Wei MF. Letter to the Editor: Yin Yang 1 in inflammatory memory and progression susceptibility in Helicobacter pylori–associated gastric cancer. World J Clin Oncol 2026; 17(6): 116895 [DOI: 10.5306/wjco.116895]
Corresponding Author of This Article
Meng-Fan Wei, Zhejiang Chinese Medical University, School of Medical Technology and Information Engineering, Puyan Street, Binjiang District, Hangzhou 310053, Zhejiang Province, China. 202312210701027@zcmu.edu.cn
Research Domain of This Article
Gastroenterology & Hepatology
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letter
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Wei MF. Letter to the Editor: Yin Yang 1 in inflammatory memory and progression susceptibility in Helicobacter pylori–associated gastric cancer. World J Clin Oncol 2026; 17(6): 116895 [DOI: 10.5306/wjco.116895]
World J Clin Oncol. Jun 24, 2026; 17(6): 116895 Published online Jun 24, 2026. doi: 10.5306/wjco.116895
Letter to the Editor: Yin Yang 1 in inflammatory memory and progression susceptibility in Helicobacter pylori–associated gastric cancer
Meng-Fan Wei
Meng-Fan Wei, Zhejiang Chinese Medical University, School of Medical Technology and Information Engineering, Hangzhou 310053, Zhejiang Province, China
Author contributions: Wei MF drafted the manuscript.
Conflict-of-interest statement: The author has no relevant conflicts of interest.
Corresponding author: Meng-Fan Wei, Zhejiang Chinese Medical University, School of Medical Technology and Information Engineering, Puyan Street, Binjiang District, Hangzhou 310053, Zhejiang Province, China. 202312210701027@zcmu.edu.cn
Received: November 24, 2025 Revised: December 16, 2025 Accepted: February 2, 2026 Published online: June 24, 2026 Processing time: 210 Days and 20.5 Hours
Abstract
Chen et al recently published a study in World Journal of Clinical Oncology, demonstrated that Helicobacter pylori induces Yin Yang 1 (YY1) expression and activates the Janus kinase 2-signal transducer and activator of transcriptional protein 3 pathway, thereby promoting epithelial–mesenchymal transition and gastric cancer progression. This commentary highlights how their findings refine the mechanistic understanding of a chronic infection–driven oncogenic cascade and positions YY1 as a central regulator linking inflammatory stimulation with malignant evolution. When considered within the broader framework of inflammatory memory and epigenetic imprinting, the sustained upregulation of YY1 across precancerous stages suggests that YY1 may function as a molecular imprint of chronic injury and a determinant of individual susceptibility to disease progression.
Core Tip: This commentary discusses the study by Chen et al, which demonstrated that Yin Yang 1 (YY1) mediates Helicobacter pylori (H. pylori)-induced activation of the Janus kinase 2-signal transducer and activator of transcriptional protein 3 pathway and epithelial–mesenchymal transition in gastric cancer. By integrating recent work on innate and epithelial inflammatory memory with the broader biology of YY1 in malignancy, this article proposes that sustained and heterogeneous upregulation of YY1 may represent an inflammation-derived transcriptional imprint and an early determinant of susceptibility to disease progression. These insights open new directions for risk stratification and pathway-targeted prevention in H. pylori-infected individuals.
