Author

Alfonso Bellacosa

Fox Chase Cancer CenterORCID 0000-0001-6278-6801Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cancer Biology· 2 Cell Biology· 2

Signature Assays, Organisms & Methods

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Organism:human· 4 Research Focus:differential expression· 2 Assay:DNA methylation· 2 Research Focus:drug response / drug discovery· 2 Approach:experimental assay· 2 Organism:mouse· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1

Frequent Co-Authors

Colin R. GodingiD· 2 shared Évelyne SageiD· 2 shared Jérémy H. RaymondiD· 2 shared Lionel LarueiD· 2 shared Madeleine Le CoziD· 2 shared Marie PouteauxiD· 2 shared Martin Walsh· 2 shared Michael HAMM· 2 shared

Activity by Year

2026-2026 · peak 4/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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2 shared papersCell Biology

Colin R. GodingORCID

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4 papers

Recent·Most cited

Cell BiologybioRxivPreprintOct 22, 2026

BRN2 preserves the melanocyte lineage following ionizing radiation

Jérémy H. Raymond, Madeleine Le Coz, Zackie Aktary…·Lionel Larue

This study shows BRN2 is essential for preserving melanocyte lineage integrity after ionizing radiation, but not for normal maintenance.

DOI 10.64898/2026.10.18.759918

𝕏 PostBluesky

Cell BiologybioRxivPreprintOct 4, 2026

BRN2 suppresses stress-induced hair greying

Jérémy H. Raymond, Madeleine Le Coz, Zackie Aktary…·Lionel Larue

This study identifies BRN2 as a regulator of melanocyte stem cell resilience under genotoxic stress, showing its role in preventing irradiation-induced hair greying.

DOI 10.64898/2026.09.28.754993

𝕏 PostBluesky

Cancer BiologybioRxivPreprintSep 22, 2026

DNMT1-Mediated Epigenetic Reprogramming Drives KMT2A Amplifications and Rearrangements

Madison A. Lineberger, Zach H. Gray, Benjamin I. Ferman…·Johnathan R. Whetstine

The paper identifies a DNA-histone methylation axis that drives KMT2A amplifications and rearrangements in leukemia, revealing therapeutic targets.

DOI 10.64898/2026.09.21.753283

humanDNA methylation

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Cancer BiologyCell Reports MedicinePeer-reviewedMar 1, 2026

Pol is a functional dependency and therapeutic vulnerability in DNMT3A deficient leukemia cells

Bac Viet Le, Umeshkumar M. Vekariya, Monika Maria Toma…·Tomasz Skórski

This study identifies Polθ as a therapeutic target in DNMT3A-mutated leukemia by showing its essential role in DNA repair and replication fork restart, and demonstrates that its inhibition enhances standard therapies.

1 citation

humanDNA methylation

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