A common cancer gene works in part by helping tumours to evade immune cells.

Dean Felsher of Stanford University in California and his colleagues studied the effects of MYC — a gene that is often overexpressed in cancer — in a mouse model of a type of leukaemia. They found that higher MYC expression levels increased the production of two proteins, PD-L1 and CD47, that help cancer cells to hide from the immune system. When MYC was inactivated, CD47 and PD-L1 levels dropped and tumour size decreased. Tumour data from humans showed a strong link between levels of MYC expression and levels of these immune-evasion signals.

People with cancers that overexpress MYC could benefit from treatments that boost the immune attack against tumours, the authors suggest.

Science http://doi.org/bc7p (2016)