A Boston University- and US Army Research Institute of Infectious Diseases-led team presents findings from a genome sequencing analysis of the Egyptian rousette (Rousettus aegyptiacus), a bat host capable of asymptomatically carrying filoviruses such as Marburg virus. The researchers put together a 1.9 billion base draft genome assembly from short- and long-read sequences, uncovering almost 19,700 predicted protein-coding genes supported by available RNA sequence and protein data. Their phylogenetic and comparative genomic analyses provided a look at the bat's relationships, while identifying immune gene expansions, diversifications, and signaling changes that boost bat tolerance to viral infection. These and other features in the new genome "strengthen the notion of the unique biology of bats," the authors note, "and suggest the existence of a distinct immunomodulatory mechanism used to control viral infection."
Canadian researchers report on results from a phylogenetic analysis on nearly 300 prostate cancers, uncovering features ranging from tumor sub-clonal architecture to mutation patterns marking earlier and later stages of prostate tumor evolution. The team analyzed new and previously generated genome sequence data for matched tumor and normal samples from 293 individuals with localized prostate cancer, turning to somatic single nucleotide changes and copy number shifts to profile tumor sub-clones. In more than half of the tumors, the analysis unearthed multiple tumor sub-clones, which were considered alongside the patients' clinicopathological features. Where 61 percent of prostate cancer patients with high-risk, polyclonal tumors went on to relapse after primary therapy, for example, such relapse occurred in just 7 percent of individuals with monoclonal tumors, prompting the authors to suggest that "multiple sub-clones in an index biopsy may be necessary, but not sufficient, for relapse of localized prostate cancer."
A team from the US, Korea, and Japan describes its "chemistry-first" strategy for finding personalized lung cancer treatment targets. The researchers began by profiling more than 202,100 chemical library compounds in combination with 96 non-small cell lung cancer lines, matched normal samples from a subset of the same individuals, and four immortalized bronchial epithelial lung cell lines, assessed by RNA sequencing, exome sequencing, SNP arrays, reverse phase protein arrays, and/or other approaches. Based on 171 genetic-chemical associations identified there, they attempted to tease out druggable targets in lung cancer patients lacking clear treatment targets. Based on their results, the authors argue that "many undeveloped avenues remain open for productive pursuit of tumor-intrinsic precision medicine."