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To date, comprehensive sequencing efforts have elucidated the genomic landscapes of multiple cancer entities and increased our understanding of tumor biology [1]. The identification of tumor-specific somatic mutations associated with respective cellular pathways has paved the way for targeted therapies [2]. Hence somatic mutations may serve as predictive biomarkers of tumor response and may guide clinicians in their decisions about treatment options. The inclusion of genomic data in treatment decisions has frequently been referred to as “personalized medicine ” or “precision medicine”. Although personalized medicine appears to be extremely attractive, a potential drawback is that tumor genomes are instable and that clones resistant to a given therapy can take over. As a consequence sequencing information obtained from
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Auer et al. (2013) studied this question.
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