ReviewClinical epigenetics2026
DNMT3A in cancer: from epigenetic writer to oncogenic driver.
Review in Clinical epigenetics, 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
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer is the leading cause of mortality, accounting for one in six deaths worldwide. Despite the emergence of new therapies, cancer mortality remains high. Cancer cells share many traits, such as reprogrammed metabolism and exacerbated proliferation. All these alterations are in part orchestrated by changes in gene expression, notably due to the reshaping of the epigenetic landscape, including DNA methylation marks. Over the past decades, the enzymes responsible for DNA methylation, the DNA methyltransferases (DNMTs), have emerged as important actors in tumorigenesis and therefore as therapeutic targets of choice. Of particular interest is DNMT3A, which plays a critical role in de novo DNA methylation and has been strongly implicated in the pathogenesis of acute myeloid leukemia. Considering the large number of recent studies, this review aims to provide an up-to-date view of knowledge regarding DNMT3A-dependant DNA methylation and its implications for cancer pathophysiology. This review highlights the central position of DNMT3A in cell proliferation, metabolic reprogramming and drug resistance in tumor cells, reinforcing the need for further studies on this protein, which appears to be a key therapeutic target.
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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.