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Mutations that harm cancer cells accumulate in tumors - despite selective pressures against them - because cancer cells do not genetically recombine and mutate rapidly. These mutations cause proteotoxic stress that can be clinically targeted.

To study the genomic complexity of lung cancers and model tumor growth from initiation, we developed a new technology. We’re now using this technology to mathematically-describe the heterogeneity of tumor growth and identify pharmacogenomic interactions in vivo.