Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Two studies have shown that DNA polymerase-θ (POLQ) promotes an alternative form of non-homologous end-joining (alt-NHEJ) and suppresses homologous recombination (HR) in mammalian cells. The activity of alt-NHEJ is essential for the survival of cells deficient in HR.
Stites and Trampontet al. used mathematical modelling with verification in cells and cancer genome data to understand the effects of weakly activating RAS mutations. They found that pairs of mutations within the RAS pathway might be able to act together to create a selective advantage in human tumours.
Hosteet al. discuss whether allergic immune responses, which have been observed to be protective against some types of cancer, can be activated to target cancer, and what the mechanism of antitumour allergic responses might be.
Two studies have examined how manipulation of energy availability by cancer cells, mediated by changes in microRNAs (miRNAs), can fuel metastatic colonization.
Madsenet al. have delineated the roles of components of the striatin-interacting phosphatase and kinase (STRIPAK) complex in cancer cell migration and metastasis, which may explain why some of these proteins are overexpressed or mutated in cancer.
Yodaet al. have shown that mutations in G protein-β (Gβ) subunits occur in haematological malignancies and can transform cells. Mutant Gβ can also confer resistance to different therapeutic kinase inhibitors.
Why do inherited germline mutations in common cancer-associated genes cause a restricted pattern of tissue-specific malignancies, but when somatic mutations occur in these genes they exhibit far less tissue restriction?
