J. Ross Chapman
Ph.D
Professor of Genome Maintenance Biology
- CRUK CDF, Lister Fellow & EMBO Young Investigator
- Principal Investigator - Genome Integrity Group
Genome stability and DNA repair mechanisms in cancer and genome diversification
Ross Chapman started his career in research in 2002, working as a Research Assistant at the MRC Genome Damage and Stability Centre (University of Sussex, UK). In 2006, he went on to join Prof. Steve Jackson’s laboratory (Gurdon Institute, Cambridge), where his PhD research focused on the regulated assembly of DNA repair and signalling complexes at sites of DNA breaks. As a Sir Henry Wellcome Fellow, Ross continued for a short postdoc in the Jackson laboratory, before leaving in 2010 to join Prof. Simon Boulton’s laboratory at Cancer Research UK Clare Hall Laboratories (London), now part of the present-day Francis Crick Institute. There he studied the regulated interplay between the non-homologous end joining and homologous recombination DNA repair pathways, and their role in immune system development, carcinogenesis and cancer’s response to therapy. Establishing his group in 2013 at the Wellcome Centre for Human Genetics (Nuffield Department of Medicine, University of Oxford), he was elected to Associate Professor in 2017. In 2020 his laboratory moved to join the MRC Molecular Haematology Unit (Oxford), where Ross holds Cancer Research UK and Lister Institute Fellowships. He is also a current member of the EMBO Young Investigator Programme.
The Chapman group’s major research is on genetic recombination mechanisms, and in particular, the role of the major DNA double strand break repair pathways. His group is particularly interested in how cells and different tissues strike an appropriate equilibrium between accurate and mutagenic DNA repair mechanisms, as a means to understand why faults in this regulation lead to cancer and immune-deficiency disorders. An end goal will be to devise innovative strategies to exploit these faults in cancer therapies.
Recent publications
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BLM and BRCA1-BARD1 coordinate complementary mechanisms of joint DNA molecule resolution.
Journal article
Tsukada K. et al, (2024), Mol Cell, 84, 640 - 658.e10
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Shieldin and CST co-orchestrate DNA polymerase-dependent tailed-end joining reactions independently of 53BP1-governed repair pathway choice
Preprint
KING A. et al, (2023)
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Single-cell multi-omics identifies chronic inflammation as a driver of TP53-mutant leukemic evolution.
Journal article
Rodriguez-Meira A. et al, (2023), Nat Genet, 55, 1531 - 1541
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53BP1-shieldin-dependent DSB processing in BRCA1-deficient cells requires CST-Polα-primase fill-in synthesis.
Journal article
Mirman Z. et al, (2022), Nat Cell Biol, 24, 51 - 61
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BARD1 reads H2A lysine 15 ubiquitination to direct homologous recombination.
Journal article
Becker JR. et al, (2021), Nature, 596, 433 - 437
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Defective ALC1 nucleosome remodeling confers PARPi sensitization and synthetic lethality with HRD.
Journal article
Hewitt G. et al, (2021), Mol Cell, 81, 767 - 783.e11
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Targeting TRIM37-driven centrosome dysfunction in 17q23-amplified breast cancer.
Journal article
Yeow ZY. et al, (2020), Nature, 585, 447 - 452
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Functional Radiogenetic Profiling Implicates ERCC6L2 in Non-homologous End Joining.
Journal article
Francica P. et al, (2020), Cell Rep, 32
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An essential role for the Zn2+ transporter ZIP7 in B cell development.
Journal article
Anzilotti C. et al, (2019), Nat Immunol, 20, 350 - 361
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H4K20me0 recognition by BRCA1-BARD1 directs homologous recombination to sister chromatids.
Journal article
Nakamura K. et al, (2019), Nat Cell Biol, 21, 311 - 318