Frontiers in Clinical Drug Research - Anti-Cancer Agents: Volume 5 -  - E-Book

Frontiers in Clinical Drug Research - Anti-Cancer Agents: Volume 5 E-Book

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Frontiers in Clinical Drug Research - Anti-Cancer Agents is a book series intended for pharmaceutical scientists, postgraduate students and researchers seeking updated and critical information for developing clinical trials and devising research plans in anti-cancer research. Reviews in each volume are written by experts in medical oncology and clinical trials research and compile the latest information available on special topics of interest to oncology researchers.
The fifth volume of the book features reviews on biochemical inhibitors (second-generation protein kinase Inhibitors, histone deacetylase inhibitors, immune checkpoint inhibitors, EGFR Tyrosine Kinase inhibitors, non-coding RNAs), apoptosis, and physical exercise therapy for cancer patients undergoing chemotherapy. The treatment strategies in this volume cover cancers such as acute myeloid leukemia, gastrointestinal cancer, breast cancer and lung cancer.

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Table of Contents
Welcome
Table of Contents
Title
BENTHAM SCIENCE PUBLISHERS LTD.
End User License Agreement (for non-institutional, personal use)
Usage Rules:
Disclaimer:
Limitation of Liability:
General:
PREFACE
List of Contributors
Second-Generation Protein Kinase Inhibitor – A Focus on Quizartinib, A Promising Targeted Therapy for High-Risk FLT3+ Patients with Acute Myeloid Leukemia
Abstract
INTRODUCTION
FIRST-GENERATION FLT3 TYROSINE KINASE INHIBITORS
SECOND-GENERATION FLT3 TYROSINE KINASE INHIBITOR QUIZARTINIB
Clinical Pharmacology
Studies with Quizartinib Used as Monotherapy
Combination Studies with Intensive Chemotherapy
Quizartinib as Maintenance Therapy
Terminal Myeloid Differentiation
Toxicity
Drug-Drug Interactions
Inhibition of c-KIT
PERSPECTIVES WITH OTHER SECOND- OR THIRD-GENERATION FLT3 TYROSINE KINASE INHIBITORS
CONCLUSIONS
CONSENT FOR PUBLICATION
CONFLICT OF INTEREST
ACKNOWLEDGEMENT
REFERENCES
Physical Exercise for Cancer Patients Treated with Chemotherapy
Abstract
INTRODUCTION
Breast Cancer
Physical, Psychological, and Psychosocial Side Effects During and After Chemotherapy
Decreased Physical Function During and After Chemotherapy
Type of Physical Exercise (Aerobic, Resistance Training, or Combined, Flexibility)
Prostate
Physical, Psychological, and Psychosocial Side Effects During and After Chemotherapy
Decreased Physical Function During and After Chemotherapy
Type of Physical Exercise (Aerobic, Resistance Training, or Combined, Flexibility)
Lung
Physical, Psychological, and Psychosocial Side Effects During and After Chemotherapy
Decreased Physical Function During and After Chemotherapy
Type of Physical Exercise (Aerobic, Resistance Training, or Combined, Flexibility)
Colon and Rectum
Physical, Psychological, and Psychosocial Side Effects During and After Chemotherapy
Decreased Physical Function During and After Chemotherapy
Type of Physical Exercise (Aerobic, Resistance Training, or Combined, Flexibility)
Stomach (Gastric)
Physical, Psychological, and Psychosocial Side Effects During and After Chemotherapy
Decreased Physical Function During and After Chemotherapy
Type of Physical Exercise (Aerobic, Resistance Training, or Combined, Flexibility)
Esophagus
Physical, Psychological, and Psychosocial Side Effects During and After Chemotherapy
Decreased Physical Function During and After Chemotherapy
Type of Physical Exercise (Aerobic, Resistance Training, or Combined, Flexibility)
Lymphoma, Leukemia (Adult)
Physical, Psychological, and Psychosocial Side Effects During and After Chemotherapy
Decreased Physical Function During and After Chemotherapy
Type of Physical Exercise (Aerobic, Resistance Training, or Combined, Flexibility)
Lymphoma, Leukemia (Child and Adolescent)
Physical, Psychological, and Psychosocial Side Effects During and After Chemotherapy
Decreased Physical Function During and After Chemotherapy
Type of Physical Exercise (Aerobic, Resistance Training, or Combined, Flexibility)
Gynecologic Cancer as Cervical, Endometrial Cancer, Ovarian
Physical, Psychological, and Psychosocial Side Effects During and After Chemotherapy
Decreased Physical Function During and After Chemotherapy
Type of Physical Exercise (Aerobic, Resistance Training, or Combined, Flexibility)
Others (Liver, Pancreas, Gallbladder, Bile Duct, Urinary Bladder, Skin, Oral, Thyroid Gland)
Physical, Psychological, and Psychosocial Side Effects During and After Chemotherapy
Decreased Physical Function During and After Chemotherapy
Type of Physical Exercise (Aerobic, Resistance Training, or Combined, Flexibility)
Managing Risk Using Physical Exercise for Cancer Patients Treated with Chemotherapy
Recommendation for Physical Exercise
Physical Exercise Prolongs Survival and Reduces Mortality
CONCLUSION
ABBREVIATIONS
CONSENT FOR PUBLICATION
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Cancer Immune Evasion in Gastrointestinal Cancer: Can this be Overcome by Combination of Histone Deacetylase and Immune Checkpoint Inhibitors?
Abstract
INTRODUCTION
MECHANISMS OF TUMOUR IMMUNE EVASION
Direct Cellular Interactions
Altered Expression of Co-receptor Molecules
Fas/Fas-ligand Interactions
Interference with MHC Complex Expression and Assembly
Tumour Environment Manipulation
Tumour Microenvironment
Regulatory T-Cell Invasion
IMMUNE CHECKPOINT INHIBITORS
Mechanisms of Action of Immune Checkpoint Inhibitors
CTLA-4 and Anti CTLA-4 Therapy
PD-1/PD-L1 and Anti-PD-1/PD-L1 Therapy
Clinical Trials of Immune Checkpoint Inhibitors in Gastrointestinal and Pancreatic Tumours
Gastric Cancer
Colorectal Cancer
Pancreatic Cancer
HISTONE DEACETYLASE INHIBITORS
Clinical Trials of Histone Deacetylase Inhibitors in Gastrointestinal and Pancreatic Cancers
Gastrointestinal Cancer
Pancreatic Cancer
HR23B: A Marker of CXD101 Sensitivity
Can We Reverse Immunoediting by Treating with Histone Deacetylase (HDAC) Inhibitors?
CONCLUSION
Consent for Publication
Conflict of Interest
Acknowledgements
REFERENCES
Long Non-Coding RNAs in Cancer Progression: Implication for Anti-Cancer Therapy
Abstract
INTRODUCTION
OVERVIEW OF LONG NON-CODING RNA BIOLOGY
MECHANISM OF ACTION
Nucleic lncRNAs Act in cis
Nucleic lncRNAs Act in trans
Nucleic lncRNAs Function in Alternative Splicing
Cytoplasmic lncRNAs Regulate RNA Sstability
Cytoplasmic lncRNA in Protein Modification
Competing Endogenous RNAs
Endogenous Small Interfering RNA Formation
LONG NON-CODING RNA IN CANCER
TARGETING LONG NON-CODING RNA FOR CANCER THERAPY
RNA Interference
Antisense Oligonucleotides
Aptamers
Chemistry and Delivery of RNA-based Therapeutics
Small Molecules
CRISPR System
Therapeutic Manipulation of LncRNAs
CONCLUSION
ACKNOWLEDGMENT
CONFLICT OF INTEREST
REFERENCE
Ros-Mediated Induction of Apoptosis in Breast Cancer Cells
Abstract
INTRODUCTION
THE ROLE OF ROS IN BREAST CANCER CELLS
CONCLUSION
ACKNOWLEDGMENT
CONFLICT OF INTEREST
REFERENCES
Generations of Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors: A Battle against Drug Resistant Lung Cancer
Abstract
INTRODUCTION
FIRST GENERATION OF EGFR-TKIs
STRUCTURES AND MECHANISM OF ACTION
GEFITINIB
Clinical Efficacy
Safety and Tolerability
Quality of Life (QoL) Analysis
ERLOTINIB
Clinical Efficacy as a First-line Treatment
Clinical Efficacy as a Maintenance Treatment
Quality of Life (QoL) Analysis
Safety and Tolerability
ICOTINIB
Clinical Efficacy
Safety and Tolerability
Quality of Life (QoL) Analysis
EGFR EXON 19 DELETION IS MORE SENSITIVE THAN EXON 21 L858R TO FIRST GENERATION EGFR TKIs
DRUG RESISTANCE TO FIRST GENERATION EGFR TKIs
DRUG COMBINATION APPROACHES TO OVERCOME RESISTANCE TO FIRST GENERATION EGFR TKIs
SECOND GENERATION OF EGFR-TKIs
STRUCTURE AND MECHANISM OF ACTION
AFATINIB
Clinical Efficacy: Comparison with Cytotoxic Chemotherapy
Clinical Efficacy: Comparison with Gefitinib
Safety and Tolerability
Quality of Life Analysis
DACOMITINIB
Clinical Efficacy as a First-line Treatment
Clinical Efficacy as a Second-line Treatment
Clinical Efficacy as a Third-line or Beyond Treatment
Quality of Life Analysis
CANERTINIB
NERATINIB
DRUG RESISTANCE TO SECOND GENERATION EGFR TKI (AFATINIB)
THIRD-GENERATION OF EGFR-TKIs
STRUCTURES AND MECHANISM OF ACTION
OSIMERTINIB
Clinical Efficacy
Clinical Use in Patients with Leptomeningeal Metastases (LM)
Safety and Tolerability
Quality of Life (QoL) Analysis
ROCILETINIB
OLMUTINIB
ASP8273
EGF816
PF-06747775
DRUG RESISTANCE TO THIRD-GENERATION EGFR TKI (OSIMERTINIB)
CLINICAL MODES OF DISEASE PROGRESSION IN EGFR TKI-TREATED PATIENTS AND SUBSEQUENT MANAGEMENT
CONCLUDING REMARKS
CONSENT FOR PUBLICATION
CONFLICT OF INTEREST
ACKNOWLEDGEMENT
REFERENCES

Frontiers in Clinical DrugResearch - Anti-Cancer Agents

(Volume 5)

Edited By

Atta-ur-Rahman, FRS

Honorary Life Fellow,
Kings College, University of Cambridge,Cambridge,UK

BENTHAM SCIENCE PUBLISHERS LTD.

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PREFACE

Frontiers in Clinical Drug Research - Anti-Cancer Agents presents recent developments in various therapeutic approaches against different types of cancer. The book is a valuable resource for pharmaceutical scientists, postgraduate students and researchers seeking updated and critical information for developing clinical trials and devising research plans in anti-cancer research. The chapters are written by authorities in the field. The contents of this volume represent exciting recent researches on Acute Myeloid Leukemia, Chemotherapy, Gastrointestinal Cancer, Anti-cancer Therapy, Breast Cancer Cells, and Lung Cancer. I hope that the readers will find these reviews valuable and thought provoking so that they may trigger further research in the quest for the new and novel therapies against cancers.

I am grateful for the timely efforts made by the editorial personnel, especially Mr. Mahmood Alam (Director Publications), and Mr. Shehzad Naqvi (Editorial Manager Publications) at Bentham Science Publishers.

Atta-ur-Rahman, FRSHonorary Life Fellow Kings College University of Cambridge UK

List of Contributors

Atsuhiro TsubakiInstitute for Human Movement and Medical Sciences, Niigata University of Health and Welfare, Niigata, JapanAndrew J. SandersCardiff China Medical Research Collaborative, Cardiff University School of Medicine, Cardiff University, Heath Park, Cardiff, UKChang GongGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetic and Gene Regulation, Breast Tumor Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Varna, ChinaDavid KerrRadcliffe Department of Medicine, University of Oxford, UKEtienne PaubelleHematology Department, University of Arizonaospices Civils de Lyon, Lyon-Sud Hospital, Pierre Bénite, FranceIşıl YıldırımBeykent University, Vocational School, The University of Hong Kong, Istanbul, TurkeyJack B. FuDepartment of Palliative, Rehabilitation Integrative Medicine, University of Texas MD Anderson Cancer Center, Houston, TX, USAKenneth K.W. ToSchool of Pharmacy, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, ChinaOnyinyechi DuruDepartment of Oncology, Nottingham University Hospital, City Campus, Nottingham, UKShinichiro MorishitaInstitute for Human Movement and Medical Sciences, Niigata University of Health and Welfare, Niigata, JapanWen G. JiangCardiff China Medical Research Collaborative, Cardiff University School of Medicine, Cardiff University, Heath Park, Cardiff, UKWing-Sum TongSchool of Pharmacy, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, ChinaXavier ThomasHematology Department, University of Arizonaospices Civils de Lyon, Lyon-Sud Hospital, Pierre Bénite, FranceYuequan ShiChina Medical University, Liaoning, ChinaZifang ZouChina Medical University, Liaoning, ChinaZihao LiuGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetic and Gene Regulation, Breast Tumor Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Varna, China

Second-Generation Protein Kinase Inhibitor – A Focus on Quizartinib, A Promising Targeted Therapy for High-Risk FLT3+ Patients with Acute Myeloid Leukemia

Xavier Thomas*,Etienne Paubelle
Hematology Department, Hospices Civils de Lyon, Lyon-Sud Hospital, Pierre Bénite, France

Abstract

Fms-like tyrosine kinase 3 (FLT3) is one of the most commonly mutated genes in acute myeloid leukemia (AML). While first-generation FLT3 tyrosine kinase inhibitors are relatively non-specific for FLT3 with other potential targets, the next-generation inhibitors appear more potent and selective. Among them quizartinib is the most clinically advanced. The greater potency and selectivity of this drug promises greater efficacy and less toxicity in FLT3-mutated AML. It is currently studied across virtually all disease settings, and its use in combination with chemotherapy appears promising in FLT3+ patients. In this review, we summarize the current data on quizartinib and the encouraging clinical data that have also emerged with other second- or further-generation FLT3 inhibitors, after recalling results observed with first-generation inhibitors.

Keywords: Acute Myeloid Leukemia, Chemotherapy, c-Kit Inhibition, FLT3 inhibitors, Prognosis, Quizartinib, Relapse, Targeted Therapy, Treatment, Tyrosine Kinase Inhibitors.
*Corresponding author Xavier Thomas: Hematology Department, Hospices Civils de Lyon, Lyon-Sud Hospital, Bât. 1G, 165 chemin du Grand Revoyet, 69495 Pierre Bénite, France; Tel: +33478862235; Fax: +33472678880; E-mail: [email protected]