Version 1
: Received: 21 June 2024 / Approved: 21 June 2024 / Online: 24 June 2024 (04:30:16 CEST)
How to cite:
Tanabe, S.; Quader, S.; Ono, R.; Cabral, H.; Aoyagi, K.; Yokozaki, H.; Sasaki, H.; Perkins, E. The Pathway Flow Starting From Chronic Reactive Oxygen Species Leading to Human Treatment-Resistant Gastric Cancer. Preprints2024, 2024061539. https://doi.org/10.20944/preprints202406.1539.v1
Tanabe, S.; Quader, S.; Ono, R.; Cabral, H.; Aoyagi, K.; Yokozaki, H.; Sasaki, H.; Perkins, E. The Pathway Flow Starting From Chronic Reactive Oxygen Species Leading to Human Treatment-Resistant Gastric Cancer. Preprints 2024, 2024061539. https://doi.org/10.20944/preprints202406.1539.v1
Tanabe, S.; Quader, S.; Ono, R.; Cabral, H.; Aoyagi, K.; Yokozaki, H.; Sasaki, H.; Perkins, E. The Pathway Flow Starting From Chronic Reactive Oxygen Species Leading to Human Treatment-Resistant Gastric Cancer. Preprints2024, 2024061539. https://doi.org/10.20944/preprints202406.1539.v1
APA Style
Tanabe, S., Quader, S., Ono, R., Cabral, H., Aoyagi, K., Yokozaki, H., Sasaki, H., & Perkins, E. (2024). The Pathway Flow Starting From Chronic Reactive Oxygen Species Leading to Human Treatment-Resistant Gastric Cancer. Preprints. https://doi.org/10.20944/preprints202406.1539.v1
Chicago/Turabian Style
Tanabe, S., Hiroki Sasaki and Edward Perkins. 2024 "The Pathway Flow Starting From Chronic Reactive Oxygen Species Leading to Human Treatment-Resistant Gastric Cancer" Preprints. https://doi.org/10.20944/preprints202406.1539.v1
Abstract
The injury causes resistance in human gastric cancer (GC). This Adverse Outcome Pathway (AOP) entitled “Increases in cellular reactive oxygen species (ROS) and chronic ROS leading to human treatment-resistant gastric cancer (GC)” consists of molecular initiating event (MIE) as “Increases in cellular ROS” and “Chronic ROS”, followed by series of key events (KEs); “porcupine-induced Wnt secretion and Wnt signaling activation”, “beta-catenin activation”, “epithelial-mesenchymal transition (EMT), and adverse outcome (AO) as “human treatment-resistant GC” in the sequence. ROS has multiple roles in disease such as development and progression of cancer, or apoptotic induction causing anti-tumor effects. In this AOP, we focus on the role of sustained levels of chronic ROS to induce the therapy-resistance in human GC. EMT, which is cellular phenotypic change from epithelial to mesenchymal-like features, demonstrates cancer stem cell (CSC)-like characteristics in human GC. EMT is induced by Wnt/beta-catenin signaling, providing the rationale to have Wnt secretion and beta-catenin activation as KEs in the AOP.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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