6;References;115
10;Apoptosis in Cutaneous Melanoma;127
10.1;Introduction;128
10.2;Mechanisms of Apoptosis in Melanoma;129
10.3;Bcl-2;130
10.4;p53;130
10.5;Apaf-1;131
10.6;Inhibitors of Apoptosis (IAP);134
10.7;Conclusion;136
10.8;References;137
11;Apoptosis in Carcinogenesis and Chemotherapy – Esophageal Cancer;142
11.1;Introduction;142
11.2;Apoptosis and Esophageal Squamous Cell Carcinoma;145
11.3;Apoptosis and Esophageal Adenocarcinoma;156
11.4;References;163
12;Molecular Targets in Gastric Cancer and Apoptosis;172
12.1;Introduction;172
12.2;Epidemiology;173
12.3;Pathological Classification;174
12.4;Conventional Treatment Options;175
12.5;Molecular Aspects of Gastric Cancer;178
12.6;Apoptotic Pathways in Gastric Cancer;188
12.7;Apoptosis-Targeting in Gastric Cancer;192
12.8;Cancer Stem Cells, MicroRNAs and Potential Cancer Therapeutics;195
12.9;Conclusions;196
12.10;References;197
13;Apoptosis and the Tumor Microenvironment in Hematologic Malignancies;208
13.1;Introduction;208
13.2;The Role of the Tumor Microenvironment in Hematologic Tumorigenesis and Tumor Cell Survival;210
13.3;The Role of the Tumor Microenvironment in Drug Resistance;215
13.4;Overcoming Drug Resistance in Hematologic Malignancies;222
13.5;Conclusions;226
13.6;References;226
14;Bcl-2 Family Members in Hepatocellular Carcinoma ( HCC) – Mechanisms and Therapeutic Potentials;234
14.1;Introduction;234
14.2;Physiological Role of Bcl-2 Family Members in Liver;235
14.3;Bcl-2 Family Members and Hepatocarcinogenesis;238
14.4;Bcl-2 Family Members in HCC Treatment;241
14.5;Conclusions;244
14.6;References;244
15;Apoptosis in the Development and Treatment of Laryngeal Cancer: Role of p53, Bcl- 2 and Clusterin;251
15.1;Introduction;251
15.2;Role of p53 and bcl-2 in Layngeal Intraepithelial Neoplasia;254
15.3;P53 and Laryngeal Cancer;255
15.4;Bcl-2 and Laryngeal Cancer;256
15.5;Clusterin and Laryngeal Cancer;258
15.6;Conclusions;259
15.7;References;259
16;Cyclooxygenase 2 and its Metabolites: Implications for Lung Cancer Therapy;264
16.1;Introduction;264
16.2;Apoptosis in Lung Cancer;266
16.3;COX-2 in Lung Cancer;269
16.4;Prostaglandins and its Enzymes/Inhibitors;272
16.5;Prostaglandins in Lung cancer;274
16.6;COX-2 Inhibitors and Chemotherapy;276
16.7;Conclusions;278
16.8;References;278
17;Roles of Negative and Positive Growth Regulators in Nasopharyngeal Carcinoma;286
17.1;Introduction;286
17.2;Negative Growth Regulators of NPC;287
17.3;Positive Growth Regulators of NPC;294
17.4;Conclusion;299
17.5;References;300
18;Cellular Signaling Mechanisms in Pancreatic Apoptosis;308
18.1;Introduction;308
18.2;Apoptosis;309
18.3;Position for Figure;310
18.4;Signaling Pathways in Pancreatic Apoptosis;310
18.5;Death Receptor Mediated Signaling Pathways;311
18.6;Apoptotic Factors in Pancreatic Cancer;312
18.7;Mitochondrial Signaling Pathways in Pancreatic Apoptosis;313
18.8;Biomarkers of Apoptosis;314
18.9;Apoptosis Mediated by Caspase Inhibitors;315
18.10;Apoptosis Mediated by the IAP Family;316
18.11;Apoptosis Mediated by G-Protein Coupled Mechanisms;317
18.12;Apoptosis Mediated by Inositol Polyphosphates;318
18.13;Changes in Cellular Levels of Inositol Polyphosphates During Apoptosis;319
18.14;Treatment Agents That Induce Apoptosis in Pancreatic Cells;320
18.15;Position for Table;323
18.16;Diagnostic Markers for Pancreatic Cancer;323
18.17;Therapeutic Approaches to Identify Diagnostic Biomarkers for Pancreatic Cancer;324
18.18;Diet and Risk Factors for Pancreatic Cancer;325
18.19;Role of Oxidative Stress in Pancreatic Cancer and Prevention;326
18.20;Nutritional Impact on Pancreatic Apoptosis;327
18.21;Conclusions;328
18.22;References;328
19;Strategies to Circumvent Resistance to Apoptosis in Prostate Cancer Cells by Targeted Necrosis;339
19.1;Introduction;340
19.2;Conclusion;356
19.3;References;357
20;Carcinogenesis and Therapeutic Strategies for Thyroid Cancer;359
20.1;Introduction;359
20.2;Activation of TSHR-Gsp Pathway Is Involved in Benign Thyroid Lesions;362
20.3;Receptor Tyrosine Kinase-Ras-Raf Pathway is Constitutively Activated in Approximately 70% of all Thyroid Cancers and is an Important Potential Therapeutic Target for Thyroid Cancer;363
20.4;PI3K-AKT Pathway is Overactive in Development and Progression of Thyroid Cancer and is also a Novel Therapeutic Target for Thyroid Cancer;365
20.5;Angiogenesis in Thyroid Cancer;367
20.6;Several Functional ProteinsWere Overexpressed in Thyroid Cancer;368
20.7;Molecules Involved in Cellular Differentiation and Adhesion Is Decreased in the Progression of Thyroid Cancer;369
20.8;Estrogen Is a Proliferative Factor for Thyroid Cancer;371
20.9;Mutation of p53 is Common and Is a Target of Gene Therapy in Thyroid Cancer;372
20.10;Alteration of Apoptotic Pathways in Thyroid Cancer;373
20.11;Selenium Deficiency Is a Risk Factor for Thyroid Cancer Development;376
20.12;NIS Expression and Therapeutic Potential in Thyroid Cancer;376
20.13;Conclusions;377
20.14;References;378
21;Index;387



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