Ming RJ, Liu HW. Letter to the Editor: Not one disease - ethnic-specific mutational pathways redefine precision oncology in esophageal cancer. World J Gastroenterol 2026; 32(27): 116615 [DOI: 10.3748/wjg.116615]
Corresponding Author of This Article
Hua-Wen Liu, MD, Professor, Department of Oncology, Chongqing University Three Gorges Hospital, No. 165 Xincheng Road, Chongqing 404010, China. liuhuawen@cqu.edu.cn
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Genetics & Heredity
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letter
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Ming RJ, Liu HW. Letter to the Editor: Not one disease - ethnic-specific mutational pathways redefine precision oncology in esophageal cancer. World J Gastroenterol 2026; 32(27): 116615 [DOI: 10.3748/wjg.116615]
World J Gastroenterol. Jul 21, 2026; 32(27): 116615 Published online Jul 21, 2026. doi: 10.3748/wjg.116615
Letter to the Editor: Not one disease - ethnic-specific mutational pathways redefine precision oncology in esophageal cancer
Rui-Jie Ming, Hua-Wen Liu
Rui-Jie Ming, Hua-Wen Liu, Department of Oncology, Chongqing University Three Gorges Hospital, Chongqing 404010, China
Author contributions: Ming RJ wrote the original draft; Liu HW contributed to reviewing and editing; Ming RJ and Liu HW participated in drafting the manuscript; both authors have read and approved the final version of the manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Hua-Wen Liu, MD, Professor, Department of Oncology, Chongqing University Three Gorges Hospital, No. 165 Xincheng Road, Chongqing 404010, China. liuhuawen@cqu.edu.cn
Received: November 17, 2025 Revised: January 7, 2026 Accepted: February 4, 2026 Published online: July 21, 2026 Processing time: 230 Days and 21.8 Hours
Abstract
Precision oncology in esophageal squamous cell carcinoma has long operated under the implicit assumption that it is a single biological entity. In a study published in the World Journal of Gastroenterology, Wei et al provide a compelling and definitive challenge to this monolithic view. Through whole-exome sequencing of Han and Kazakh populations, they revealed not just different driver genes, but fundamentally distinct carcinogenic processes: A predominance of the apolipoprotein B messenger RNA-editing enzyme catalytic polypeptide-related mutational signatures in the Han cohort vs signatures of defective DNA mismatch repair in the Kazakh group. This finding transcends descriptive genomics; it suggests that esophageal squamous cell carcinoma in these populations may represent two different diseases at the molecular level. Clinically, this has profound implications. It questions the global applicability of clinical trial data derived from homogeneous populations and argues for the urgent need to incorporate ethnic diversity into genomic databases and trial design. Most provocatively, the authors uncover a crucial paradox: The Kazakh cohort, despite having poorer historical survival, exhibits a higher tumor mutational burden, a biomarker that paradoxically suggests the potential for heightened sensitivity to immune checkpoint inhibitors. This study is therefore a landmark, shifting the paradigm from treating a single cancer type to tailoring therapy based on distinct, ethnic-specific mutational etiologies.
Core Tip: This letter highlights that esophageal squamous cell carcinoma is not a single entity but comprises ethnically distinct molecular subtypes. While Han patients exhibit the apolipoprotein B messenger RNA-editing enzyme catalytic polypeptide-related signatures, Kazakh patients show defective mismatch repair. We emphasize a critical paradox: Despite worse historical survival, Kazakh tumors display high tumor mutational burden, suggesting potential sensitivity to immunotherapy. These findings urge the integration of ethnic genomics into clinical trial design to transform therapeutic strategies for underrepresented populations.
