The clustering of galaxies in the SDSS-III Baryon Oscillation Spectroscopic Survey : BAO measurement from the LOS-dependent power spectrum of DR12 BOSS galaxies

HGM is grateful for support from the UK Science and Technology Facilities Council through the grant ST/I001204/1. WJP is grateful for support from the UK Science and Technology Facilities Research Council through the grant ST/I001204/1, and the European Research Council through the grant “Darksurvey”, reference 614030. FSK acknowledges the support of the Karl-Schwarzschild Program from the Leibniz Society.[abridged] We present an anisotropic analysis of the baryonic acoustic oscillation (BAO) scale in the twelfth and final data release of the Baryonic Oscillation Spectroscopic Survey (BOSS). We independently analyse the LOWZ and CMASS galaxy samples: the LOWZ sample contains contains 361\,762 galaxies with an effective redshift of $z_{\rm LOWZ}=0.32$, and the CMASS sample consists of 777\,202 galaxies with an effective redshift of $z_{\rm CMASS}=0.57$. We extract the BAO peak position from the monopole power spectrum moment, $\alpha_0$, and from the $\mu^2$ moment, $\alpha_2$. We report $H(z_{\rm LOWZ})r_s(z_d)=(11.64\pm0.62)\cdot10^3\,{\rm km}s^{-1}$ and $D_A(z_{\rm LOWZ})/r_s(z_d)=6.85\pm0.17$ with a cross-correlation coefficient of $r_{HD_A}=0.42$, for the LOWZ sample; and $H(z_{\rm CMASS})r_s(z_d)=(14.56\pm0.38)\cdot10^3\,{\rm km}s^{-1}$ and $D_A(z_{\rm CMASS})/r_s(z_d)=9.42\pm0.13$ with a cross-correlation coefficient of $r_{HD_A}=0.51$, for the CMASS sample. We combine these results with the measurements of the BAO peak position in the monopole and quadrupole correlation function of the same dataset \citep[][companion paper]{Cuestaetal2015} and report the consensus values: $H(z_{\rm LOWZ})r_s(z_d)=(11.64\pm0.70)\cdot10^3\,{\rm km}s^{-1}$ and $D_A(z_{\rm LOWZ})/r_s(z_d)=6.76\pm0.15$ with $r_{HD_A}=0.35$ for the LOWZ sample; and $H(z_{\rm CMASS})r_s(z_d)=(14.66\pm0.42)\cdot10^3\,{\rm km}s^{-1}$ and $D_A(z_{\rm CMASS})/r_s(z_d)=9.47\pm0.13$ with $r_{HD_A}=0.54$ for the CMASS sample.Publisher PDFPeer reviewe

Interaction between the microbiome and TP53 in human lung cancer.

BACKGROUND: Lung cancer is the leading cancer diagnosis worldwide and the number one cause of cancer deaths. Exposure to cigarette smoke, the primary risk factor in lung cancer, reduces epithelial barrier integrity and increases susceptibility to infections. Herein, we hypothesize that somatic mutations together with cigarette smoke generate a dysbiotic microbiota that is associated with lung carcinogenesis. Using lung tissue from 33 controls and 143 cancer cases, we conduct 16S ribosomal RNA (rRNA) bacterial gene sequencing, with RNA-sequencing data from lung cancer cases in The Cancer Genome Atlas serving as the validation cohort. RESULTS: Overall, we demonstrate a lower alpha diversity in normal lung as compared to non-tumor adjacent or tumor tissue. In squamous cell carcinoma specifically, a separate group of taxa are identified, in which Acidovorax is enriched in smokers. Acidovorax temporans is identified within tumor sections by fluorescent in situ hybridization and confirmed by two separate 16S rRNA strategies. Further, these taxa, including Acidovorax, exhibit higher abundance among the subset of squamous cell carcinoma cases with TP53 mutations, an association not seen in adenocarcinomas. CONCLUSIONS: The results of this comprehensive study show both microbiome-gene and microbiome-exposure interactions in squamous cell carcinoma lung cancer tissue. Specifically, tumors harboring TP53 mutations, which can impair epithelial function, have a unique bacterial consortium that is higher in relative abundance in smoking-associated tumors of this type. Given the significant need for clinical diagnostic tools in lung cancer, this study may provide novel biomarkers for early detection

Interaction between the microbiome and TP53 in human lung cancer

Abstract Background Lung cancer is the leading cancer diagnosis worldwide and the number one cause of cancer deaths. Exposure to cigarette smoke, the primary risk factor in lung cancer, reduces epithelial barrier integrity and increases susceptibility to infections. Herein, we hypothesize that somatic mutations together with cigarette smoke generate a dysbiotic microbiota that is associated with lung carcinogenesis. Using lung tissue from 33 controls and 143 cancer cases, we conduct 16S ribosomal RNA (rRNA) bacterial gene sequencing, with RNA-sequencing data from lung cancer cases in The Cancer Genome Atlas serving as the validation cohort. Results Overall, we demonstrate a lower alpha diversity in normal lung as compared to non-tumor adjacent or tumor tissue. In squamous cell carcinoma specifically, a separate group of taxa are identified, in which Acidovorax is enriched in smokers. Acidovorax temporans is identified within tumor sections by fluorescent in situ hybridization and confirmed by two separate 16S rRNA strategies. Further, these taxa, including Acidovorax, exhibit higher abundance among the subset of squamous cell carcinoma cases with TP53 mutations, an association not seen in adenocarcinomas. Conclusions The results of this comprehensive study show both microbiome-gene and microbiome-exposure interactions in squamous cell carcinoma lung cancer tissue. Specifically, tumors harboring TP53 mutations, which can impair epithelial function, have a unique bacterial consortium that is higher in relative abundance in smoking-associated tumors of this type. Given the significant need for clinical diagnostic tools in lung cancer, this study may provide novel biomarkers for early detection