Novel Sensitizing Agents for Therapeutic Anti-EGFR Antibodies

Shi Hu

• Publisher: Academic Press
• Year: 2022
• Print ISBN:
  9780128215845
• eBook ISBN:
  9780128215852
• Topic: Biological Sciences
• Subtopic: Biology
• Index: Biological Sciences

Novel Sensitizing Agents for Therapeutic Anti-EGFR Antibodies presents a description of the sensitizers used to overcome resistance to anti-EGFR targeted antibody therapies in cancer, including novel engineered antibody drugs and other sensitizers. The book gives insights into the landscape of anti-EGFR based cancer treatments, the challenges of targeted therapy, and a glimpse into the future of antibody therapy. It offers pertinent science information on strategies used for the rational design and discovery of novel sensitizing agents, and in addition, translational studies involving pre-clinical and clinical design. This book is an indispensable resource for cancer researchers, medicinal chemists and other biomedical scientists.Finally, the book covers basic science strategies used in drug discovery and preclinical evaluation focused on EGFR blockage resistance, as well as clinical trial methodology, including clinical pharmacokinetics and imaging to address issues of efficacy evaluation of the new anticancer sensitizers for anti-EGFR drug resistance. - Presents detailed descriptions on the history, chemistry, mechanism of action, structure-function relationships, pharmacology, side effects, dosing and formulation of new sensitizers to anti-EGFR antibodies - Provides molecular structures for all novel anticancer drugs, along with strategies to overcome resistance to anti-EGFR antibodies - Encompasses up-to-date information on the cancer drug discovery process, including new research tools, tumor-targeting strategies, and fundamental concepts in emerging areas of precision medicine

Table of contents

• Cover
• Front Matter
• Table of Contents
• Copyright
• Cover Image Insert
• Aims and Scope of Series “Breaking Tolerance to Antibody-Mediated Immunotherapy”
• About the Series Editor
• Aims and Scope of Volume
• About the Volume Editor
• Preface
• Contributors
• List of Illustrations
• List of Tables
• Chapter 1 : Current status of anti-EGFR agents
• Chapter 2 : Molecular mechanisms of resistance to the EGFR monoclonal antibody cetuximab
• Chapter 3 : MM-151 overcomes acquired resistance to cetuximab and panitumumab in colorectal cancers harboring EGFR extracellular domain mutations
• Chapter 4 : Sym004 anti-EGFR antibody mixture overcomes resistance to anti-EGFR antibodies in metastatic colorectal cancer
• Chapter 5 : Broad RTK-targeted therapy overcomes molecular heterogeneity-driven resistance to cetuximab via vectored immunoprophylaxis in colorectal cancer
• Chapter 6 : Pan-HER, an antibody mixture, simultaneously targeting EGFR, HER2, and HER3 effectively overcomes resistance to anti-EGFR antibodies
• Chapter 7 : Four-in-one antibodies have superior cancer inhibitory activity against EGFR, HER2, HER3, and VEGF through disruption of HER/MET crosstalk
• Chapter 8 : Overcoming acquired resistance to cetuximab by combining EGFR- and HER3-neutralizing monoclonal antibodies
• Chapter 9 : Dual targeting of EGFR and HER3 with MEHD7945A overcomes acquired resistance to EGFR inhibitors and radiation
• Chapter 10 : Targeting ERBB2 overcomes resistance to the anti-EGFR therapeutic antibody cetuximab
• Chapter 11 : CT16: A dual antibody targeting both EGFR and Notch suppresses EGFR blockage and radiation resistance by decreasing tumor-initiating cell frequency
• Chapter 12 : BET inhibition overcomes receptor tyrosine kinase-mediated cetuximab resistance in HNSCC
• Chapter 13 : Dual inhibition of EGFR and c-Src by cetuximab and dasatinib combined with FOLFOX chemotherapy in patients with metastatic colorectal cancer
• Chapter 14 : A novel bispecific antibody targeting EGFR and cMet is effective against EGFR inhibitor-resistant lung tumors
• Chapter 15 : Use of MET kinase inhibitors to overcome cetuximab resistance in colorectal cancer
• Chapter 16 : EGFR- and VEGF(R)-targeted small molecules show synergistic activity in colorectal cancer models refractory to combinations of monoclonal antibodies
• Chapter 17 : Antitumor activity of the VEGFR inhibitor ZD6474 in human cancer cells resistant to anti-EGFR therapy
• Chapter 18 : Antibody-mediated delivery of anti-KRAS-siRNA overcomes therapy resistance in colon cancer
• Chapter 19 : Primary and acquired resistance of colorectal cancer cells to anti-EGFR antibodies converge on MEK/ERK pathway activation and can be overcome by combined MEK/EGFR inhibition
• Chapter 20 : MEK1/2 inhibitors AS703026 and AZD6244 may be potential therapies for KRAS-mutated colorectal cancer that is resistant to EGFR monoclonal antibody therapy
• Chapter 21 : EGFR/JIP-4/JNK2 signaling attenuates cetuximab-mediated radiosensitization of squamous cell carcinoma cells
• Chapter 22 : EGFR/Notch antagonists enhance the response to inhibitors of the PI3K-Akt pathway by decreasing tumor-initiating cell frequency
• Chapter 23 : Inhibition of SLC1A5 sensitizes colorectal cancer to cetuximab
• Chapter 24 : Targeting of PYK2 synergizes with EGFR antagonists in basal-like TNBC and circumvents HER3-associated resistance via the NEDD4–NDRG1 axis
• Chapter 25 : Overcoming acquired resistance to EGFR-targeted therapy by regulating autophagy
• Chapter 26 : Hedgehog signaling alters reliance on EGF receptor signaling and mediates anti-EGFR therapeutic resistance in head and neck cancer
• Chapter 27 : Novel Toll-like receptor 9 agonist induces epidermal growth factor receptor (EGFR) inhibition and synergistic antitumor activity with EGFR inhibitors
• Chapter 28 : Targeted cancer therapy: The future of drug combinations
• Index
• A