ReviewJournal of translational medicine2026
Post-translational modification networks in tumor radiosensitivity: mechanistic insights and therapeutic opportunities.
Review in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
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Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundRadiotherapy is a central modality in cancer management, yet intrinsic and acquired radioresistance and dose-limiting normal tissue toxicities continue to constrain durable tumor control. Beyond genetic and transcriptional programs, post-translational modifications (PTMs) provide rapid and reversible regulation that can rewire radiation responses across tumor and stromal compartments. MAIN BODY: This review synthesizes recent advances defining how major PTM axes, including ADP-ribosylation, ubiquitination and deubiquitination, neddylation, SUMOylation, methylation, acetylation, and lactylation, shape tumor radiosensitivity and radiation-induced injury. We highlight mechanistic links to DNA damage recognition and repair pathway choice, chromatin remodeling, checkpoint control, and cell-fate decisions encompassing apoptosis and ferroptosis. We further discuss how PTM-driven metabolic and redox adaptation influences post-irradiation signaling, and how PTMs modulate anti-tumor immunity by affecting immunogenic cell death, antigen presentation, cytokine networks, and immune checkpoint regulation within the tumor microenvironment. In addition, we summarize emerging evidence for reciprocal crosstalk between PTM enzymes and non-coding RNAs, which can act as upstream regulators, scaffolds, or effectors to reinforce context-specific modification patterns and therapeutic vulnerabilities.
conclusionsViewing radioresponse through a PTM-network lens reveals actionable nodes for radiosensitization and radioprotection. Targeting PTM writers, erasers, and readers, alone or in rational combinations with radiotherapy, DNA damage response inhibitors, epigenetic agents, and immunotherapy, may overcome resistance while improving the therapeutic window. Future efforts should prioritize context-specific biomarkers, on-target toxicity management, and mechanism-informed trial designs to translate PTM-guided strategies into clinically meaningful gains.
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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.