Tumor genome sequences present an opportunity to learn about mechanisms causing mutations, usually resulting from disturbances in DNA replication or repair -- a common occurence in cancers.

Genomics also presents an opportunity of how these mutagenic mechanisms can be better exploited to selectively target cancer cells, improving treatment prospects.  I will describe our statistical methods for detecting somatic mutation clustering , and an application thereof to classify mutation signatures resulting from the APOBEC cytosine deaminases (Mas-Ponte & Supek, Nature Genetics 2020). 

Moreover, I will describe a combined experimental and genomic study to uncover the unique vulnerability of APOBEC-overexpressing lung cancer cells the HMCES DNA protective enzyme -- demonstrating a novel of synthetic lethal relationship (Biayna, ..., Supek* and Stracker*, PLOS Biology 2021). 

Finally I will comment on our recent analyses that systematically examined various types of mutation signatures, including APOBEC and many others, as drug sensitivity markers in  cancer cell line panels (Levatic, Salvadores, Fuster & Supek, 2021 biorxiv).
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