ArticleArchives of toxicology2026
The role of cytotoxicity in the process of carcinogenesis.
Article in Archives of toxicology, 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enhanced cancer prevalence findings restricted to high, cytotoxic dose levels in long-term animal cancer studies are generally assumed to be a consequence of-indirect or secondary-mutational effects, e.g. DNA damage mediated by generation of reactive oxygen species (ROS) or replication errors occurring during regenerative cell proliferation. An alternative explanation is provided by recent findings suggesting that cell lysis caused by cytotoxic doses of non-genotoxic agents may give rise to tumor promotion by selective growth stimulation of pre-existing (already mutated) dormant tumor precursor cells. This growth stimulation is assumed to be mediated by damage-associated molecular pattern (DAMP) signaling ("sterile inflammation"). Here, we discuss the differing views on cancer findings observed only at high cytotoxic doses in particular with respect to the implications for the risk assessment of the agents.
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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.