ReviewCell death discovery2026
The "Hit-and-Run" legacy: epigenetic locking and the survival switch in H. pylori-associated gastric cancer.
Review in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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0 citing papers in PubMed.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mortality associated with gastric cancer (GC) is mostly attributed to metastasis that is resistant to therapy, presenting a therapeutic challenge that frequently continues even after effective eradication of Helicobacter pylori (H. pylori). This paper addresses the "eradication paradox" by introducing a novel conceptual framework, the "Survival Switch" hypothesis: H. pylori infection not only induces a temporary epithelial-mesenchymal transition (EMT) but also stabilizes gastric epithelial cells in a persistent, drug-resistant "Hybrid Epithelial/Mesenchymal (Hybrid E/M) state." We systematically outline this evolutionary trajectory through three distinct phases: (1) The Igniter: The virulence factor Cytotoxin-associated gene A (CagA) compromises junctional integrity and commandeers YAP/ZEB1 signaling to initiate plasticity; (2) The Lock: A "Hit-and-Run" mechanism establishes "epigenetic scarring," specifically methyltransferase-like 3 (METTL3)-mediated N
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.