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Statements

Subject Item
n2:RIV%2F46747885%3A24510%2F11%3A%230000325%21RIV12-MSM-24510___
rdf:type
n11:Vysledek skos:Concept
rdfs:seeAlso
http://www.biomedcentral.com/1471-2407/11/327
dcterms:description
Background: Several predisposition loci for hereditary prostate cancer (HPC) have been suggested, including HPCX1 at Xq27-q28, but due to the complex structure of the region, the susceptibility gene has not yet been identified. Methods: In this study, nonsense-mediated mRNA decay (NMD) inhibition was used for the discovery of truncating mutations. Six prostate cancer (PC) patients and their healthy brothers were selected from a group of HPCX1-linked families. Expression analyses were done using Agilent 44 K oligoarrays, and selected genes were screened for mutations by direct sequencing. In addition, microRNA expression levels in the lymphoblastic cells were analyzed to trace variants that might alter miRNA expression and explain partly an inherited genetic predisposion to PC. Results: Seventeen genes were selected for resequencing based on the NMD array, but no truncating mutations were found. The most interesting variant was MAGEC1 p.Met1?. An association was seen between the variant and unselected PC (OR = 2.35, 95% CI = 1.10-5.02) and HPC (OR = 3.38, 95% CI = 1.10-10.40). miRNA analysis revealed altogether 29 miRNAs with altered expression between the PC cases and controls. miRNA target analysis revealed that 12 of them also had possible target sites in the MAGEC1 gene. These miRNAs were selected for validation process including four miRNAs located in the X chromosome. The expressions of 14 miRNAs were validated in families that contributed to the significant signal differences in Agilent arrays. Conclusions: Further functional studies are needed to fully understand the possible contribution of these miRNAs and MAGEC1 start codon variant to PC. Background: Several predisposition loci for hereditary prostate cancer (HPC) have been suggested, including HPCX1 at Xq27-q28, but due to the complex structure of the region, the susceptibility gene has not yet been identified. Methods: In this study, nonsense-mediated mRNA decay (NMD) inhibition was used for the discovery of truncating mutations. Six prostate cancer (PC) patients and their healthy brothers were selected from a group of HPCX1-linked families. Expression analyses were done using Agilent 44 K oligoarrays, and selected genes were screened for mutations by direct sequencing. In addition, microRNA expression levels in the lymphoblastic cells were analyzed to trace variants that might alter miRNA expression and explain partly an inherited genetic predisposion to PC. Results: Seventeen genes were selected for resequencing based on the NMD array, but no truncating mutations were found. The most interesting variant was MAGEC1 p.Met1?. An association was seen between the variant and unselected PC (OR = 2.35, 95% CI = 1.10-5.02) and HPC (OR = 3.38, 95% CI = 1.10-10.40). miRNA analysis revealed altogether 29 miRNAs with altered expression between the PC cases and controls. miRNA target analysis revealed that 12 of them also had possible target sites in the MAGEC1 gene. These miRNAs were selected for validation process including four miRNAs located in the X chromosome. The expressions of 14 miRNAs were validated in families that contributed to the significant signal differences in Agilent arrays. Conclusions: Further functional studies are needed to fully understand the possible contribution of these miRNAs and MAGEC1 start codon variant to PC.
dcterms:title
NMD and microRNA expression profiling of the HPCX1 locus reveal MAGEC1 as a candidate prostate cancer predisposition gene. NMD and microRNA expression profiling of the HPCX1 locus reveal MAGEC1 as a candidate prostate cancer predisposition gene.
skos:prefLabel
NMD and microRNA expression profiling of the HPCX1 locus reveal MAGEC1 as a candidate prostate cancer predisposition gene. NMD and microRNA expression profiling of the HPCX1 locus reveal MAGEC1 as a candidate prostate cancer predisposition gene.
skos:notation
RIV/46747885:24510/11:#0000325!RIV12-MSM-24510___
n11:predkladatel
n14:orjk%3A24510
n3:aktivita
n16:V
n3:aktivity
V
n3:cisloPeriodika
AUG 2
n3:dodaniDat
n4:2012
n3:domaciTvurceVysledku
n13:6819443
n3:druhVysledku
n20:J
n3:duvernostUdaju
n15:S
n3:entitaPredkladatele
n12:predkladatel
n3:idSjednocenehoVysledku
216095
n3:idVysledku
RIV/46747885:24510/11:#0000325
n3:jazykVysledku
n10:eng
n3:klicovaSlova
NONSENSE-MEDIATED DECAY; MESSENGER-RNA DECAY; MICROARRAY ANALYSIS; SUSCEPTIBILITY LOCUS; HOST GENES; IDENTIFICATION; INHIBITION; MUTATIONS; FAMILIES; FINLAND
n3:klicoveSlovo
n5:IDENTIFICATION n5:MUTATIONS n5:SUSCEPTIBILITY%20LOCUS n5:INHIBITION n5:FINLAND n5:HOST%20GENES n5:FAMILIES n5:NONSENSE-MEDIATED%20DECAY n5:MESSENGER-RNA%20DECAY n5:MICROARRAY%20ANALYSIS
n3:kodStatuVydavatele
GB - Spojené království Velké Británie a Severního Irska
n3:kontrolniKodProRIV
[406E1A55144C]
n3:nazevZdroje
BMC Cancer
n3:obor
n18:FD
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
9
n3:rokUplatneniVysledku
n4:2011
n3:svazekPeriodika
11
n3:tvurceVysledku
Mattila, Henna Isotalo, Jarkko Vihinen, Mauno Ikonen, Tarja Oja, Hannu Schleutker, Johanna Tammela, Teuvo L. J. Schindler, Martin Wahlfors, Tiina
n3:wos
294286700001
s:issn
1471-2407
s:numberOfPages
11
n17:doi
10.1186/1471-2407-11-327
n19:organizacniJednotka
24510