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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.
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.
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.
Protein-linked DNA breaks can be formed through the abortive activity of topoisomerases — this Review discusses the roles of such breaks during transcription and in triggering gene deletions and translocations in cancer.
Mutations in the gene encoding DNA methyltransferase 3A (DNMT3A) have been reported in patients with various haematological malignancies, suggesting that DNMT3A could be a tumour suppressor. In this Review, Yanget al. put data from basic science studies into clinical context, opening stimulating discussions regarding possible new therapeutic avenues.
This Analysis uses the published literature to form a DNA damage response network and then uses this to identify potential synthetic lethal interactions and to assess the druggability of proteins in the DNA damage response network.
Lynch syndrome is caused by heterozygous mutations and epimutations in mismatch repair genes, which lead to specific pathologies, including increased risk of multiple types of cancer and microsatellite instability. Lynch syndrome has been pivotal to the history of understanding hereditary cancer-prone syndromes and continues to lead the way in our understanding of the risk and treatment of familial cancers.
