"(Re)Visions of the Unicorn: The Case of Scève's Délie (1544)."

The unicorn is a ubiquitous figure redolent with symbolic meaning in the visual culture of the high and late Middle Ages. It is primarily a symbol of Christ in bestiaries and the Physiologus tradition, the hunt for the unicorn is an allegory of the Passion, but scenes of the unicorn near fountains or water sources suggest the latemedieval perception of the horn as a panacea. Beyond this, the one-horned creature represents courtly love as the poet-lover falls prey to the beautiful virgin. Because of this variety, unicorns also populate the genre of emblems1 - an allegorical mode of representation derived from medieval bestiaries consisting of three parts: title, image, and motto. While scholars have shown the significance2 of unicorns in a range of literary and visual arts,3 little scholarship has examined unicorn iconography in early emblem books of 1540s Europe nor has there been much formal analysis of emblem images combined with literary analysis of the accompanying text in emblem books.4 This article considers the shift of unicorn iconography from the allegory of Christ in medieval bestiaries to the symbol of poet-lover in Maurice Scève’s early emblem book Délie, object de plus haulte vertu (1544). The article title indicates a “vision” or sighting of the unicorn in antiquity, the revisions of written and visual depictions throughout history, and the unicorn’s gaze in emblems

Germline variation at 8q24 and prostate cancer risk in men of European ancestry

Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and 52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p < 4.28 × 10−15), including three risk variants that have yet to be reported. From a polygenic risk score (PRS) model, derived to assess the cumulative effect of risk variants at 8q24, men in the top 1% of the PRS have a 4-fold (95%CI = 3.62–4.40) greater risk compared to the population average. These 12 variants account for ~25% of what can be currently explained of the familial risk of prostate cancer by known genetic risk factors. These findings highlight the overwhelming contribution of germline variation at 8q24 on prostate cancer risk which has implications for population risk stratification

Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants

Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Peer reviewe