یادداشتهای مربوط به کتابنامه ، واژه نامه و نمایه های داخل اثر
متن يادداشت
Includes bibliographical references and index.
یادداشتهای مربوط به مندرجات
متن يادداشت
Intro; Aims and Scope; Series Editor Biography; Acknowledgment; Preface; Contents; Contributors; About the Editors; Chapter 1: Introduction to the Acquisition of Resistance to Targeted Therapy; 1.1 Introduction; 1.2 Molecular Events Leading to the Acquisition of Resistance to Targeted Therapy; 1.2.1 Alterations in Drug Target Expression to Prevent Therapeutic Action; 1.2.2 Activation of Compensatory Pathways; 1.2.3 Activation of Alternative Pathways to Ensure Survival; 1.2.4 Epigenome: Regulating Acquired Resistance and Modifying Drug Activity
متن يادداشت
1.3 Cellular Events Contributing to the Development of Resistance1.3.1 Transformation/Dedifferentiation Mechanisms and Indirect Resistance to Therapeutic Action; 1.3.2 The Tumor Microenvironment and the Development of Resistance to Targeted Therapies; 1.3.3 The Activity of Drug Efflux Transporters; 1.3.4 Other Considerations of Mechanisms Potentially Contributing to the Acquisition of Resistance; 1.4 Specific Mechanisms of Acquired Resistance to Select Targeted Therapies; 1.4.1 Mechanisms of Resistance to Anti-Angiogenic Therapy; 1.4.2 Resistance to Tyrosine Kinase Inhibitors
متن يادداشت
1.4.3 Resistance to Anti-Apoptosis Inhibitors1.5 Future Directions of Targeted Therapy; References; Chapter 2: Targeting the Tumor Microenvironment to Overcome Resistance to Therapy; 2.1 Introduction; 2.2 Key Components of the Tumor Microenvironment That Contribute to the Acquisition of Resistance; 2.2.1 Extracellular Matrix Regulation of Invasion and Metastasis; 2.2.2 Soluble Factors in the Tumor Microenvironment Modulate Tumor-Stromal Crosstalk; 2.2.3 Inflammation and Immunity Modulate the Tumorigenic Niche; 2.2.4 The Angiogenic Switch in Tumorigenesis
متن يادداشت
2.2.5 Exosomes Are the Transporters of the Tumor Microenvironment2.3 Targeting the Tumor Microenvironment to Overcome Resistance to Therapy; 2.3.1 Discovering a Novel Role of Neuraminidase-1 Activity in Multistage Tumorigenesis; 2.3.2 Role of GPCR Transactivation in Neuraminidase-1 Activity; 2.3.3 Targeting Neuraminidase-1 Activity as the Achilles Heel of the Tumor Microenvironment; 2.4 Conclusions; References; Chapter 3: Current Challenges and Applications of Oncolytic Viruses in Overcoming the Development of Resistance to Therapies in Cancer; 3.1 Introduction; 3.2 Types of Oncolytic Viruses
متن يادداشت
3.2.1 Adenovirus3.2.2 Herpes Simplex Virus 1 (HSV-1); 3.2.3 Vaccinia Virus (VV); 3.2.4 Reovirus Type 3 Dearing; 3.2.5 Measles Virus (MV); 3.2.6 Poliovirus (PV); 3.2.7 Coxsackievirus (CV); 3.2.8 Vesicular Stomatitis Virus (VSV); 3.2.9 Maraba Virus (MRB); 3.3 Oncolytic Viral Targeting of the Tumor Vasculature; 3.4 Targeting Components of the Tumor Extracellular Matrix with Virotherapy to Overcome Therapy Resistance; 3.4.1 Tumor Extracellular Matrix Limits Oncolytic Virus Efficacy; 3.4.2 ECM-Modifying OVs Can Overcome ECM-Mediated Resistance
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یادداشتهای مربوط به خلاصه یا چکیده
متن يادداشت
Targeted therapies were initially developed to exploit the upregulation and dependence on key oncogenic pathways critical to cancer progression. Additionally, they also presented as a method to overcome chemoresistance by supplementing conventional therapeutic regimens with targeted therapies. However, the development of resistance to these combinatorial approaches has led to the reassessment of currently available therapeutic options to overcome resistance to targeted therapy. This book aims to provide an update on the advancements in the therapeutic arms race between cancer, clinicians and scientists alike to overcome resistance to targeted therapies. Subject experts provide a comprehensive overview of the challenges and solutions to resistance to several conventional targeted therapies in addition to providing a discussion on broad topics including targeting components of the tumor microenvironment, emerging therapeutic options, and novel areas to be explored concerning nanotechnology and the epigenome.