ArticlebioRxiv : the preprint server for biology2025
Epigenomic dynamics of clonal evolution reveal new regulators of leukemic growth.
Article in bioRxiv : the preprint server for biology, 2025. 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, 1 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
- Updated by
Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanisms driving cell growth during clonal evolution in leukemia are not fully understood. We focused on epigenomic regulation of this process by analyzing the changes of chromatin marks and gene expression in independent leukemic clones evolving towards increased growth. The evolved subclones lost their growth differential ex vivo but restored it upon secondary transplantation, suggesting molecular memory of their evolutionary stage. Genome-wide, clonal evolution was associated with clone-specific gradual modulation of chromatin states and expression levels, with a surprising preferential trend of reversing the prior changes observed at the early leukemic stage. We leveraged clonal specificity of these modulation patterns to focus on the core gene set of potential growth regulators with consistent changes of expression and chromatin marks that were maintained in vivo and ex vivo in both independent clones. We selected three of these genes as candidates (Irx5 and Plag1 as growth suppressors and Smad1 as a driver) and validated their predicted growth effects by overexpression in leukemic subclones. AML patient data confirmed IRX5 and SMAD1 as markers of AML status in patients, suggesting that multiomic analysis of clonal evolution in a mouse model is a valuable predictive approach relevant to human AML.
Identifiers
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.