ReviewMolecular oncology2026
Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer.
Review in Molecular oncology, 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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Authors and funding
8 authors.
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Abstract
Various environmental and endogenous stressors, including ultraviolet (UV) radiation, cytotoxins, and dysregulated translation, can induce ribosome stalling and collisions, disrupting protein homeostasis. The ribotoxic stress response (RSR) is a cellular surveillance mechanism that senses translational stress and activates stress signaling via the MAP3 kinase ZAKα and the stress-activated protein kinases (SAPKs) p38 and JNK. This review outlines the molecular mechanisms behind RSR, distinguishes RSR from other translational stress response pathways, such as the well-studied integrated stress response (ISR), discusses the role of RSR in key cellular processes, and presents new evidence linking RSR to cancer biology. We explore how ribotoxic stress is exploited by chemotherapeutic agents and other compounds to induce cancer cell death, and the potential limitations of such therapeutic strategy. Finally, we highlight future considerations for inducing the RSR pathway in cancer, highlighting both therapeutic potential and the challenges in this emerging field.
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