Author

Ana M. Dopico-Fernandez

University of OxfordORCID 0009-0007-7314-3319Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Molecular Biology· 2 Cancer Biology· 1

Signature Assays, Organisms & Methods

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Assay:ChIP-seq· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Organism:human· 2 Assay:ATAC-seq· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Approach:deep learning· 1

Frequent Co-Authors

Catherine ChahrouriD· 3 shared James O. J. DaviesiD· 3 shared Thomas A. MilneiD· 3 shared Alastair SmithiD· 2 shared Anindita RoyiD· 2 shared Huimin GengiD· 2 shared Irene A.G. RobertsiD· 2 shared Joe R. HarmaniD· 2 shared

Activity by Year

2023-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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3 shared papersMolecular Biology

Catherine ChahrourORCID

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3 papers

Recent·Most cited

Molecular BiologybioRxivPreprintFeb 19, 2026

FACT safeguards promoter topology by maintaining nucleosomes and restricting chromatin factor spreading

Ana M. Dopico-Fernandez, Hangpeng Li, Catherine Chahrour…·Thomas A. Milne

This study shows FACT maintains promoter topology by preserving nucleosomes and preventing chromatin factor spreading into gene bodies.

1 citation

ChIP-seqexperimental assay

𝕏 PostBluesky

Cancer BiologyBloodPeer-reviewedJul 29, 2025

Enhancer heterogeneity in acute lymphoblastic leukemia drives differential gene expression between patients

Alastair Smith, Nicholas Denny, Catherine Chahrour…·Thomas A. Milne

This study identifies enhancer heterogeneity as a driver of transcriptional differences in KMT2A::AFF1 ALL patients, revealing patient-specific enhancer activity at oncogenes.

8 citationstop 2%

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Molecular BiologyNature CommunicationsPeer-reviewedAug 25, 2023

PAF1 and FACT cooperate with MLL-AF4 to drive enhancer activity in leukemia

Nicholas T. Crump, Alastair Smith, Laura Godfrey…·Thomas A. Milne

This study identifies PAF1 and FACT as essential for enhancer activity in MLL-AF4-driven leukemia by maintaining histone acetylation and enhancer-promoter interactions.

27 citations

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