ArticleCell stem cell2017
Dominating the Negative: How DNMT3A Mutations Contribute to AML Pathogenesis.
Article in Cell stem cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed, 5 citations in OpenAlex.
- Double mutant DNMT3A AML: a unique subtype experiencing increased DNA damage and poor prognosis.Blood advances · 2025Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Somatic mutations in DNMT3A are one of the most prevalent genetic abnormalities found in acute myeloid leukemia (AML) patients. A new study by Guryanova et al. sheds mechanistic insight into how the most common DNMT3A variant protein contributes to AML using a combination of mouse genetics and primary patient samples.
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What OpenQuestion holds
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.