Author

Malgorzata Gozdecka

University of CambridgeORCID 0000-0002-3134-1276Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Research Focus:benchmarking· 1 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Assay:DNA methylation· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

Brian J.P. HuntlyiD· 2 shared George S. VassiliouiD· 2 shared Alfonso BellacosaiD· 1 shared Anna-Mariya Kukuyan· 1 shared Bac Viet LeiD· 1 shared Berthold GöttgensiD· 1 shared David Lara‐AstiasoiD· 1 shared Dhoyazan AzaziiD· 1 shared

Activity by Year

2025-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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2 shared papersCancer Biology

Brian J.P. HuntlyORCID

Mutual co-authors in cluster

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2 papers

Recent·Most cited

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

Bac Viet Le, Umeshkumar M. Vekariya, Monika Maria Toma, Margaret Nieborowska-Skorska, Marie‐Christine Caron, Malgorzata Gozdecka, Zayd Haydar, Martin Walsh, Jayashri Ghosh, Elaine Vaughan‐Williams, Paulina Podszywalow‐Bartnicka, Anna-Mariya Kukuyan, Sylwia Ziółkowska, Jessica Atkins, Emir Hadzijusufovic, , 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.

Cell Reports Medicine · Mar 1, 2026Peer-reviewedCancer Biology

Delayed Trp53 activation protects Dnmt3a-mutant hematopoietic stem cells from inflammatory attrition.

Ludovica Marando, George Giotopoulos, Pedro Madrigal, Dhoyazan Azazi, Ryan J. Asby, María Eréndira Calleja-Cervantes, Muxin Gu, David Lara‐Astiaso, Nicola K. Wilson, Rebecca Hannah, Jaana Bagri, Emily F. Calderbank, Elisa Laurenti, Elsa Bernard, Sarah J. Horton, , Brian J.P. Huntly

This study shows that DNMT3A R882H mutant HSCs resist inflammatory stress through delayed p53 activation, leading to clonal expansion and increased AML risk.

bioRxiv · Jan 27, 2025 · PreprintMolecular Biology