Targeted Therapies in Esophageal Squamous Cell Carcinoma
Summary
Esophageal squamous cell carcinoma (ESCC) remains a formidable clinical challenge, owing to its genetic heterogeneity, high metastatic potential and resistance to conventional chemoradiotherapy. Targeted therapies seek to exploit molecular vulnerabilities—most notably dysregulated receptor tyrosine kinases such as the epidermal growth factor receptor (EGFR), aberrant signalling pathways (for example Wnt/β-catenin and PI3K/AKT) and factors within the tumour microenvironment that foster immune evasion and radioresistance. Small-molecule inhibitors and monoclonal antibodies directed against EGFR have delivered proof-of-concept activity, while emerging targets including neurotrophic receptor tyrosine kinase 2 (NTRK2), Src family kinases and components of DNA-damage response networks are under investigation. The current paradigm emphasises biomarker-driven patient selection, combination regimens pairing targeted agents with radiotherapy or immunotherapy, and adaptive strategies to overcome acquired resistance. Global efforts continue to refine dosing, minimise toxicity and enhance durable responses in diverse populations.
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Targeted Therapies in Esophageal Squamous Cell Carcinoma publication trend
The graph below shows the total number of articles in targeted therapies in esophageal squamous cell carcinoma across all publications each year (not limited to Nature Index journals).
Technical terms
Epidermal growth factor receptor (EGFR): A cell-surface receptor tyrosine kinase that, when aberrantly activated, drives tumour proliferation and survival.
Tyrosine kinase inhibitor (TKI): A small molecule that blocks phosphorylation activity of specific kinases to disrupt oncogenic signalling.
Patient-derived xenograft (PDX): A preclinical model in which human tumour tissue is implanted into immunodeficient mice to evaluate therapeutic responses.
Tumour microenvironment (TME): The complex milieu of stromal cells, immune infiltrates and extracellular matrix that influences tumour growth and treatment sensitivity.
Wnt/β-catenin pathway: A signalling cascade regulating cell proliferation and differentiation, often co-opted in cancer to promote stemness and metastasis.
References
- Clinical efficacy and identification of factors confer resistance to afatinib (tyrosine kinase inhibitor) in EGFR-overexpressing esophageal squamous cell carcinoma. Signal Transduction and Targeted Therapy (2024).
- Mouse avatar models of esophageal squamous cell carcinoma proved the potential for EGFR-TKI afatinib and uncovered Src family kinases involved in acquired resistance. Journal of Hematology & Oncology (2018).
- SAMD9 Promotes Postoperative Recurrence of Esophageal Squamous Cell Carcinoma by Stimulating MYH9‐Mediated GSK3β/β‐Catenin Signaling. Advanced Science (2023).
- Mechanisms of radiotherapy resistance and radiosensitization strategies for esophageal squamous cell carcinoma. Molecular Cancer (2023).
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