عوامل حساس‌کننده‌ی نوین برای پادتن‌های درمانی ضد EGFR ۲۰۲۲
Novel Sensitizing Agents for Therapeutic Anti-EGFR Antibodies 2022

1. Cover

2. Front Matter

3. Table of Contents

4. Copyright

5. Cover Image Insert

6. Aims and Scope of Series “Breaking Tolerance to Antibody-Mediated Immunotherapy”

7. About the Series Editor

8. Aims and Scope of Volume

9. About the Volume Editor

10. Preface

11. Contributors

12. List of Illustrations

13. List of Tables

14. Chapter 1 : Current status of anti-EGFR agents

15. Chapter 2 : Molecular mechanisms of resistance to the EGFR monoclonal antibody cetuximab

16. Chapter 3 : MM-151 overcomes acquired resistance to cetuximab and panitumumab in colorectal cancers harboring EGFR extracellular domain mutations

17. Chapter 4 : Sym004 anti-EGFR antibody mixture overcomes resistance to anti-EGFR antibodies in metastatic colorectal cancer

18. Chapter 5 : Broad RTK-targeted therapy overcomes molecular heterogeneity-driven resistance to cetuximab via vectored immunoprophylaxis in colorectal cancer

19. Chapter 6 : Pan-HER, an antibody mixture, simultaneously targeting EGFR, HER2, and HER3 effectively overcomes resistance to anti-EGFR antibodies

20. Chapter 7 : Four-in-one antibodies have superior cancer inhibitory activity against EGFR, HER2, HER3, and VEGF through disruption of HER/MET crosstalk

21. Chapter 8 : Overcoming acquired resistance to cetuximab by combining EGFR- and HER3-neutralizing monoclonal antibodies

22. Chapter 9 : Dual targeting of EGFR and HER3 with MEHD7945A overcomes acquired resistance to EGFR inhibitors and radiation

23. Chapter 10 : Targeting ERBB2 overcomes resistance to the anti-EGFR therapeutic antibody cetuximab

24. Chapter 11 : CT16: A dual antibody targeting both EGFR and Notch suppresses EGFR blockage and radiation resistance by decreasing tumor-initiating cell frequency

25. Chapter 12 : BET inhibition overcomes receptor tyrosine kinase-mediated cetuximab resistance in HNSCC

26. Chapter 13 : Dual inhibition of EGFR and c-Src by cetuximab and dasatinib combined with FOLFOX chemotherapy in patients with metastatic colorectal cancer

27. Chapter 14 : A novel bispecific antibody targeting EGFR and cMet is effective against EGFR inhibitor-resistant lung tumors

28. Chapter 15 : Use of MET kinase inhibitors to overcome cetuximab resistance in colorectal cancer

29. Chapter 16 : EGFR- and VEGF(R)-targeted small molecules show synergistic activity in colorectal cancer models refractory to combinations of monoclonal antibodies

30. Chapter 17 : Antitumor activity of the VEGFR inhibitor ZD6474 in human cancer cells resistant to anti-EGFR therapy

31. Chapter 18 : Antibody-mediated delivery of anti-KRAS-siRNA overcomes therapy resistance in colon cancer

32. 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

33. 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

34. Chapter 21 : EGFR/JIP-4/JNK2 signaling attenuates cetuximab-mediated radiosensitization of squamous cell carcinoma cells

35. Chapter 22 : EGFR/Notch antagonists enhance the response to inhibitors of the PI3K-Akt pathway by decreasing tumor-initiating cell frequency

36. Chapter 23 : Inhibition of SLC1A5 sensitizes colorectal cancer to cetuximab

37. Chapter 24 : Targeting of PYK2 synergizes with EGFR antagonists in basal-like TNBC and circumvents HER3-associated resistance via the NEDD4–NDRG1 axis

38. Chapter 25 : Overcoming acquired resistance to EGFR-targeted therapy by regulating autophagy

39. Chapter 26 : Hedgehog signaling alters reliance on EGF receptor signaling and mediates anti-EGFR therapeutic resistance in head and neck cancer

40. Chapter 27 : Novel Toll-like receptor 9 agonist induces epidermal growth factor receptor (EGFR) inhibition and synergistic antitumor activity with EGFR inhibitors

41. Chapter 28 : Targeted cancer therapy: The future of drug combinations

42. Index

43. A