ReviewDisease models & mechanisms2025
The physiological functions of ascorbate in the development of cancer.
Review in Disease models & mechanisms, 2025. 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.
- Loss of vitamin C biosynthesis protects from the pathology of a parasitic infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
The metabolite ascorbate (vitamin C) is synthesized endogenously in most animals or, in humans and some other species, obtained from the diet. Its role in cancer development is controversial. Addition of ascorbate to cultured cells or high-dose administration in animals can inhibit growth of many cancers, but most of these effects are caused by non-physiological biochemical activities. Few experiments have tested the physiological roles of ascorbate in cancer development by depleting it in physiological settings. Ascorbate depletion inhibits the activity of ten-eleven translocation (TET) enzymes in hematopoietic and leukemia cells and accelerates myeloid leukemia development. Many clinical trials have tested ascorbate supplementation in cancers and shown little or no evidence that it has a beneficial role. I propose that depletion experiments are needed to define the cancers in which ascorbate has a physiological role, establish its cellular and molecular targets, and provide a rationale for clinical trials.
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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 OpenQuestion graph.