The Panchromatic Hubble Andromeda Treasury: Triangulum Extended Region (PHATTER) I. Ultraviolet to Infrared Photometry of 22 Million Stars in M33

We present panchromatic resolved stellar photometry for 22 million stars in the Local Group dwarf spiral Triangulum (M33), derived from Hubble Space Telescope (HST) observations with the Advanced Camera for Surveys (ACS) in the optical (F475W, F814W), and the Wide Field Camera 3 (WFC3) in the near ultraviolet (F275W, F336W) and near-infrared (F110W, F160W) bands. The large, contiguous survey area covers $\sim$14 square kpc and extends to 3.5 kpc (14 arcmin, or 1.5-2 scale lengths) from the center of M33. The PHATTER observing strategy and photometry technique closely mimic those of the Panchromatic Hubble Andromeda Treasury (PHAT), but with updated photometry techniques that take full advantage of all overlapping pointings (aligned to within $<$5-10 milliarcseconds) and improved treatment of spatially-varying point spread functions. The photometry reaches a completeness-limited depth of F475W$\sim$28.5 in the lowest surface density regions observed in M33 and F475W$\sim$26.5 in the most crowded regions found near the center of M33. We find the young populations trace several relatively tight arms, while the old populations show a clear, looser two-armed structure. We present extensive analysis of the data quality including artificial star tests to quantify completeness, photometric uncertainties, and flux biases. This stellar catalog is the largest ever produced for M33, and is publicly available for download by the community.Comment: 38 pages, 6 tables, 25 figures, accepted for publication in ApJ

VII Scandinavian Copd Research Symposium, Holmenkollen, Oslo 18th-19th November 2016

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Seabirds reveal mercury distribution across the North Atlantic

Author contributionsC.A. and J.F. designed research; C.A., B. Moe, A.T., S.D., V.S.B., B. Merkel, J.Å., and J.F. performed research; C.A., B. Moe, M.B.-F., A.T., S.D., V.S.B., B. Merkel, J.Å., J.L., C.P.-P., and J.F. analyzed data; C.A., B.M., V.S.B., and J.F. sample and data collection, data coordination and management, statistical methodology; H.S. sample and data contribution and Data coordination and management; D.G., M.B.-F., F. Amélineau, F. Angelier, T.A.-N., O.C., S.C.-D., J.D., K.E., K.E.E., A.E., G.W.G., M.G., S.A.H., H.H.H., M.K.J., Y. Kolbeinsson, Y. Krasnov, M.L., J.L., S.-H.L., B.O., A.P., C.P.-P., T.K.R., G.H.S., P.M.T., T.L.T., and P.B. sample and data contribution; A.T., P.F. and S.D. sample and data contribution and statistical methodology; J.Å. statistical methodology; J.F. supervision; and C.A., B. Moe, H.S., D.G., A.T., S.D., V.S.B., B. Merkel, J.Å., F. Amélineau, F. Angelier, T.A.-N., O.C., S.C.-D., J.D., K.E., K.E.E., A.E., P.F., G.W.G., M.G., S.A.H., H.H.H., Y. Kolbeinsson, Y. Krasnov, S.-H.L., B.O., A.P., T.K.R., G.H.S., P.M.T., T.L.L., P.B., and J.F. wrote the paper.Peer reviewe

Retrospective evaluation of whole exome and genome mutation calls in 746 cancer samples

Funder: NCI U24CA211006Abstract: The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC) curated consensus somatic mutation calls using whole exome sequencing (WES) and whole genome sequencing (WGS), respectively. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2,658 cancers across 38 tumour types, we compare WES and WGS side-by-side from 746 TCGA samples, finding that ~80% of mutations overlap in covered exonic regions. We estimate that low variant allele fraction (VAF < 15%) and clonal heterogeneity contribute up to 68% of private WGS mutations and 71% of private WES mutations. We observe that ~30% of private WGS mutations trace to mutations identified by a single variant caller in WES consensus efforts. WGS captures both ~50% more variation in exonic regions and un-observed mutations in loci with variable GC-content. Together, our analysis highlights technological divergences between two reproducible somatic variant detection efforts

Genomic profiling of intrahepatic cholangiocarcinoma: refining prognosis and identifying therapeutic targets

BACKGROUND: The molecular alterations that drive tumorigenesis in intrahepatic cholangiocarcinoma (ICC) remain poorly defined. We sought to determine the incidence and prognostic significance of mutations associated with ICC among patients undergoing surgical resection. METHODS: Multiplexed mutational profiling was performed using nucleic acids that were extracted from 200 resected ICC tumor specimens from 7 centers. The frequency of mutations was ascertained and the effect on outcome was determined. RESULTS: The majority of patients (61.5 %) had no genetic mutation identified. Among the 77 patients (38.5 %) with a genetic mutation, only a small number of gene mutations were identified with a frequency of >5 %: IDH1 (15.5 %) and KRAS (8.6 %). Other genetic mutations were identified in very low frequency: BRAF (4.9 %), IDH2 (4.5 %), PIK3CA (4.3 %), NRAS (3.1 %), TP53 (2.5 %), MAP2K1 (1.9 %), CTNNB1 (0.6 %), and PTEN (0.6 %). Among patients with an IDH1-mutant tumor, approximately 7 % were associated with a concurrent PIK3CA gene mutation or a mutation in MAP2K1 (4 %). No concurrent mutations in IDH1 and KRAS were noted. Compared with ICC tumors that had no identified mutation, IDH1-mutant tumors were more often bilateral (odds ratio 2.75), while KRAS-mutant tumors were more likely to be associated with R1 margin (odds ratio 6.51) (both P < 0.05). Although clinicopathological features such as tumor number and nodal status were associated with survival, no specific mutation was associated with prognosis. CONCLUSIONS: Most somatic mutations in resected ICC tissue are found at low frequency, supporting a need for broad-based mutational profiling in these patients. IDH1 and KRAS were the most common mutations noted. Although certain mutations were associated with ICC clinicopathological features, mutational status did not seemingly affect long-term prognosis

Sex differences in oncogenic mutational processes

Sex differences have been observed in multiple facets of cancer epidemiology, treatment and biology, and in most cancers outside the sex organs. Efforts to link these clinical differences to specific molecular features have focused on somatic mutations within the coding regions of the genome. Here we report a pan-cancer analysis of sex differences in whole genomes of 1983 tumours of 28 subtypes as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium. We both confirm the results of exome studies, and also uncover previously undescribed sex differences. These include sex-biases in coding and non-coding cancer drivers, mutation prevalence and strikingly, in mutational signatures related to underlying mutational processes. These results underline the pervasiveness of molecular sex differences and strengthen the call for increased consideration of sex in molecular cancer research.Sex differences have been observed in multiple facets of cancer epidemiology, treatment and biology, and in most cancers outside the sex organs. Efforts to link these clinical differences to specific molecular features have focused on somatic mutations within the coding regions of the genome. Here we report a pan-cancer analysis of sex differences in whole genomes of 1983 tumours of 28 subtypes as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium. We both confirm the results of exome studies, and also uncover previously undescribed sex differences. These include sex-biases in coding and non-coding cancer drivers, mutation prevalence and strikingly, in mutational signatures related to underlying mutational processes. These results underline the pervasiveness of molecular sex differences and strengthen the call for increased consideration of sex in molecular cancer research.Peer reviewe