Contact information
Research groups
Michael McClellan
Post-doctoral Fellow
Mutations, either germline or spontaneous, are the primary cause of all cancers, yet currently there are limited methods that can detect non-clonal mutations. We have developed a technique to plug the gap in our understanding of the origin of mutations at the single molecule level and are currently using it to explore the interplay between polymerase error rate and DNA modification.
Prior to working in Ludwig Cancer Research I completed a PhD at the University of Sussex under the supervision of Professor Michelle West. The project employed ChIP sequencing and gene expression analysis to investigate the host targets of Epstein-Barr virus latent antigens.
Recent publications
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Human DNA polymerase ε is a source of C>T mutations at CpG dinucleotides
Journal article
Tomkova M. et al, (2024), Nature Genetics, 56, 2506 - 2516
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In Vitro Site Directed Mutagenesis.
Journal article
McClellan MJ., (2023), Methods Mol Biol, 2633, 87 - 95
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The non-canonical SMC protein SmcHD1 antagonises TAD formation and compartmentalisation on the inactive X chromosome
Journal article
Gdula MR. et al, (2019), Nature Communications, 10
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Correction: Telomere length and genetics are independent colorectal tumour risk factors in an evaluation of biomarkers in normal bowel
Journal article
Fernandez-Rozadilla C. et al, (2018), British Journal of Cancer, 118, 1683 - 1683
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Erratum to “DNA Replication and associated repair pathways are involved in the mutagenesis of methylated cytosine”[DNA Repair, 62 (2018) 1–7]
Journal article
Tomkova M. et al, (2018), DNA Repair, 65, 79 - 79