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Hata, Niederstet al. present data suggesting that genetic resistance to the epidermal growth factor receptor (EGFR) inhibitor gefitinib can develop either through selection of clones carrying a pre-existing resistance mutation, or through the eventual de novodevelopment of a resistance mutation in cells that survive initial therapy.
Roybalet al. have designed a system in which two tumour antigens are required to effectively induce T cell activation through chimeric antigen receptors, which in principle could improve the efficacy and safety of T cell therapies.
A new study reports how tracking the evolution of resistance in serial biopsies revealed the molecular mechanisms by which a patient with metastatic non-small-cell lung cancer became resensitized to crizotinib.
An analysis by Tomasetti and Vogelstein prompted considerable debate about the origins of the genetic mutations that drive tumour initiation. Further fuel to this debate has recently been provided by an analysis from Wuet al.
A study inCancer Cell reports that the growth of some isocitrate dehydrogenase 1 (IDH1)-mutant cancers is dependent on their addiction to NAD+, a metabolic vulnerability that can be targeted by drugs that are already in clinical trials.
Nguyen, Pellacaniet al. report data suggesting that a slow multi-step evolutionary process might not be required to generate mammary tumours following KRAS-G12D expression, and that KRAS-G12D-expressing tumours can rapidly accumulate heterogeneous clones.
