Research progress on the mechanisms of resistance to cetuximab targeted therapy in head and neck squamous cell carcinoma.
10.13201/j.issn.2096-7993.2025.06.016
- Author:
Lulu LIU
1
;
Dan LUO
1
;
Wenqing ZHANG
2
;
Zhenfeng SUN
1
Author Information
1. Department of Otolaryngology Head and Neck surgery，Shanghai General Hospital，Shanghai Jiao Tong University School Of Medicine，Shanghai，200080，China.
2. Department of Otolaryngology，Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine.
- Publication Type:English Abstract
- Keywords:
cetuximab;
head and neck squamous cell carcinoma;
resistance mechanisms;
targeted therapy
- MeSH:
Humans;
Cetuximab/therapeutic use*;
Drug Resistance, Neoplasm;
Squamous Cell Carcinoma of Head and Neck/drug therapy*;
Head and Neck Neoplasms/drug therapy*;
ErbB Receptors/metabolism*;
Tumor Microenvironment;
Epithelial-Mesenchymal Transition;
Molecular Targeted Therapy;
Antineoplastic Agents, Immunological/therapeutic use*
- From:
Journal of Clinical Otorhinolaryngology Head and Neck Surgery
2025;39(6):582-589
- CountryChina
- Language:Chinese
-
Abstract:
Head and neck squamous cell carcinoma （HNSCC） is one of the ten most common cancers worldwide and is one of the refractory cancers with a poor prognosis in otorhinolaryngology-head and neck surgery. Cetuximab is widely used in the clinical treatment of HNSCC and has been approved by the FDA as a first-line chemotherapeutic agent. However, its efficacy varies significantly among different individuals. Therefore, exploring the resistance mechanisms of cetuximab in the treatment of HNSCC and screening for sensitive populations are essential for the precision treatment of head and neck cancer. This article summarizes the research progress on cetuximab resistance mechanisms in HNSCC, and the main aspects include: alterations in epidermal growth factor receptor （EGFR） and its ligands, changes in downstream effectors of EGFR, bypass activation and crosstalk, epithelial-mesenchymal transition, epigenetic modifications, and immunosuppression in the tumor microenvironment.
