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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
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
Core Tip

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.

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