I am speaking at #AACR25 this afternoon on our latest work on somatic mutations in normal tissues. If you are attending AACR, feel free to drop by and say hello.
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If you are looking for an exciting postdoc position, please see below! Adrian Baez Ortega (a former member of the group) is starting an independent group at the University of Cambridge on the evolution of transmissible cancers and is recruiting. tinyurl.com/pdra-cambridge

A huge thanks to the many friends and colleagues at Sanger and elsewhere who have made this possible. Particular thanks to the brilliant Andrew Lawson, Pan Nicola and Fede Abascal. Stef Lensing on R&D. And the TwinsUK team and donors for making this collection possible. 🙏19/n

Multivariate regression models then enable mutational epidemiology studies on how exposures and cancer risk factors, such as age, tobacco or alcohol, alter the acquisition and selection of somatic mutations. 16/n

By analysing how the frequency of driver mutations increases with age, we also gained new and unexpected insights into the mode of clonal growth in oral epithelium, which suggests that clonal expansions are highly constrained. 15/n

The high number of positively selected mutations in multiple genes provides high-resolution maps of selection across coding and non-coding sites, a form of in vivo saturation mutagenesis. This reveals very interesting patterns of selection within genes. 14/n

We found 49 genes under positive selection driving clonal expansions in the oral epithelium, over 62,000 driver mutations, and evidence of negative selection in some genes. 12/n

In the new preprint, we present a new NanoSeq protocol with full genome coverage, compatible with targeted or exome capture, with <5e-9 error rate in single DNA molecules. This yields accurate somatic mutation rates, signatures and driver landscapes from any tissue or cell population. 10/n