Steven A. Roberts

The paper identifies transient squamous-state excursions in cancer cells as a source of APOBEC3A mutagenesis, linking it to lineage-state plasticity rather than persistent inflammation.

The paper identifies APOBEC3A as the main RNA editor in human cells and viruses, showing its preference for specific motifs in mRNA and viral RNA.

This study identifies factors influencing 8-oxoG-induced mutagenesis in human cells, revealing a hierarchical DNA repair network and chromatin structure effects on mutation patterns.

The paper shows that a hypomorphic mutation in RPA subunit rfa1-t33 in yeast enhances APOBEC-induced mutagenesis and alters mutation spectra.

This paper identifies genetic modifiers of APOBEC-induced mutagenesis in yeast and human tumors, revealing factors that influence mutation patterns and DNA repair mechanisms.

This study shows the yeast Shu complex prevents mutagenesis from 3meC lesions by binding to them and reducing replication errors.

This study elucidates how DNA Polymerase Theta identifies microhomologies during repair and shows how this process leads to genomic scars in cancer.

The paper analyzes whole-genome sequencing data from cancer samples to identify genomic footprints of telomere maintenance mechanisms, finding specific telomere variant repeat patterns associated with ATRX/DAXX mutations.

The paper examines how somatic structural variations affect TAD boundaries and gene regulation in human cancers using whole genome sequencing data.

This study analyzes chromothripsis in 2,658 cancers using whole-genome sequencing, finding it prevalent across multiple cancer types with complex structural alterations.