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A recent study shows that smoking-induced epigenetic changes in lung epithelium occur even before malignant transformation, and sensitize the cells to allow a single key oncogenic event to initiate the growth of a tumour.
Konget al. report a mechanism that underlies tumour 'drug addiction' in melanoma cell lines and mouse models involving an ERK2-dependent phenotype switch, which might have clinical implications for the use of alternating treatment strategies with targeted therapies.
Zhanget al. report that CD8+tumour-infiltrating T lymphocytes exposed to a hypoglycaemic and hypoxic tumour microenvironment enhance PPARα signalling and fatty acid catabolism to partially preserve effector functions and increase the efficacy of immunotherapy in melanoma mouse models.
Despite advances in targeting oncogenic driver mutations, advanced-stage non-small-cell lung cancer (NSCLC) remains largely incurable due to therapeutic resistance. This Review focuses on how understanding the mechanisms of resistance to targeted therapies in NSCLC can inform improved treatment strategies.
This Review by Mitchellet al. summarizes how engineering and the physical sciences have advanced oncology by highlighting four important areas: the physical microenvironment of the tumour, drug delivery, cellular and molecular imaging, and microfluidics and microfabrication.
Several types of human tumour are dependent on mutations in BRAF. This led to the development of RAF inhibitors, which prolong patient survival but are limited by resistance. This Review discusses the recent advances in our understanding of BRAF oncogenic signalling, RAF inhibitor activity and the implementation of this knowledge for the development of next-generation inhibitors.
Genome-wide association studies (GWAS) uncover the impact of genetic variation on the risk of many common cancers. This Review discusses current insights and how understanding the biological basis of these associations is required to maximise the clinical benefit of GWAS.
