The Wilkinson Microwave Anisotropy Probe WMAP has mapped the entire sky in five frequency bands between 23 and 94 GHz with polarization sensitive radiometers. We present three-year full-sky maps of the polarization and analyze them for foreground emission and cosmological implications. These observations open up a new window for understanding the universe. WMAP observes significant levels of polarized foreground emission due to both Galactic synchrotron radiation and thermal dust emission. The least contaminated channel is at 61 GHz. Informed by a model of the Galactic foreground emission, we subtract the foreground emission from the maps. In the foreground corrected maps, for l=2-6, we detect l(l+1) C_l^{EE} / (2 pi) = 0.086 +-0.029 microkelvin^2. This is interpreted as the result of rescattering of the CMB by free electrons released during reionization and corresponds to an optical depth of tau = 0.10 +- 0.03. We see no evidence for B-modes, limiting them to l(l+1) C_l^{BB} / (2 pi) = -0.04 +- 0.03 microkelvin^2. We find that the limit from the polarization signals alone is r<2.2 (95% CL) corresponding to a limit on the cosmic density of gravitational waves of Omega_{GW}h^2 < 5 times 10^{-12}. From the full WMAP analysis, we find r<0.55 (95% CL) corresponding to a limit of Omega_{GW}h^2 < 10^{-12} (95% CL).Comment: 105 pgs, 28 figs. Accepted version of the 3-year paper as posted to http://lambda.gsfc.nasa.gov/product/map/dr2/map_bibliography.cfm in January 200

Copy number variants (CNVs) account for a major proportion of human genetic polymorphism and have been predicted to have an important role in genetic susceptibility to common disease. To address this we undertook a large, direct genome-wide study of association between CNVs and eight common human diseases. Using a purpose-designed array we typed ∼19,000 individuals into distinct copy-number classes at 3,432 polymorphic CNVs, including an estimated ∼50% of all common CNVs larger than 500 base pairs. We identified several biological artefacts that lead to false-positive associations, including systematic CNV differences between DNAs derived from blood and cell lines. Association testing and follow-up replication analyses confirmed three loci where CNVs were associated with disease—IRGM for Crohn’s disease, HLA for Crohn’s disease, rheumatoid arthritis and type 1 diabetes, and TSPAN8 for type 2 diabetes—although in each case the locus had previously been identified in single nucleotide polymorphism (SNP)-based studies, reflecting our observation that most common CNVs that are well-typed on our array are well tagged by SNPs and so have been indirectly explored through SNP studies. We conclude that common CNVs that can be typed on existing platforms are unlikely to contribute greatly to the genetic basis of common human diseases.

Andrea Sottoriva, Trevor Graham and colleagues analyze tumor sequencing data and show that a substantial proportion of cancers of many different types are characterized by neutral evolution resulting in a characteristic power-law distribution of the mutant allele frequencies. This neutral framework provides a new way to interpret cancer genomic data and to discriminate between functional and non-functional intratumoral heterogeneity. Despite extraordinary efforts to profile cancer genomes, interpreting the vast amount of genomic data in the light of cancer evolution remains challenging. Here we demonstrate that neutral tumor evolution results in a power-law distribution of the mutant allele frequencies reported by next-generation sequencing of tumor bulk samples. We find that the neutral power law fits with high precision 323 of 904 cancers from 14 types and from different cohorts. In malignancies identified as evolving neutrally, all clonal selection seemingly occurred before the onset of cancer growth and not in later-arising subclones, resulting in numerous passenger mutations that are responsible for intratumoral heterogeneity. Reanalyzing cancer sequencing data within the neutral framework allowed the measurement, in each patient, of both the in vivo mutation rate and the order and timing of mutations. This result provides a new way to interpret existing cancer genomic data and to discriminate between functional and non-functional intratumoral heterogeneity.

We report the observation of the $X(3872)$ in the $J/\psi {\pi }^{+}{\pi }^{-}$ channel, with $J/\psi$ decaying to ${\mu }^{+}{\mu }^{-}$, in $p\overline{p}$ collisions at $\sqrt{s}=1.96\mathrm{T}\mathrm{e}\mathrm{V}$. Using approximately $230{\mathrm{p}\mathrm{b}}^{-1}$ of data collected with the Run II D0 detector, we observe $522\pm 100$ $X(3872)$ candidates. The mass difference between the $X(3872)$ state and the $J/\psi$ is measured to be $774.9\pm 3.1(\mathrm{s}\mathrm{t}\mathrm{a}\mathrm{t})\pm 3.0(\mathrm{s}\mathrm{y}\mathrm{s}\mathrm{t})\mathrm{M}\mathrm{e}\mathrm{V}/c^2$. We have investigated the production and decay characteristics of the $X(3872)$ and find them to be similar to those of the $\psi (2S)$ state.