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A family-based genome-wide association study of chronic rhinosinusitis with nasal polyps implicates several genes in the disease pathogenesis.

Abstract The pathogenesis of chronic rhinosinusitis with nasal polyps is largely unknown. Previous studies have given valuable information about genetic variants associated with this disease but much is still unexplained. Our goal was to identify genetic markers and genes associated with susceptibility to chronic rhinosinusitis with nasal polyps using a family-based genome-wide association study.
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Journal Title plos one
Publication Year Start




PMID- 29253858
OWN - NLM
STAT- In-Process
LR  - 20171224
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 12
DP  - 2017
TI  - A family-based genome-wide association study of chronic rhinosinusitis with nasal
      polyps implicates several genes in the disease pathogenesis.
PG  - e0185244
LID - 10.1371/journal.pone.0185244 [doi]
AB  - BACKGROUND: The pathogenesis of chronic rhinosinusitis with nasal polyps is
      largely unknown. Previous studies have given valuable information about genetic
      variants associated with this disease but much is still unexplained. Our goal was
      to identify genetic markers and genes associated with susceptibility to chronic
      rhinosinusitis with nasal polyps using a family-based genome-wide association
      study. METHODS: 427 patients (293 males and 134 females) with CRSwNP and 393
      controls (175 males and 218 females) were recruited from several Swedish
      hospitals. SNP association values were generated using DFAM (implemented in
      PLINK) and Efficient Mixed Model Association eXpedited (EMMAX). Analyses of
      pathway enrichment, gene expression levels and expression quantitative trait loci
      were then performed in turn. RESULTS: None of the analysed SNPs reached genome
      wide significant association of 5.0 x 10-8. Pathway analyses using our top 1000
      markers with the most significant association p-values resulted in 138 target
      genes. A comparison between our target genes and gene expression data from the
      NCBI Gene Expression Omnibus database showed significant overlap for 36 of these 
      genes. Comparisons with data from expression quantitative trait loci showed the
      most skewed allelic distributions in cases with chronic rhinosinusitis with nasal
      polyps compared with controls for the genes HLCS, HLA-DRA, BICD2, VSIR and
      SLC5A1. CONCLUSION: Our study indicates that HLCS, HLA-DRA, BICD2, VSIR and
      SLC5A1 could be involved in the pathogenesis of chronic rhinosinusitis with nasal
      polyps. HLA-DRA has been associated with chronic rhinosinusitis with nasal polyps
      in previous studies and HLCS, BICD2, VSIR and SLC5A1 may be new targets for
      future research.
FAU - Bohman, Anton
AU  - Bohman A
AUID- ORCID: http://orcid.org/0000-0001-6875-603X
AD  - Department of Otorhinolaryngology, Uppsala University Hospital, Uppsala, Sweden.
FAU - Juodakis, Julius
AU  - Juodakis J
AD  - Department of Obstetrics and Gynecology, Institute of Clinical Sciences,
      Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
FAU - Oscarsson, Martin
AU  - Oscarsson M
AD  - Department of Otorhinolaryngology, Skaraborg Hospital, Skovde, Sweden.
FAU - Bacelis, Jonas
AU  - Bacelis J
AD  - Department of Obstetrics and Gynecology, Institute of Clinical Sciences,
      Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
FAU - Bende, Mats
AU  - Bende M
AD  - Department of Otorhinolaryngology, Skaraborg Hospital, Skovde, Sweden.
FAU - Torinsson Naluai, Asa
AU  - Torinsson Naluai A
AD  - Department of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska 
      Academy, University of Gothenburg, Gothenburg, Sweden.
LA  - eng
PT  - Journal Article
DEP - 20171218
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
PMC - PMC5734761
EDAT- 2017/12/19 06:00
MHDA- 2017/12/19 06:00
CRDT- 2017/12/19 06:00
PHST- 2017/02/17 00:00 [received]
PHST- 2017/09/09 00:00 [accepted]
PHST- 2017/12/19 06:00 [entrez]
PHST- 2017/12/19 06:00 [pubmed]
PHST- 2017/12/19 06:00 [medline]
AID - 10.1371/journal.pone.0185244 [doi]
AID - PONE-D-17-06556 [pii]
PST - epublish
SO  - PLoS One. 2017 Dec 18;12(12):e0185244. doi: 10.1371/journal.pone.0185244.
      eCollection 2017.