Evidence map›Paper›PMID 40773517›Full record

ArticlePLoS computational biology2025

Machine learning on multiple epigenetic features reveals H3K27Ac as a driver of gene expression prediction across patients with glioblastoma.

Yusuke Suita, Hardy Bright, Yuan Pu, Merih Deniz Toruner, Jordan Idehen, Nikos Tapinos, Ritambhara Singh

Abstract read
In one paragraph

Article in PLoS computational biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Yusuke SuitaLaboratory of Cancer Epigenetics and Plasticity, Department of Neurosurgery, Brown University, Providence, Rhode Island, United States of America.ORCID 0000-0002-8387-4162
Hardy BrightData Science Institute, Brown University, Providence, Rhode Island, United States of America.
Yuan PuCenter for Computational Molecular Biology, Brown University, Providence, Rhode Island, United States of America.ORCID 0009-0008-4227-1833
Merih Deniz TorunerLaboratory of Cancer Epigenetics and Plasticity, Department of Neurosurgery, Brown University, Providence, Rhode Island, United States of America.ORCID 0000-0001-7447-8654
Jordan IdehenDepartment of Computer Science, Brown University, Providence, Rhode Island, United States of America.
Nikos TapinosLaboratory of Cancer Epigenetics and Plasticity, Department of Neurosurgery, Brown University, Providence, Rhode Island, United States of America.ORCID 0000-0002-3798-5363
Ritambhara SinghCenter for Computational Molecular Biology, Brown University, Providence, Rhode Island, United States of America.ORCID 0000-0002-7523-160X

Funding

Deep learning for understanding gene regulation in diseases via 'omics' integrationR35HG011939 · NHGRI · BROWN UNIVERSITY · PI SINGH, RITAMBHARA · 2021 to 2025
$1.9M
NHGRI NIH HHS R35 HG011939
6 · The paper itself

Abstract

Epigenetic mechanisms play a crucial role in driving transcript expression and shaping the phenotypic plasticity of glioblastoma stem cells (GSCs), contributing to tumor heterogeneity and therapeutic resistance. These mechanisms dynamically regulate the expression of key oncogenic and stemness-associated genes, enabling GSCs to adapt to environmental cues and evade targeted therapies. Importantly, epigenetic reprogramming allows GSCs to transition between cellular states, including therapy-resistant mesenchymal-like phenotypes, underscoring the need for epigenetic-targeting strategies to disrupt these adaptive processes. Understanding these epigenetic drivers of gene expression provides a foundation for novel therapeutic interventions aimed at eradicating GSCs and improving glioblastoma outcomes. Using machine learning (ML), we employ cross-patient prediction of transcript expression in GSCs by combining epigenetic features from various sources, including ATAC-seq, CTCF ChIP-seq, RNAPII ChIP-seq, H3K27Ac ChIP-seq, and RNA-seq. We investigate different ML and deep learning (DL) models for this task and ultimately build our final pipeline using XGBoost. The model trained on one patient generalizes to other 11 patients with high performance. Notably, H3K27Ac alone from a single patient is sufficient to predict gene expression in all 11 patients. Furthermore, the distribution of H3K27Ac peaks across the genomes of all patients is remarkably similar. These findings suggest that GSCs share a common distributional pattern of enhancer activity characterized by H3K27Ac, which can be utilized to predict gene expression in GSCs across patients. In summary, while GSCs are known for their transcriptomic and phenotypic heterogeneity, we propose that they share a common epigenetic pattern of enhancer activation that defines their underlying transcriptomic expression pattern. This pattern can predict gene expression across patient samples, providing valuable insights into the biology of GSCs.

Indexed as

Brain NeoplasmsEpigenesis, GeneticGlioblastomaHistonesMachine LearningComputational BiologyGene Expression ProfilingGene Expression Regulation, NeoplasticHumansNeoplastic Stem CellsHistones

Identifiers

PMID40773517
PMCPMC12352877

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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.