ArticleNature cancer2025
TRIM28-dependent developmental heterogeneity determines cancer susceptibility through distinct epigenetic states.
Article in Nature cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- Chronic High-Fat Diet Does Not Alter Overall Cancer Incidence in Trp53R270H/+ Mice.Cancer research communications · 2026Article
- Roles of TIF1β in Leukemic Stem Cell Through SETDB1-Dependent and Independent Mechanisms.Cancer science · 2026Review
- Decoding epigenetic and transcriptional landscapes: DNA methylome-transcriptome integration reveals novel drivers in 4NQO-Induced esophageal squamous cell carcinoma mouse model.Clinical epigenetics · 2025Article
- GECSI: Large-scale chromatin state imputation from gene expression.bioRxiv : the preprint server for biology · 2025Article
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18 authors.
Funding
Abstract
Mutations in cancer risk genes increase susceptibility, but not all carriers develop cancer. Indeed, while DNA mutations are necessary drivers of cancer, only a small subset of mutated cells go on to cause the disease. To date, the mechanisms underlying individual cancer susceptibility remain unclear. Here, we took advantage of a unique mouse model of intrinsic developmental heterogeneity (Trim28
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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.