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This Week in Science: Nov 3, 2017

In Science this week, two independent research teams publish studies showing how gut bacteria can influence cancer patients' responses to immunotherapy. In the first, investigators examined the effect antibiotics have on the outcomes lung or kidney cancer patients undergoing immunotherapy with PD-1 inhibitors. They found that patients who had recently taken antibiotics have reduced survival compared with those who had not. Analysis of patients' gut microbes showed that an abundance of the bacterium Akkermansia muciniphila was associated with the best clinical outcome. Further experimentation showed that mice given the bacteria experienced increased immune system efficiency. In the second study, researchers showed that melanoma patients who respond better to PD-1 inhibitors have greater gut microbe diversity and abundance of certain bacteria. By analyzing gut microbiome samples from 112 patients, the team discovered that those whose microbiomes were enriched with the bacteria Faecalibacterium and Clostridiales were more likely to respond to treatment and to experience longer, progression-free survival. Patients whose gut microbiomes were enriched with Bacteroidales bacteria experienced the opposite effect. An analysis of patient immune responses suggested that those with the beneficial microbes tended to have more immune cells and better immune system activity. GenomeWeb has more on these here.

And in Science Translational Medicine, a group of US and German researchers publishes a study indicating that inhibition of a particular DNA repair pathway may help treat some childhood solid tumors, which are often difficult to treat due to their rapid development of drug resistance. The scientists found that many childhood solid tumors express the active DNA transposase PGBD5, which can promote site-specific genomic rearrangements in human cells, and that human cells deficient in nonhomologous end joining (NHEJ) cannot tolerate PGBD5 expression. Treating PGBD5-expression cancer cells with the NHEJ inhibitor AZD6738 triggered apoptosis, while combining AZD6738 with the DNA-damaging chemotherapeutic agent cisplatin resulted in enhanced apoptosis and regression of human neuroblastoma and medulloblastoma tumors in mouse models.