The Pineal Gland and Cancer
Neuroimmunoendocrine Mechanisms in Malignancy
(Sprache: Englisch)
Three years ago, most authors contributing to this book gathered at the Heinrich Fabri Institute of the University of Tübingen at Blaubeuren near Ulm in Germany for the third conference on "Pineal Gland and Cancer". In 1987, the late Derek Gupta organized...
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Klappentext zu „The Pineal Gland and Cancer “
Three years ago, most authors contributing to this book gathered at the Heinrich Fabri Institute of the University of Tübingen at Blaubeuren near Ulm in Germany for the third conference on "Pineal Gland and Cancer". In 1987, the late Derek Gupta organized the second meeting and published the first book on the topic, 10 years after Vera Lapin, as part of the 25th anniversary celebrations of the Vienna Cancer Research Institute, had held the first meeting. It was in Vienna during the 1930s and 1940s that W. Bergmann and P. Engel demonstrated that pineal extracts possess growth inhibitory properties on experimental rodent tumors and R. Hofstätter reported favorable results when these extracts were given to cancer patients. In the 1970s, Vera Lapin and others reported that surgical removal of the pineal gland (pinealectomy) stimulates experimental tumor growth rendering fundamental support for an involvement of the pineal gland in malignancy. A focal question of past and present research in this field is whether the pineal gland exerts its tumor inhibitory activity primarily or exclusively via melatonin. Currently, it appears that the action of melatonin on experimental tumor growth criti cally depends on the circadian timing of its administration as weH as on the type and stage of cancer, and that primarily highly differentiated tumor ceHs are controHed. Initial clinical applications of the pineal hormone for incurable cancers raise hopes for a promising future use, particularly when combined with other therapies (e. g.
Inhaltsverzeichnis zu „The Pineal Gland and Cancer “
Section I: Significance of the Pineal Gland and Its Hormone Melatonin1 Some Historical Remarks Concerning Research on the Pineal Gland and Cancer
- References
2 Biology of the Pineal Gland and Melatonin in Humans
2.1 Introduction
2.2 The Pineal Gland in Animal Species
2.2.1 Structural Aspects, Innervation, and Pinealocyte Receptors
2.2.2 Melatonin (MEL) Synthesis and the Regulation of Its Day/Night Rhythm
2.2.3 The Influence of Light and Darkness on MEL Formation
2.2.4 The Function of MEL in Non-Human Mammals
2.2.5 Influence of Magnetic and Electromagnetic Fields on the Pineal Gland
2.3 The Human Pineal Gland and MEL
2.3.1 General Aspects
2.3.2 Release and Fate of MEL
2.3.3 Interindividual Variation of MEL Secretion
2.3.4 Day/Night Rhythm of MEL Formation in Humans
2.3.5 Influence of Light and Dark on MEL Secretion
2.3.6 Seasonal Differences in MEL Secretion
2.3.7 MEL Secretion in Old Age and Pineal Calcification
2.3.8 Various Factors Influencing MEL Secretion
2.3.9 MEL and Seasonal Affective Disorder
2.3.10 Electromagnetic and Magnetic Fields
2.3.11 Function of MEL in Humans
2.4 Conclusions
- References
3 The Role of Melatonin in the Neuroendocrine System: Multiplicity of Sites and Mechanisms of Action
3.1 Melatonin Is a Universal Time-Related Signal
3.2 Sites of Melatonin Action Are Multiple
3.3 Melatonin Promotes GABAergic Responses in SCN and the Brain
3.4 Melatonin Acts on Cells Through cAMP- and Non-cAMP-Signal Transduction Pathways
3.5 Melatonin Interacts with Cytoskeletal Proteins
3.6 Melatonin Exerts Antioxidant Effects
3.7 Melatonin Restores Amplitude of Circadian Rhythm in Chronic Inflammation or Aging
3.8 Concluding Remarks
- References
4 The Pineal Gland and Chronobiologic History: Mind and Spirit as Feedsidewards in Time Structures for Prehabilitation
4.1 Introduction
4.2 Render Measurable What as Yet Is Not: Emotion, Mind, and Spirit
4.3 Let Us Learn That We Do Not Know Even What We Should Know
4.4 Tarquini and
... mehr
Pineal Gland History
4.5 Anatomical-Clinical Associations
4.6 The Homeostatic Melatonin Era
4.7 Sampling and Assessing Chronomes
4.8 Subtle Human Melatonin Rhythms
4.9 Pineal Gland and Adrenal Cortex, Feedsidewards
4.10 Circaseptans
4.11 The Need for Dense Sampling Before the Ruling Out of Rhythms and Presence of Melatonin
4.12 A Controversy Resolved
4.13 Summary
- References
5 Melatonin Involvement in Cancer: Methodological Considerations
5.1 Introduction
5.2 Chronoradiotherapy
5.3 Historical Perspective
5.4 Chronochemotherapy
5.5 Need for Marker Rhythmometry
5.6 Chronorisk
5.7 Rhythm Scrambling
5.8 Lessons from Studies on Pituitary Grafts With and Without a Hypothalamus
5.9 Methodological Considerations
5.9.1 Specificity
5.9.2 Risk Versus Disease
5.9.3 Melatonin as an Oncostatic Drug: Importance of Timing
5.9.4 Coordination Via Feedsidewards: Importance of Circaseptans
5.9.5 Environmental Effects from Near and Far
5.10 Concluding Remarks
- References
Section II: Effect of Tumor Growth on the Production and Secretion of Pineal Melatonin
6 Analysis of Melatonin in Patients with Cancer of the Reproductive System
6.1 Introduction
6.2 Methodological Considerations and Problems Encountered in Estimating the Function of the Pineal Gland in Cancer Patients
6.2.1 Analytical Methods
6.2.2 Parameters Interfering with the Estimation of Pineal Function in Patients
6.3 Studies on Patients with Breast Cancer
6.4 Studies on Patients with Gynecological Cancers
6.4.1 Endometrial Cancer
6.4.2 Ovarian Cancer
6.5 Studies on Patients with Prostate Cancer
- References
7 Melatonin in Patients with Cancer of Extra-Reproductive Location
7.1 Introduction
7.2 Patients and Methods
7.3 Results
7.3.1 Nocturnal Urinary aMT6s Excretion in Cancer Patients
7.3.2 Correlations of Nocturnal Urinary aMT6s Excretion with Immunocytochemical Parameters Measured in Gastrointestinal and Lung Cancer
7.3.3 Correlations Among Intratumoral Parameters in Gastrointestinal Cancers
7.4 Discussion
7.4.1 Melatonin Secretion in Human Cancer Patients
7.4.2 Correlation Between MT Production and Proliferative Activity in Tumor Cells
7.4.3 Correlation Among Tumoral Parameters
7.5 Conclusion
- References
8 The Modulation of Melatonin in Tumor-Bearing Animals: Underlying Mechanisms and Possible Significance for Prognosis
8.1 Introduction
8.2 Studies with Chemically-Induced Mammary Cancers
8.2.1 Acute Effects of DMBA-Administration on Circulating Melatonin: Evidence for an Induction of the Hepatic Degradation of the Hormone
8.2.2 The Effects of DMBA-Induced Mammary Tumor Growth on Circulating Melatonin and the Pineal Melatonin Biosynthetic Pathway
8.3 Studies with Serial Transplants Derived from DMBA-Induced Mammary Cancers
8.3.1 Early Passage: Localized Carcinosarcoma
8.3.2 Late Passages: Metastasizing Sarcoma
8.4 Studies with Chemically Induced Colon Cancers
8.5 Conclusions and Considerations
- References
9 The Pineal Gland, Melatonin, and Neoplastic Growth: Morphological Approach
9.1 Introduction
9.2 Morphological Studies of Tumors Following Melatonin Treatment and Pinealectomy
9.3 Pineal Morphology in Tumor-Bearing Animals
9.4 Pineal Morphology in Human Malignancy
- References
Section III: Effects of Melatonin and of Unidentified Pineal Products on Tumor Growth
10 In Vitro Effects of Melatonin on Tumor Cells
10.1 Introduction
10.2 Effects of Melatonin on Breast Cancer Cells
10.2.1 Effects of Melatonin on Proliferation of Breast Cancer Cells In Vitro
10.2.2 Effects of Melatonin on the Metastatic Behavior of Breast Cancer Cells
10.2.3 Influence of Melatonin on Active Cell Death of Mammary Cancer Cells
10.2.4 Mechanisms of the Oncostatic Action of Melatonin In Vitro
10.3 Effect of Melatonin on Melanoma Cells
10.4 Effect of Melatonin on Cancer Cells from Female Reproductive Organs
10.5 Effect of Melatonin on Other Neoplasms
10.6 Conclusions
- References
11 Melatonin and Colon Carcinogenesis
11.1 Introduction
11.2 Effect of Melatonin on Colon Carcinoma Development
11.2.1 Inhibitory Effect of Melatonin on 1,2-Dimethylhydrazine-Induced Colon Carcinogenesis in Rats
11.2.2 Effect of Melatonin on Colon Tumor Growth In Vitro and In Vivo
11.3 Early Stages of 1,2-Dimethylhydrazine-Induced Colon Carcinogenesis As Targets for the Effect of Melatonin
11.3.1 Effect of Melatonin on the Genotoxic Action of 1,2-Dimethylhydrazine
11.3.2 Effect of a Single 1,2-Dimethylhydrazine Administration on Free Radical Processes in Rats
11.3.3 Effect of Melatonin on Free Radical Processes in Rats
11.3.4 Carbohydrate and Lipid Metabolism in Rats Exposed to a Single Dose of 1,2-Dimethylhydrazine
11.3.5 Effect of 1,2-Dimethylhydrazine on the Neuroendocrine System of Rats
11.4 Effect of Melatonin on Late Stages of 1,2-Dimethylhydrazine-Induced Colon Carcinogenesis
11.4.1 Free Radical Processes in Rats with Colon Tumors Induced by 1,2-Dimethylhydrazine: Effect of Melatonin
11.4.2 Effect of Melatonin on Proliferative Activity and Apoptosis in Colon Mucosa and Colon Tumors Induced by 1,2-Dimethylhydrazine in Rats
11.4.3 Pineal Function in Rats with Colon Tumors Induced by 1,2-Dimethylhydrazine
11.4.4 Melatonin-Containing Cells in the Intestinal Mucosa of Rats with 1,2-Dimethylhydrazine-Induced Colon Tumors: Effect of Exogenous Melatonin
11.4.5 Disturbances in Carbohydrate and Lipid Metabolism During Carcinogenesis Induced by 1,2-Dimethylhydrazine in Rats
11.4.6 Effect of Melatonin on Carbohydrate and Lipid Metabolism in Rats with Colon Tumors Induced by 1,2-Dimethylhydrazine
11.4.7 Possible Effect of Melatonin on the Immune System in Rats Exposed to 1,2-Dimethylhydrazine
11.5 Conclusion
- References
12 Role of Extrapineal Melatonin and Related APUD Series Peptides in Malignancy
12.1 Introduction
12.2 Extrapineal Melatonin: Cellular Localization, Role, and Significance Within the Diffuse Neuroendocrine System
12.3 Extrapineal MT and APUD Series Peptides: Possible Participation in Endogenous Mechanisms of Tumor Growth
12.4 Extrapineal Melatonin and Tumor Radiosensitivity: New Approaches for Modification of Antitumor Therapy
12.5 General Conclusion and Future Perspectives
- References
13 A Survey of the Evidence That Melatonin and Unidentified Pineal Substances Affect Neoplastic Growth
13.1 Introduction
13.2 The Role of the Pineal Hormone Melatonin
13.2.1 The Effects of Melatonin in Relation to Malignant Growth
13.2.2 The Effects of Melatonin in Relation to the Immune System and Stress
13.3 Effects of Yet Unknown Pineal Substances on Malignant Cells in Culture
13.3.1 Extracts of Ovine Pineal Glands
13.3.2 Extracts of Rat Pineals
13.3.3 Studies on an Unidentified Bovine Pineal Substance Which Inhibits MCF-7 Cell Growth in Vitro
13.4 Possible Presence of Kynurenines and Kynurenamines in Pineal Extracts
13.5 The Possible Significance of a Bovine Pineal Gland-Derived Decapeptide for the Growth of Malignant Cells in Vivo
13.6 Summary
- References
14 Experimental Studies of the Pineal Gland Preparation Epithalamin
14.1 Introduction
14.2 Epithalamin - a Low Molecular Weight Peptide Preparation
14.3 Effect of Epithalamin on the Life Span of Mice, Rats, and Drosophila melanogaster
14.4 The Influence of Epithalamin on the Function of the Nervous, Endocrine, and Immune Systems of Young and Old Rats
14.5 The Effect of Epithalamin on Spontaneous Tumor Development in Rats and Mice
- References
Section IV: Mechanisms of Action of Melatonin on Tumor Cells
A. Actions Via the Endocrine System
15 An Overview of the Neuroendocrine Regulation of Experimental Tumor Growth by Melatonin and Its Analogues and the Therapeutic Use of Melatonin in Oncology
15.1 Introduction
15.2 Effects of Melatonin and Its Analogues on Experimental Cancer Growth
15.2.1 Melatonin and Breast Cancer
15.2.2 Melatonin and Melanoma
15.2.3 Melatonin and Sarcoma
15.2.4 Melatonin and Other Tumors
15.3 Melatonin Binding in Neoplastic Tissues
15.3.1 Mouse Melanoma
15.3.2 Hamster Melanoma
15.3.3 Human Melanoma
15.3.4 Murine Mammary Cancer
15.3.5 Human Breast Cancer
15.3.6 Human Benign Prostatic Hyperplasia
15.3.7 Other Immortalized Cell Lines
15.4 Potential Melatonin Signal Transduction Mechanisms in Neoplastic Cells
15.4.1 Cyclic AMP and G Proteins
15.4.2 Phosphoinositide Metabolism
15.4.3 Nonmelatonin Receptor Expression
15.4.4 Transcriptional Regulation
15.4.5 Genomic Interactions
15.4.6 Calcium/Calmodulin (Ca2+/CaM) and the Cytoskeleton
15.4.7 Redox Mechanisms: Glutathione and Nitric Oxide
15.4.8 Tumor Linoleic Acid Uptake and Metabolism
15.5 Melatonin in the Chemoendocrine Therapy of Human Malignancies
15.6 Conclusions
- References
16 Modulation of the Estrogen Response Pathway in Human Breast Cancer Cells by Melatonin
16.1 Introduction
16.2 Melatonin and Breast Cancer
16.3 Melatonin Receptors
16.3.1 Membrane-Associated, G Protein-Linked Melatonin Receptors
16.3.2 Nuclear Melatonin Receptors
16.4 Melatonin and the Estrogen Response Pathway
16.4.1 Melatonin Modulation of ER Expression
16.4.2 Melatonin Modulation of Estrogen-Regulated Genes
16.4.3 Melatonin Modulation of ER Transactivation
16.5 Conclusions
- References
17 Benign and Tumor Prostate Cells as Melatonin Target Sites
17.1 Effects of Melatonin on the Prostate Gland In Vivo
17.2 Melatonin Action in Prostate Epithelial Cells In Vitro
17.2.1 Benign Prostate Hypertrophy Cells
17.2.2 Prostate Cancer Cells
17.3 Melatonin Action in Prostate Epithelial Cells: Towards a Unifying Hypothesis
- References
B. Actions Via the Immune System
18 Neuroimmunomodulation Via the Autonomic Nervous System
18.1 Introduction
18.2 Adrenergic In Vivo Effects on Immune Functions
18.3 Cholinergic Immunomodulation
18.4 Conclusions
- References
19 Melatonin and Immune Functions
19.1 Evidence of an Immunoregulatory Role of Melatonin (MEL)
19.2 Protective Effects of MEL on ?2-Adrenergic Immunosuppression in Rats
19.3 CD4+ Lymphocytes and Monocytes/Macrophages as Targets of MEL Activity
19.4 Possible Mechanisms of Action of MEL on Immune Cells
19.4.1 MEL Membrane Receptors on Immune Cells
19.4.2 MEL as a Ligand for the Nuclear Receptors RZR-? and RZR-?
19.4.3 MEL as a Calmodulin Antagonist
19.4.4 MEL as Antioxidant
19.5 Conclusion
- References
20 Melatonin and the Immune System: Therapeutic Potential in Cancer, Viral Diseases, and Immunodeficiency States
20.1 Neuroimmune Interactions with the Environment
20.2 Melatonin and the Immune-Hematopoietic System
20.2.1 Functional Effects
20.2.2 Cytokines Which Mediate the Effect of Melatonin
20.2.3 Melatonin Receptors
20.2.4 Clinical Trials
20.2.5 Mechanism of Action
20.3 Conclusion
- References
21 Melatonin Rhythms in Mice: Role in Autoimmune and Lymphoproliferative Diseases
21.1 Introduction
21.2 Melatonin Endogenous Rhythm in Mice
21.3 The Role of Pineal Gland and Melatonin in Autoimmune and Lymphoproliferative Diseases
21.3.1 Autoimmune Diabetes
21.3.2 Collagen-Induced Arthritis
21.3.3 Induced T Cell Leukemia
21.4 Conclusions
- References
22 Mechanisms Involved in the Immunomodulatory Effects of Melatonin on the Human Immune System
22.1 Introduction
22.2 Effects of Melatonin on the Immune System
22.3 Mechanisms of Action of Melatonin: The Membrane Receptor
22.4 Nuclear Receptors for Melatonin in the Immune System
22.5 The Physiological Role of Membrane Receptors Versus Nuclear Receptors
- References
- C Actions Via Neural Pathways
23 The Role of the Pineal Gland in Neural Control of Cell Proliferation in Healthy and Malignant Tissue
23.1 Introduction
23.2 The Role of the Autonomic Nervous System in the Control of Normal and Neoplastic Crypt Cell Proliferation in the Gut
23.3 Efferent Neural Connections Between the Pineal Gland and the Autonomic Nervous System
23.4 The Enteric Nervous System and Its Possible Role in Neural Control of Crypt Cell Proliferation in the Normal Gut. Is It Suitably Located?
23.5 Neural Control of Normal Cell Proliferation in Organs Other Than the Gastrointestinal System
23.6 The Precise Role of the Pineal Gland in the Normal Mechanism of Control of Proliferation in the Gastrointestinal Tract
23.7 The Role of the Pineal Gland in Induction or Promotion of Malignancy: How Important is It?
23.8 Further Consideration of the Role of Melatonin in the Control of Normal Crypt Cell Proliferation in the Gut
23.9 The Possible Role of the Pineal as a Modulator of Neuroendocrine Activity in Controlling Tumor Growth (Rather Than a Direct Effect Via the Autonomic Nervous System or Changes in the Level of Melatonin Secretion)
23.10 The Relationship Between Pinealectomy and Melatonin Levels in the Body
23.11 Are Any Other Possible Antitumor Factors Produced by the Pineal Gland Besides Melatonin, and Could These Be Involved in the Physiological Control of Malignancy?
23.12 Relationship of Pinealectomy and Its Effects on the Intestinal Crypts with Similar Effects on the Crypts Associated with Limbic Lesions
23.13 Is it Possible That the Pineal Gland Acts Directly on the Crypts Via the Limbic System and the Autonomic Nervous System?
23.14 Does the Pineal Gland Act on the Crypts Via the Limbic System Indirectly by Affecting the General Level of Excitability of the Brain, i. e. Not a Specific Effect on the Limbic System?
23.15 Conclusions
- References
D. Molecular Mechanisms of Action
24 Reactive Oxygen Species, DNA Damage, and Carcinogenesis: Intervention with Melatonin
24.1 Introduction
24.2 Endogenous Oxidative Damage to DNA
24.3 Reactive Oxygen Species and DNA Damage
24.4 Lipid Peroxidation and DNA Damage
24.5 Melatonin as a Free Radical Scavenger
24.6 Melatonin as an Antioxidant
24.7 Concluding Remarks
- References
25 Could the Antiproliferative Effect of Melatonin Be Exerted Via the Interaction of Melatonin with Calmodulin and Protein Kinase C?
25.1 Introduction
25.2 Calmodulin Involvement in Cell Proliferation: Effects of Melatonin
25.3 Protein Kinase C Involvement in Cell Proliferation: Effects of Melatonin
25.4 Concluding Remarks
- References
Section V: Oncotherapeutic Potential of Melatonin
26 Efficacy of Melatonin in the Immunotherapy of Cancer Using Interleukin-2
26.1 Introduction
26.2 Materials and Methods
26.3 Results
26.4 Discussion
- References
27 Melatonin Cancer Therapy
27.1 Introduction
27.2 Undisputed Biological Effects of Melatonin in Human Beings
27.3 Melatonin Affects Sleep and Body Temperature
27.4 Light, Melatonin and the Manipulation of Circadian Orientation
27.5 The Pineal, Melatonin, and Cancer
27.6 Circadian Cytokinetic Rhythms
27.7 Melatonin in Human Cancer Therapy
27.8 Does Melatonin Benefit Human Beings with Cancer?
27.9 Lissoni's Broad Phase II Trials
27.10 Lissoni's Disease-Specific Randomized Controlled Clinical Trials of Melatonin
27.11 Lissoni's Randomized Controlled Trials of Melatonin Plus Interleukin-2 vs Interleukin-2 Alone
27.12 Melatonin Trials of Other Investigators
27.13 Minimal Clinical Trial Design for the Productive Study of Melatonin
27.14 A Useful Melatonin Study Design
27.15 Objective, Physiologic Measurement of Fatigue Needed
27.16 Chronobiology and Drug Development
- References
Section VI: Electromagnetic Fields and Cancer: The Possible Role of Melatonin
28 Circadian Disruption and Breast Cancer
28.1 Background
28.2 Light and Melatonin
28.3 Electric and Magnetic Fields and Melatonin
28.4 Breast Cancer in Blind Women
28.5 Conclusion
- References
29 Breast Cancer and Use of Electric Power: Experimental Studies on the Melatonin Hypothesis
29.1 Introduction
29.2 The Melatonin Hypothesis
29.3 Effect of ELF MFs on Melatonin Levels
29.4 Effect of ELF MFs on Breast Tissue Proliferation
29.5 Effect of ELF MFs on Mammary Carcinogenesis
29.6 Effect of ELF MFs on Immune Responses to Tumor Formation
29.7 Magnetic Field Exposure and Breast Cancer: Conclusions
- References
30 Magnetic Field Exposure and Pineal Melatonin Production (Mini-Review)
30.1 Introduction
30.2 Circadian Rhythm of Melatonin Secretion
30.3 The Response of the Pineal Gland to Electromagnetic Fields: Role of Duration and Intensity of Exposure
30.4 Effect of Magnetic Field Exposure on Humans
30.5 Comments
- References
31 Nocturnal Hormone Profiles in Healthy Humans Under the Influence of Pulsed High-Frequency Electromagnetic Fields
31.1 Introduction
31.2 Materials and Methods
31.2.1 Subjects
31.2.2 Experimental Procedure
31.2.3 Protocol
31.2.4 Nocturnal Hormone Profiles
31.2.5 Data Analysis
31.3 Results
31.4 Discussion
- References
32 Weak High-Frequency (Radiofrequency, Microwave) Electromagnetic Fields: Epidemiological Evidence of Their Impact on Cancer Development and Reproductive Outcome
32.1 Introduction
32.2 Studies
32.2.1 Cancer Studies
32.2.2 Studies on Reproduction
32.3 Conclusions
32.3.1 Cancer Studies
32.3.2 Studies on Reproduction
- References
4.5 Anatomical-Clinical Associations
4.6 The Homeostatic Melatonin Era
4.7 Sampling and Assessing Chronomes
4.8 Subtle Human Melatonin Rhythms
4.9 Pineal Gland and Adrenal Cortex, Feedsidewards
4.10 Circaseptans
4.11 The Need for Dense Sampling Before the Ruling Out of Rhythms and Presence of Melatonin
4.12 A Controversy Resolved
4.13 Summary
- References
5 Melatonin Involvement in Cancer: Methodological Considerations
5.1 Introduction
5.2 Chronoradiotherapy
5.3 Historical Perspective
5.4 Chronochemotherapy
5.5 Need for Marker Rhythmometry
5.6 Chronorisk
5.7 Rhythm Scrambling
5.8 Lessons from Studies on Pituitary Grafts With and Without a Hypothalamus
5.9 Methodological Considerations
5.9.1 Specificity
5.9.2 Risk Versus Disease
5.9.3 Melatonin as an Oncostatic Drug: Importance of Timing
5.9.4 Coordination Via Feedsidewards: Importance of Circaseptans
5.9.5 Environmental Effects from Near and Far
5.10 Concluding Remarks
- References
Section II: Effect of Tumor Growth on the Production and Secretion of Pineal Melatonin
6 Analysis of Melatonin in Patients with Cancer of the Reproductive System
6.1 Introduction
6.2 Methodological Considerations and Problems Encountered in Estimating the Function of the Pineal Gland in Cancer Patients
6.2.1 Analytical Methods
6.2.2 Parameters Interfering with the Estimation of Pineal Function in Patients
6.3 Studies on Patients with Breast Cancer
6.4 Studies on Patients with Gynecological Cancers
6.4.1 Endometrial Cancer
6.4.2 Ovarian Cancer
6.5 Studies on Patients with Prostate Cancer
- References
7 Melatonin in Patients with Cancer of Extra-Reproductive Location
7.1 Introduction
7.2 Patients and Methods
7.3 Results
7.3.1 Nocturnal Urinary aMT6s Excretion in Cancer Patients
7.3.2 Correlations of Nocturnal Urinary aMT6s Excretion with Immunocytochemical Parameters Measured in Gastrointestinal and Lung Cancer
7.3.3 Correlations Among Intratumoral Parameters in Gastrointestinal Cancers
7.4 Discussion
7.4.1 Melatonin Secretion in Human Cancer Patients
7.4.2 Correlation Between MT Production and Proliferative Activity in Tumor Cells
7.4.3 Correlation Among Tumoral Parameters
7.5 Conclusion
- References
8 The Modulation of Melatonin in Tumor-Bearing Animals: Underlying Mechanisms and Possible Significance for Prognosis
8.1 Introduction
8.2 Studies with Chemically-Induced Mammary Cancers
8.2.1 Acute Effects of DMBA-Administration on Circulating Melatonin: Evidence for an Induction of the Hepatic Degradation of the Hormone
8.2.2 The Effects of DMBA-Induced Mammary Tumor Growth on Circulating Melatonin and the Pineal Melatonin Biosynthetic Pathway
8.3 Studies with Serial Transplants Derived from DMBA-Induced Mammary Cancers
8.3.1 Early Passage: Localized Carcinosarcoma
8.3.2 Late Passages: Metastasizing Sarcoma
8.4 Studies with Chemically Induced Colon Cancers
8.5 Conclusions and Considerations
- References
9 The Pineal Gland, Melatonin, and Neoplastic Growth: Morphological Approach
9.1 Introduction
9.2 Morphological Studies of Tumors Following Melatonin Treatment and Pinealectomy
9.3 Pineal Morphology in Tumor-Bearing Animals
9.4 Pineal Morphology in Human Malignancy
- References
Section III: Effects of Melatonin and of Unidentified Pineal Products on Tumor Growth
10 In Vitro Effects of Melatonin on Tumor Cells
10.1 Introduction
10.2 Effects of Melatonin on Breast Cancer Cells
10.2.1 Effects of Melatonin on Proliferation of Breast Cancer Cells In Vitro
10.2.2 Effects of Melatonin on the Metastatic Behavior of Breast Cancer Cells
10.2.3 Influence of Melatonin on Active Cell Death of Mammary Cancer Cells
10.2.4 Mechanisms of the Oncostatic Action of Melatonin In Vitro
10.3 Effect of Melatonin on Melanoma Cells
10.4 Effect of Melatonin on Cancer Cells from Female Reproductive Organs
10.5 Effect of Melatonin on Other Neoplasms
10.6 Conclusions
- References
11 Melatonin and Colon Carcinogenesis
11.1 Introduction
11.2 Effect of Melatonin on Colon Carcinoma Development
11.2.1 Inhibitory Effect of Melatonin on 1,2-Dimethylhydrazine-Induced Colon Carcinogenesis in Rats
11.2.2 Effect of Melatonin on Colon Tumor Growth In Vitro and In Vivo
11.3 Early Stages of 1,2-Dimethylhydrazine-Induced Colon Carcinogenesis As Targets for the Effect of Melatonin
11.3.1 Effect of Melatonin on the Genotoxic Action of 1,2-Dimethylhydrazine
11.3.2 Effect of a Single 1,2-Dimethylhydrazine Administration on Free Radical Processes in Rats
11.3.3 Effect of Melatonin on Free Radical Processes in Rats
11.3.4 Carbohydrate and Lipid Metabolism in Rats Exposed to a Single Dose of 1,2-Dimethylhydrazine
11.3.5 Effect of 1,2-Dimethylhydrazine on the Neuroendocrine System of Rats
11.4 Effect of Melatonin on Late Stages of 1,2-Dimethylhydrazine-Induced Colon Carcinogenesis
11.4.1 Free Radical Processes in Rats with Colon Tumors Induced by 1,2-Dimethylhydrazine: Effect of Melatonin
11.4.2 Effect of Melatonin on Proliferative Activity and Apoptosis in Colon Mucosa and Colon Tumors Induced by 1,2-Dimethylhydrazine in Rats
11.4.3 Pineal Function in Rats with Colon Tumors Induced by 1,2-Dimethylhydrazine
11.4.4 Melatonin-Containing Cells in the Intestinal Mucosa of Rats with 1,2-Dimethylhydrazine-Induced Colon Tumors: Effect of Exogenous Melatonin
11.4.5 Disturbances in Carbohydrate and Lipid Metabolism During Carcinogenesis Induced by 1,2-Dimethylhydrazine in Rats
11.4.6 Effect of Melatonin on Carbohydrate and Lipid Metabolism in Rats with Colon Tumors Induced by 1,2-Dimethylhydrazine
11.4.7 Possible Effect of Melatonin on the Immune System in Rats Exposed to 1,2-Dimethylhydrazine
11.5 Conclusion
- References
12 Role of Extrapineal Melatonin and Related APUD Series Peptides in Malignancy
12.1 Introduction
12.2 Extrapineal Melatonin: Cellular Localization, Role, and Significance Within the Diffuse Neuroendocrine System
12.3 Extrapineal MT and APUD Series Peptides: Possible Participation in Endogenous Mechanisms of Tumor Growth
12.4 Extrapineal Melatonin and Tumor Radiosensitivity: New Approaches for Modification of Antitumor Therapy
12.5 General Conclusion and Future Perspectives
- References
13 A Survey of the Evidence That Melatonin and Unidentified Pineal Substances Affect Neoplastic Growth
13.1 Introduction
13.2 The Role of the Pineal Hormone Melatonin
13.2.1 The Effects of Melatonin in Relation to Malignant Growth
13.2.2 The Effects of Melatonin in Relation to the Immune System and Stress
13.3 Effects of Yet Unknown Pineal Substances on Malignant Cells in Culture
13.3.1 Extracts of Ovine Pineal Glands
13.3.2 Extracts of Rat Pineals
13.3.3 Studies on an Unidentified Bovine Pineal Substance Which Inhibits MCF-7 Cell Growth in Vitro
13.4 Possible Presence of Kynurenines and Kynurenamines in Pineal Extracts
13.5 The Possible Significance of a Bovine Pineal Gland-Derived Decapeptide for the Growth of Malignant Cells in Vivo
13.6 Summary
- References
14 Experimental Studies of the Pineal Gland Preparation Epithalamin
14.1 Introduction
14.2 Epithalamin - a Low Molecular Weight Peptide Preparation
14.3 Effect of Epithalamin on the Life Span of Mice, Rats, and Drosophila melanogaster
14.4 The Influence of Epithalamin on the Function of the Nervous, Endocrine, and Immune Systems of Young and Old Rats
14.5 The Effect of Epithalamin on Spontaneous Tumor Development in Rats and Mice
- References
Section IV: Mechanisms of Action of Melatonin on Tumor Cells
A. Actions Via the Endocrine System
15 An Overview of the Neuroendocrine Regulation of Experimental Tumor Growth by Melatonin and Its Analogues and the Therapeutic Use of Melatonin in Oncology
15.1 Introduction
15.2 Effects of Melatonin and Its Analogues on Experimental Cancer Growth
15.2.1 Melatonin and Breast Cancer
15.2.2 Melatonin and Melanoma
15.2.3 Melatonin and Sarcoma
15.2.4 Melatonin and Other Tumors
15.3 Melatonin Binding in Neoplastic Tissues
15.3.1 Mouse Melanoma
15.3.2 Hamster Melanoma
15.3.3 Human Melanoma
15.3.4 Murine Mammary Cancer
15.3.5 Human Breast Cancer
15.3.6 Human Benign Prostatic Hyperplasia
15.3.7 Other Immortalized Cell Lines
15.4 Potential Melatonin Signal Transduction Mechanisms in Neoplastic Cells
15.4.1 Cyclic AMP and G Proteins
15.4.2 Phosphoinositide Metabolism
15.4.3 Nonmelatonin Receptor Expression
15.4.4 Transcriptional Regulation
15.4.5 Genomic Interactions
15.4.6 Calcium/Calmodulin (Ca2+/CaM) and the Cytoskeleton
15.4.7 Redox Mechanisms: Glutathione and Nitric Oxide
15.4.8 Tumor Linoleic Acid Uptake and Metabolism
15.5 Melatonin in the Chemoendocrine Therapy of Human Malignancies
15.6 Conclusions
- References
16 Modulation of the Estrogen Response Pathway in Human Breast Cancer Cells by Melatonin
16.1 Introduction
16.2 Melatonin and Breast Cancer
16.3 Melatonin Receptors
16.3.1 Membrane-Associated, G Protein-Linked Melatonin Receptors
16.3.2 Nuclear Melatonin Receptors
16.4 Melatonin and the Estrogen Response Pathway
16.4.1 Melatonin Modulation of ER Expression
16.4.2 Melatonin Modulation of Estrogen-Regulated Genes
16.4.3 Melatonin Modulation of ER Transactivation
16.5 Conclusions
- References
17 Benign and Tumor Prostate Cells as Melatonin Target Sites
17.1 Effects of Melatonin on the Prostate Gland In Vivo
17.2 Melatonin Action in Prostate Epithelial Cells In Vitro
17.2.1 Benign Prostate Hypertrophy Cells
17.2.2 Prostate Cancer Cells
17.3 Melatonin Action in Prostate Epithelial Cells: Towards a Unifying Hypothesis
- References
B. Actions Via the Immune System
18 Neuroimmunomodulation Via the Autonomic Nervous System
18.1 Introduction
18.2 Adrenergic In Vivo Effects on Immune Functions
18.3 Cholinergic Immunomodulation
18.4 Conclusions
- References
19 Melatonin and Immune Functions
19.1 Evidence of an Immunoregulatory Role of Melatonin (MEL)
19.2 Protective Effects of MEL on ?2-Adrenergic Immunosuppression in Rats
19.3 CD4+ Lymphocytes and Monocytes/Macrophages as Targets of MEL Activity
19.4 Possible Mechanisms of Action of MEL on Immune Cells
19.4.1 MEL Membrane Receptors on Immune Cells
19.4.2 MEL as a Ligand for the Nuclear Receptors RZR-? and RZR-?
19.4.3 MEL as a Calmodulin Antagonist
19.4.4 MEL as Antioxidant
19.5 Conclusion
- References
20 Melatonin and the Immune System: Therapeutic Potential in Cancer, Viral Diseases, and Immunodeficiency States
20.1 Neuroimmune Interactions with the Environment
20.2 Melatonin and the Immune-Hematopoietic System
20.2.1 Functional Effects
20.2.2 Cytokines Which Mediate the Effect of Melatonin
20.2.3 Melatonin Receptors
20.2.4 Clinical Trials
20.2.5 Mechanism of Action
20.3 Conclusion
- References
21 Melatonin Rhythms in Mice: Role in Autoimmune and Lymphoproliferative Diseases
21.1 Introduction
21.2 Melatonin Endogenous Rhythm in Mice
21.3 The Role of Pineal Gland and Melatonin in Autoimmune and Lymphoproliferative Diseases
21.3.1 Autoimmune Diabetes
21.3.2 Collagen-Induced Arthritis
21.3.3 Induced T Cell Leukemia
21.4 Conclusions
- References
22 Mechanisms Involved in the Immunomodulatory Effects of Melatonin on the Human Immune System
22.1 Introduction
22.2 Effects of Melatonin on the Immune System
22.3 Mechanisms of Action of Melatonin: The Membrane Receptor
22.4 Nuclear Receptors for Melatonin in the Immune System
22.5 The Physiological Role of Membrane Receptors Versus Nuclear Receptors
- References
- C Actions Via Neural Pathways
23 The Role of the Pineal Gland in Neural Control of Cell Proliferation in Healthy and Malignant Tissue
23.1 Introduction
23.2 The Role of the Autonomic Nervous System in the Control of Normal and Neoplastic Crypt Cell Proliferation in the Gut
23.3 Efferent Neural Connections Between the Pineal Gland and the Autonomic Nervous System
23.4 The Enteric Nervous System and Its Possible Role in Neural Control of Crypt Cell Proliferation in the Normal Gut. Is It Suitably Located?
23.5 Neural Control of Normal Cell Proliferation in Organs Other Than the Gastrointestinal System
23.6 The Precise Role of the Pineal Gland in the Normal Mechanism of Control of Proliferation in the Gastrointestinal Tract
23.7 The Role of the Pineal Gland in Induction or Promotion of Malignancy: How Important is It?
23.8 Further Consideration of the Role of Melatonin in the Control of Normal Crypt Cell Proliferation in the Gut
23.9 The Possible Role of the Pineal as a Modulator of Neuroendocrine Activity in Controlling Tumor Growth (Rather Than a Direct Effect Via the Autonomic Nervous System or Changes in the Level of Melatonin Secretion)
23.10 The Relationship Between Pinealectomy and Melatonin Levels in the Body
23.11 Are Any Other Possible Antitumor Factors Produced by the Pineal Gland Besides Melatonin, and Could These Be Involved in the Physiological Control of Malignancy?
23.12 Relationship of Pinealectomy and Its Effects on the Intestinal Crypts with Similar Effects on the Crypts Associated with Limbic Lesions
23.13 Is it Possible That the Pineal Gland Acts Directly on the Crypts Via the Limbic System and the Autonomic Nervous System?
23.14 Does the Pineal Gland Act on the Crypts Via the Limbic System Indirectly by Affecting the General Level of Excitability of the Brain, i. e. Not a Specific Effect on the Limbic System?
23.15 Conclusions
- References
D. Molecular Mechanisms of Action
24 Reactive Oxygen Species, DNA Damage, and Carcinogenesis: Intervention with Melatonin
24.1 Introduction
24.2 Endogenous Oxidative Damage to DNA
24.3 Reactive Oxygen Species and DNA Damage
24.4 Lipid Peroxidation and DNA Damage
24.5 Melatonin as a Free Radical Scavenger
24.6 Melatonin as an Antioxidant
24.7 Concluding Remarks
- References
25 Could the Antiproliferative Effect of Melatonin Be Exerted Via the Interaction of Melatonin with Calmodulin and Protein Kinase C?
25.1 Introduction
25.2 Calmodulin Involvement in Cell Proliferation: Effects of Melatonin
25.3 Protein Kinase C Involvement in Cell Proliferation: Effects of Melatonin
25.4 Concluding Remarks
- References
Section V: Oncotherapeutic Potential of Melatonin
26 Efficacy of Melatonin in the Immunotherapy of Cancer Using Interleukin-2
26.1 Introduction
26.2 Materials and Methods
26.3 Results
26.4 Discussion
- References
27 Melatonin Cancer Therapy
27.1 Introduction
27.2 Undisputed Biological Effects of Melatonin in Human Beings
27.3 Melatonin Affects Sleep and Body Temperature
27.4 Light, Melatonin and the Manipulation of Circadian Orientation
27.5 The Pineal, Melatonin, and Cancer
27.6 Circadian Cytokinetic Rhythms
27.7 Melatonin in Human Cancer Therapy
27.8 Does Melatonin Benefit Human Beings with Cancer?
27.9 Lissoni's Broad Phase II Trials
27.10 Lissoni's Disease-Specific Randomized Controlled Clinical Trials of Melatonin
27.11 Lissoni's Randomized Controlled Trials of Melatonin Plus Interleukin-2 vs Interleukin-2 Alone
27.12 Melatonin Trials of Other Investigators
27.13 Minimal Clinical Trial Design for the Productive Study of Melatonin
27.14 A Useful Melatonin Study Design
27.15 Objective, Physiologic Measurement of Fatigue Needed
27.16 Chronobiology and Drug Development
- References
Section VI: Electromagnetic Fields and Cancer: The Possible Role of Melatonin
28 Circadian Disruption and Breast Cancer
28.1 Background
28.2 Light and Melatonin
28.3 Electric and Magnetic Fields and Melatonin
28.4 Breast Cancer in Blind Women
28.5 Conclusion
- References
29 Breast Cancer and Use of Electric Power: Experimental Studies on the Melatonin Hypothesis
29.1 Introduction
29.2 The Melatonin Hypothesis
29.3 Effect of ELF MFs on Melatonin Levels
29.4 Effect of ELF MFs on Breast Tissue Proliferation
29.5 Effect of ELF MFs on Mammary Carcinogenesis
29.6 Effect of ELF MFs on Immune Responses to Tumor Formation
29.7 Magnetic Field Exposure and Breast Cancer: Conclusions
- References
30 Magnetic Field Exposure and Pineal Melatonin Production (Mini-Review)
30.1 Introduction
30.2 Circadian Rhythm of Melatonin Secretion
30.3 The Response of the Pineal Gland to Electromagnetic Fields: Role of Duration and Intensity of Exposure
30.4 Effect of Magnetic Field Exposure on Humans
30.5 Comments
- References
31 Nocturnal Hormone Profiles in Healthy Humans Under the Influence of Pulsed High-Frequency Electromagnetic Fields
31.1 Introduction
31.2 Materials and Methods
31.2.1 Subjects
31.2.2 Experimental Procedure
31.2.3 Protocol
31.2.4 Nocturnal Hormone Profiles
31.2.5 Data Analysis
31.3 Results
31.4 Discussion
- References
32 Weak High-Frequency (Radiofrequency, Microwave) Electromagnetic Fields: Epidemiological Evidence of Their Impact on Cancer Development and Reproductive Outcome
32.1 Introduction
32.2 Studies
32.2.1 Cancer Studies
32.2.2 Studies on Reproduction
32.3 Conclusions
32.3.1 Cancer Studies
32.3.2 Studies on Reproduction
- References
... weniger
Bibliographische Angaben
- 2012, Softcover reprint of the original 1st ed. 2001., 578 Seiten, Maße: 23,5 cm, Kartoniert (TB), Englisch
- Herausgegeben:Bartsch, C.; Bartsch, H.; Blask, D.E.; Cardinali, D.P.; Hrushesky, W.J.M.; Mecke, Dieter
- Verlag: Springer
- ISBN-10: 3642640036
- ISBN-13: 9783642640032
Sprache:
Englisch
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