Accelerating changes in ice mass within Greenland, and the ice sheet's sensitivity to atmospheric forcing

The recent deglaciation of Greenland is a response to both oceanic and atmospheric forcings. From 2000 to 2010, ice loss was concentrated in the southeast and northwest margins of the ice sheet, in large part due to the increasing discharge of marine-terminating outlet glaciers, emphasizing the importance of oceanic forcing. However, the largest sustained (∼10 years) acceleration detected by Gravity Recovery and Climate Experiment (GRACE) occurred in southwest Greenland, an area largely devoid of such glaciers. The sustained acceleration and the subsequent, abrupt, and even stronger deceleration were mostly driven by changes in air temperature and solar radiation. Continued atmospheric warming will lead to southwest Greenland becoming a major contributor to sea level rise

Multiple novel prostate cancer susceptibility signals identified by fine-mapping of known risk loci among Europeans

Genome-wide association studies (GWAS) have identified numerous common prostate cancer (PrCa) susceptibility loci. We have fine-mapped 64 GWAS regions known at the conclusion of the iCOGS study using large-scale genotyping and imputation in 25 723 PrCa cases and 26 274 controls of European ancestry. We detected evidence for multiple independent signals at 16 regions, 12 of which contained additional newly identified significant associations. A single signal comprising a spectrum of correlated variation was observed at 39 regions; 35 of which are now described by a novel more significantly associated lead SNP, while the originally reported variant remained as the lead SNP only in 4 regions. We also confirmed two association signals in Europeans that had been previously reported only in East-Asian GWAS. Based on statistical evidence and linkage disequilibrium (LD) structure, we have curated and narrowed down the list of the most likely candidate causal variants for each region. Functional annotation using data from ENCODE filtered for PrCa cell lines and eQTL analysis demonstrated significant enrichment for overlap with bio-features within this set. By incorporating the novel risk variants identified here alongside the refined data for existing association signals, we estimate that these loci now explain ∼38.9% of the familial relative risk of PrCa, an 8.9% improvement over the previously reported GWAS tag SNPs. This suggests that a significant fraction of the heritability of PrCa may have been hidden during the discovery phase of GWAS, in particular due to the presence of multiple independent signals within the same regio