ReviewLife medicine2026
The multistep progression of areca nut-induced oral cancer: a mechanistic roadmap from pathogenesis to precision therapy.
Review in Life medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Areca nut is classified as a Group 1 carcinogen by the International Agency for Research on Cancer. It is a widely consumed psychoactive substance with profound cultural roots in regions including Hunan, Hainan, and Taiwan of China. Its key bioactive components include alkaloids (e.g. arecoline and arecaidine) and areca nut-specific nitrosamines, that induce DNA damage, reactive oxygen species bursts, and chronic inflammation in oral tissues. Coupled with mechanical trauma from chewing, these insults drive the malignant progression of oral submucous fibrosis to oral cavity carcinomas. This review systematically outlines the pathological progression from normal oral mucosa to invasive oral cavity carcinomas, highlighting two core mediators of oral submucous fibrosis carcinogenesis: immune microenvironment reprogramming and oncogenic signaling activation. Furthermore, this review elaborates the molecular mechanisms of areca nut-induced oral cancer, providing a theoretical foundation for biomarker discovery and the development of novel therapeutic strategies. It also provides actionable guidance for reducing the incidence of areca nut-related oral cavity carcinomas and improving patient prognosis.
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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.