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Cancer Pharmacology: An Illustrated Manual of Anticancer Drugs
Proteasome Inhibitors (PIs) Can Be Viewed as the Stoppers for the Waste Disposers of the Cells
Table of Contents
Free Topics
5-Fluorouracil (5-FU)
About
Antimetabolites: Antifolates
Differentiating Agents and Microenvironment
Figure - Additional Pharmacology Considerations for Cancer Drug Marketing Applications
Figure - Polymorphism in Thiopurine Methyltransferase (TPMT)
Flowchart - Patient Selection and Study Design
Flowchart - The Flow of Biomarker Identification, Validation, and Application
Question 2.1
Question 3.2
Table - Adverse Events Related to Vinca Alkaloids
Table - Antifolate Medications, Oncologic Use, and Differences in Structures as Compared
Targeted Therapies (Small Molecules)
1. Anticancer Drug Development: An Introduction
1. Anticancer Drug Development: An Introduction
Figure(s)
1-1. Targets for Cancer Drugs
1-2. The Probability of Overall Survival in the Two Groups Calculated with the Use of the Kaplan-Meier Method
1-3. Pharmacokinetic Endpoints
1-4. Pharmacokinetics: Relation to Toxicity or Achievement of Steady State
2. Alkylating Agents
2. Alkylating Agents
Figure(s)
2-1. Mechanism of Action of DNA Alkylation by Nitrogen Mustards
2-2. Cyclophosphamide and Ifosfamide
2-3. Hemorrhagic Cystitis Related to Cyclophosphamide and Ifosfamide
2-4. Other Nitrogen Mustards
2-5. Nitrosoureas
2-6. Triazines (Three Attached Nitrogen Atoms)
2-7. Clinical Importance of Methylguanine Methyltransferase
2-8. Ethylenimines
2-9. Platinum Compounds
3. Antimetabolites: Hydroxyurea, Pyrimidine and Purine Analogs, and L-Asparaginase
3. Antimetabolites: Hydroxyurea, Pyrimidine and Purine Analogs, and L-Asparaginase
Figure(s)
3-1. Normal DNA Structure Consists of Phosphate, Deoxyribose, and Base
3-2. Ribonucleotide Reductase (RNR) is Responsible for Synthesizing Deoxyribonucleotides
3-3. Polymorphism in Thiopurine Methyltransferase (TPMT)
3-4. Asparaginases, as Amidohydrolases, Possess Both Asparaginase and Glutaminase Activity
Table(s)
3-1. Ribonucleotide Reductase Inhibition
3-2. Pyrimidine Analogs
3-3. Purine Analogs
3-4. Dosing, Monitoring, and Management of Asparaginase-Related Adverse Events
4. Antimetabolites: Antifolates
4. Antimetabolites: Antifolates
Figure(s)
4-1. Mechanisms of Folic Acid in Cell Physiology
4-2. Folic Acid Cycle as Relevant for Conversion of Deoxyuridine Monophosphate (dUMP)
4-3. Antifolate Mechanism of Action
4-4. Relative Affinities of Folate Receptor (FR) and Reduced Folate Carrier (RFC)
4-5. Polyglutamate 'Trapping' of Methotrexate (MTX)
4-6. Mechanism of Leucovorin (LV) 'Rescue' in High-Dose Methotrexate (MTX)
4-7. Urinary Excretion of High-Dose Methotrexate (MTX) and Effect of Medications and Urine pH
4-8. Mechanism of Methotrexate (MTX) Breakdown Via Glucarpidase
Table(s)
4-1. Antifolate Medications, Oncologic Use, and Differences in Structures as Compared
4-2. Antifolate Toxicities and Supportive Agents
4-3. Tetrahydrofolate (THF) Compared to Leucovorin (LV) (Folinic Acid, LV) Structure
5. Antimitotics
5. Antimitotics
Figure(s)
5-1. Cell Cycle and Temporarily Related Chromosome Cycle
5-2. Microtubules
Table(s)
5-1. Adverse Events Related to Vinca Alkaloids
6. DNA Repair, Apoptotic Pathways, CDK Inhibitors
6. DNA Repair, Apoptotic Pathways, CDK Inhibitors
Figure(s)
6-1. Function and Therapeutic Targeting of DNA Topoisomerase I and II
6-2. Targeting the DNA Damage Response Pathway
6-3. Targeting the ATR-CHK1-WEE1 Pathway to Inhibit the Replication Checkpoint
6-4. Parp Inhibitors Exemplify Synthetic Lethality
6-5. Therapeutic Activation of Apoptosis
6-6. Inhibition of the Cell Cycle and Transcription through CDK Inhibition
Table(s)
6-1. Topoisomerase Inhibitors: Clinical Considerations
6-2. Topoisomerase Inhibitors: Pharmacologic Considerations
7. Epigenetic Modulators
7. Epigenetic Modulators
Figure(s)
7-1. Chromatin Structure and Epigenetic Marks
7-2. Epigenetics Modifying Agents and the Mechanism of Action
Table(s)
7-1. Epigenetic Modifying Agents Approved for Clinical Use (as of September
8. Differentiating Agents and Microenvironment
8. Differentiating Agents and Microenvironment
Figure(s)
8-1. Tumor Stem Cells and Their Microenvironment
8-2. Effects of the Tumor Microenvironment on Pharmacokinetics
8-3. Effects of the Tumor Microenvironment on Pharmacodynamics
9. Hormonal Therapies Alone and in Combinations for Treatment of Breast Cancer
9. Hormonal Therapies Alone and in Combinations for Treatment of Breast Cancer
Figure(s)
9-1. Hormones Affecting the Breast
9-10. CDK4/CDK6 and mTOR Signaling Pathways
9-11. Selective Estrogen Receptor Degrader (SERD)
9-2. Estrogen Biosynthesis from Cholesterol Precursors in Endocrine Organs
9-3. Molecular Effect of Estrogen on the Estrogen Receptor (ER)
9-4. Estrogen-Dependent Tumor Growth
9-5. Structures of Antiestrogenic Molecules
9-6. Cellular (Nuclear and Nonnuclear Mechanisms of Estrogen Action)
9-7. Selective Estrogen Receptor Modulators
9-8. Steroid Biosynthesis Aromatase Enzyme
9-9. Aromatase Inhibitors (AIs)
Table(s)
9-1. Hormonal Agents and Combinations for Prevention and Treatment of ER
10. Male Hormonal Therapies
10. Male Hormonal Therapies
Figure(s)
10-1. Overview of Prostate Cancer (PC) Progression and Treatment
10-2. Sources of and rogens in the Human Prostate
10-3. Biosynthesis of and rogens and Other Steroid Hormones from Cholesterol
10-4. Molecular Mechanism of and rogen Receptor (AR) Activation by Dihydrotestosterone (DHT)
10-5. Physiological and Anatomical Targets of FDA-Approved 'Hormonal' Drugs for Prostate Cancer
10-6. Schematic Structure of Gonadotropin-Releasing Hormone (GnRH) Agonist Relative to Native GnRH
10-7. Chemical Structures of Abiraterone and its Prodrug, Abiraterone Acetate
10-8. Chemical Structure of Steroidal and Nonsteroidal Antiand rogens
Table(s)
10-1. Clinically Available GnRH Agonists
11. Targeted Therapies (Small Molecules)
11. Targeted Therapies (Small Molecules)
Figure(s)
11-1. Epidermal Growth Factor Receptor (EGFR) and Human Epidermal Growth Factor Receptor (HER)
11-10. Tyrosine Kinase Inhibitors (TKI)
11-2. Vascular Endothelial Growth Factor (VEGF) Receptor
11-3. Mitogen-Activated Protein Kinase (MAPK)/Extracellular Signal-Related Kinase (ERK)
11-4. Anaplastic Lymphoma Kinase (ALK) Fusion
11-5. B-Cell Receptor (BCR)-ABL Translocation and the Philadelphia Chromosome
11-6. Isocitrate Dehydrogenase (IDH) and Ten-Eleven Translocation 2 (TET2) Mutations
11-7. The B-Cell Receptor (BCR) and Bruton Tyrosine Kinase (BTK)
11-8. Janus Kinase (JAK)/Signal Transducer and Activator of Transcription (STAT) Pathway
11-9. FMS-Like Tyrosine Kinase 3 (FLT3) Receptor
12. Monoclonal Antibodies Including Immunoconjugates and Cytokine-Directed Agents
12. Monoclonal Antibodies Including Immunoconjugates and Cytokine-Directed Agents
Figure(s)
12-1. Monoclonal Antibody Structure and Classification
12-2. Naked Monoclonal Antibody Mechanism of Action
12-3. Prevention and Management of Infusion-Related Reactions Due to Monoclonal Antibodies
12-4. Elements of an Antibody-drug Conjugate (ADC)
12-5. Available Antibody-drug Conjugates
12-6. An Example of an Antibody-drug Conjugate (Ado-Trastuzumab Emtansine) in Action
12-7. Components of 90y-Ibritumomab Tiuxetan
12-8. Mechanism of Action for High-Dose Interleukin
12-9. Cytokine Toxicity Man
Table(s)
12-1. Monoclonal Antibody Class and Target Overview
12-2. Select Target-Specific Toxicities and Management
12-3. Management of Cytokine Therapy Toxicities
13. Immunotherapeutics Including Vaccines, Bispecifics, CAR-T, and Checkpoint Inhibitors
13. Immunotherapeutics Including Vaccines, Bispecifics, CAR-T, and Checkpoint Inhibitors
Figure(s)
13-1. Tumors Orchestrate a Complex Signaling Network to Evade Immune Destruction
13-2. When Functioning Normally, CD8+ T Effector Cells Can Recognize and Destroy Tumor Cells
13-3. Anti-Pd-1 and Anti-Pd-L1 Immunotherapies Have Demonstrated Unprecedented Clinical Activity
13-4. The First Approved Immune Checkpoint Inhibitors Restore Anti-Tumor Immunity
13-5. Immune Checkpoint Inhibitors Can Cause a Wide Range of Immune-Related Adverse Effects (irAEs)
13-6. Prophylactic Vaccines Stimulate the Immune System Against a Disease Not Yet Experienced by the Host
13-7. Chimeric Antigen Receptor (CAR) T-Cell Therapy and Bispecific Antibodies
Table(s)
13-1. Immune Checkpoint Inhibitors Have Transformed the Management of Multiple Cancers
14. Multiple Myeloma as a Paradigm for Multi-Targeted Intervention
14. Multiple Myeloma as a Paradigm for Multi-Targeted Intervention
Figure(s)
14-1. Immunomodulatory Drugs (IMiDs) with Their Structure Almost Resembling a Snowman
14-2. Examples of Boronic Acid (Left, Bortezomib) and Epoxyketone (Right, Carfilzomib) Proteasome Inhibitors
14-3. Proteasome Inhibitors (PIs) Can Be Viewed as the Stoppers for the Waste Disposers of the Cells
14-4. Mechanisms of Action of Daratumumab
14-5. A Description of Current Immunotherapeutic Approaches in Myeloma
14-6. Some Anti-MM Drugs with Prominent Activities Mediated Via Discrete Subcellular Organelles
15. Transplant-Related Agents
15. Transplant-Related Agents
Figure(s)
15-1. Mechanism of Action of Cyclophosphamide
15-2. Mechanism of Action of Nucleoside Analogs (NA)
15-3. Mechanism of Action of Topoisomerase Inhibitors
15-4. Mechanism of Action of Mycophenolate Mofetil (CellCept)
15-5. Mechanism of Action of High-Dose Cyclophosphamide Graft-Versus-Host Disease (GVHD) Prophylaxis
16. Basic Drug Development With Structural Considerations
16. Basic Drug Development With Structural Considerations
Figure(s)
16-1. Phases of Clinical Trials
16-2. Clinical Trial Facts
16-3. Patient Selection and Study Design
16-4. New Active Substance Launches from 2011 to 2016 by Indication
16-5. Novel Therapeutic Strategies in Oncology
Table(s)
16-1. Clinical Trial Definitions
16-2. Common Terminology Criteria for Adverse Events V4.0 (CTCAE)
16-3. Comparison Between the RECIST 1.1, the WHO, and the irRC Criteria
17. Integral Components in Development of Clinical Trials: PK/PD, Statistics, and Principles of Rational Combinatorial Therapies
17. Integral Components in Development of Clinical Trials: PK/PD, Statistics, and Principles of Rational Combinatorial Therapies
Figure(s)
17-1. Clinical Trials Life Cycle
17-10. Design of Early-Phase Clinical Trials
17-11. Early-Phase Clinical Trials Using Adaptive Designs
17-12. Pathways to Drug Development
17-13. The Flow of Biomarker Identification, Validation, and Application
17-14. The Pharmacological Audit Trial (PhAT)
17-15. Comparison of the Molecular Pharmacological Audit Trial (MoPhAT) to the Pharmacological Audit Trial (PhAT)
17-16. Biomarkers in Clinical Trials
17-2. Clinical Drug Development Triad
17-3. Basic and Translation Approach to Clinical Trials
17-4. Pharmacodynamic and Descriptive/Biological Biomarkers
17-5. Characterization and Selection of Biomarkers
17-6. Development of Biomarkers Based on Their Intended Use
17-7. Prognostic Biomarkers
17-8. Predictive Biomarkers
17-9. Targeted Cancer Therapies
18. Drug Approval and Regulatory Issues
18. Drug Approval and Regulatory Issues
Figure(s)
18-1. Indenabling Nonclinical Studies for Cancer Drugs
18-2. Getting to the Recommended Phase 2 Dose (Rp2d)
18-3. Studies Contributing to Dose Refinement
18-4. Additional Pharmacology Considerations for Cancer Drug Marketing Applications
Front Matter
Contributors
Preface
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Proteasome Inhibitors (PIs) Can Be Viewed as the Stoppers for the Waste Disposers of the Cells
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