Letter to the Editor: GEN1 as a potential therapeutic target in gastric cancer

doi:10.4251/wjgo.v18.i9.116896

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World Journal of Gastrointestinal Oncology

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1948-5204

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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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 Gastrointest Oncol. Sep 15, 2026; 18(9): 116896
Published online Sep 15, 2026. doi: 10.4251/wjgo.v18.i9.116896

Letter to the Editor: GEN1 as a potential therapeutic target in gastric cancer

Yusuf Tutar

Yusuf Tutar, Division of Medicinal Biochemistry, Department of Basic Medical Sciences, Faculty of Medicine, Recep Tayyip Erdogan University, Rize 53020, Türkiye

Yusuf Tutar, Health Sciences Faculty, Recep Tayyip Erdogan University, Rize 53020, Türkiye

Yusuf Tutar, Research and Training Hospital, Recep Tayyip Erdogan University, Rize 53020, Türkiye

Yusuf Tutar, Molecular Oncology Division, Health Sciences Institutes, Recep Tayyip Erdogan University, Rize, 53100, Türkiye

Yusuf Tutar, Molecular Medicine Division, Health Sciences Institutes, Recep Tayyip Erdogan University, Rize, 53100, Türkiye

Author contributions: Tutar Y made all the contributions.

Conflict-of-interest statement: Professor Tutar Y has nothing to disclose.

Corresponding author: Yusuf Tutar, PhD, Tenured Professor, Division of Medicinal Biochemistry, Department of Basic Medical Sciences, Faculty of Medicine, Recep Tayyip Erdogan University, Islampaşa, Rize 53020, Türkiye. yusuf.tutar@erdogan.edu.tr

Received: November 24, 2025
Revised: January 6, 2026
Accepted: January 19, 2026
Published online: September 15, 2026
Processing time: 274 Days and 24 Hours

Core Tip

Core Tip: Gastric cancer (GC) growth is driven by complex molecular pathways including genomic instability, cell cycle dysregulation, mitochondrial dysfunction, and ferroptosis. Novel data suggest that GEN1, a Holliday junction resolvase involved in DNA repair, is a key oncogenic regulator in GC that promotes tumor cell proliferation, migration, survival, and chemoresistance, and modulates ferroptosis-related pathways, suggesting that GEN1 may be a therapeutic target and that adding molecular markers related to DNA damage responses may enhance diagnostic accuracy and therapy stratification in GC.