21 research outputs found
Complementarity of Galactic radio and collider data in constraining WIMP dark matter models
In this work we confront dark matter models to constraints that may be
derived from radio synchrotron radiation from the Galaxy, taking into account
the astrophysical uncertainties and we compare these to bounds set by
accelerator and complementary indirect dark matter searches. Specifically we
apply our analysis to three popular particle physics models. First, a generic
effective operator approach, in which case we set bounds on the corresponding
mass scale, and then, two specific UV completions, the Z' and Higgs portals. We
show that for many candidates, the radio synchrotron limits are competitive
with the other searches, and could even give the strongest constraints (as of
today) with some reasonable assumptions regarding the astrophysical
uncertainties.Comment: 22 pages, 12 figure
Functional mechanisms underlying pleiotropic risk alleles at the 19p13.1 breast-ovarian cancer susceptibility locus
A locus at 19p13 is associated with breast cancer (BC) and ovarian cancer (OC) risk. Here we analyse 438 SNPs in this region in 46,451 BC and 15,438 OC cases, 15,252 BRCA1 mutation carriers and 73,444 controls and identify 13 candidate causal SNPs associated with serous OC (P=9.2 × 10-20), ER-negative BC (P=1.1 × 10-13), BRCA1-associated BC (P=7.7 × 10-16) and triple negative BC (P-diff=2 × 10-5). Genotype-gene expression associations are identified for candidate target genes ANKLE1 (P=2 × 10-3) and ABHD8 (P<2 × 10-3). Chromosome conformation capture identifies interactions between four candidate SNPs and ABHD8, and luciferase assays indicate six risk alleles increased transactivation of the ADHD8 promoter. Targeted deletion of a region containing risk SNP rs56069439 in a putative enhancer induces ANKLE1 downregulation; and mRNA stability assays indicate functional effects for an ANKLE1 3′-UTR SNP. Altogether, these data suggest that multiple SNPs at 19p13 regulate ABHD8 and perhaps ANKLE1 expression, and indicate common mechanisms underlying breast and ovarian cancer risk