Polymorphisms in thioredoxin reductase and selenoprotein K genes and selenium status modulate risk of prostate cancer.

Increased dietary intake of Selenium (Se) has been suggested to lower prostate cancer mortality, but supplementation trials have produced conflicting results. Se is incorporated into 25 selenoproteins. The aim of this work was to assess whether risk of prostate cancer is affected by genetic variants...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Catherine Méplan, Sabine Rohrmann, Astrid Steinbrecher, Lutz Schomburg, Eugène Jansen, Jakob Linseisen, John Hesketh
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/1f9227011a9b4196bdeb5cf04a6024e9
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:1f9227011a9b4196bdeb5cf04a6024e9
record_format	dspace
spelling	oai:doaj.org-article:1f9227011a9b4196bdeb5cf04a6024e92021-11-18T08:10:14ZPolymorphisms in thioredoxin reductase and selenoprotein K genes and selenium status modulate risk of prostate cancer.1932-620310.1371/journal.pone.0048709https://doaj.org/article/1f9227011a9b4196bdeb5cf04a6024e92012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23133653/?tool=EBIhttps://doaj.org/toc/1932-6203Increased dietary intake of Selenium (Se) has been suggested to lower prostate cancer mortality, but supplementation trials have produced conflicting results. Se is incorporated into 25 selenoproteins. The aim of this work was to assess whether risk of prostate cancer is affected by genetic variants in genes coding for selenoproteins, either alone or in combination with Se status. 248 cases and 492 controls from an EPIC-Heidelberg nested case-control study were subjected to two-stage genotyping with an initial screening phase in which 384 tagging-SNPs covering 72 Se-related genes were determined in 94 cases and 94 controls using the Illumina Goldengate methodology. This analysis was followed by a second phase in which genotyping for candidate SNPs identified in the first phase was carried out in the full study using Sequenom. Risk of high-grade or advanced stage prostate cancer was modified by interactions between serum markers of Se status and genotypes for rs9880056 in SELK, rs9605030 and rs9605031 in TXNRD2, and rs7310505 in TXNRD1. No significant effects of SNPs on prostate cancer risk were observed when grade or Se status was not taken into account. In conclusion, the risk of high-grade or advanced-stage prostate cancer is significantly altered by a combination of genotype for SNPs in selenoprotein genes and Se status. The findings contribute to explaining the biological effects of selenium intake and genetic factors in prostate cancer development and highlight potential roles of thioredoxin reductases and selenoprotein K in tumour progression.Catherine MéplanSabine RohrmannAstrid SteinbrecherLutz SchomburgEugène JansenJakob LinseisenJohn HeskethPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 11, p e48709 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Catherine Méplan Sabine Rohrmann Astrid Steinbrecher Lutz Schomburg Eugène Jansen Jakob Linseisen John Hesketh Polymorphisms in thioredoxin reductase and selenoprotein K genes and selenium status modulate risk of prostate cancer.
description	Increased dietary intake of Selenium (Se) has been suggested to lower prostate cancer mortality, but supplementation trials have produced conflicting results. Se is incorporated into 25 selenoproteins. The aim of this work was to assess whether risk of prostate cancer is affected by genetic variants in genes coding for selenoproteins, either alone or in combination with Se status. 248 cases and 492 controls from an EPIC-Heidelberg nested case-control study were subjected to two-stage genotyping with an initial screening phase in which 384 tagging-SNPs covering 72 Se-related genes were determined in 94 cases and 94 controls using the Illumina Goldengate methodology. This analysis was followed by a second phase in which genotyping for candidate SNPs identified in the first phase was carried out in the full study using Sequenom. Risk of high-grade or advanced stage prostate cancer was modified by interactions between serum markers of Se status and genotypes for rs9880056 in SELK, rs9605030 and rs9605031 in TXNRD2, and rs7310505 in TXNRD1. No significant effects of SNPs on prostate cancer risk were observed when grade or Se status was not taken into account. In conclusion, the risk of high-grade or advanced-stage prostate cancer is significantly altered by a combination of genotype for SNPs in selenoprotein genes and Se status. The findings contribute to explaining the biological effects of selenium intake and genetic factors in prostate cancer development and highlight potential roles of thioredoxin reductases and selenoprotein K in tumour progression.
format	article
author	Catherine Méplan Sabine Rohrmann Astrid Steinbrecher Lutz Schomburg Eugène Jansen Jakob Linseisen John Hesketh
author_facet	Catherine Méplan Sabine Rohrmann Astrid Steinbrecher Lutz Schomburg Eugène Jansen Jakob Linseisen John Hesketh
author_sort	Catherine Méplan
title	Polymorphisms in thioredoxin reductase and selenoprotein K genes and selenium status modulate risk of prostate cancer.
title_short	Polymorphisms in thioredoxin reductase and selenoprotein K genes and selenium status modulate risk of prostate cancer.
title_full	Polymorphisms in thioredoxin reductase and selenoprotein K genes and selenium status modulate risk of prostate cancer.
title_fullStr	Polymorphisms in thioredoxin reductase and selenoprotein K genes and selenium status modulate risk of prostate cancer.
title_full_unstemmed	Polymorphisms in thioredoxin reductase and selenoprotein K genes and selenium status modulate risk of prostate cancer.
title_sort	polymorphisms in thioredoxin reductase and selenoprotein k genes and selenium status modulate risk of prostate cancer.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/1f9227011a9b4196bdeb5cf04a6024e9
work_keys_str_mv	AT catherinemeplan polymorphismsinthioredoxinreductaseandselenoproteinkgenesandseleniumstatusmodulateriskofprostatecancer AT sabinerohrmann polymorphismsinthioredoxinreductaseandselenoproteinkgenesandseleniumstatusmodulateriskofprostatecancer AT astridsteinbrecher polymorphismsinthioredoxinreductaseandselenoproteinkgenesandseleniumstatusmodulateriskofprostatecancer AT lutzschomburg polymorphismsinthioredoxinreductaseandselenoproteinkgenesandseleniumstatusmodulateriskofprostatecancer AT eugenejansen polymorphismsinthioredoxinreductaseandselenoproteinkgenesandseleniumstatusmodulateriskofprostatecancer AT jakoblinseisen polymorphismsinthioredoxinreductaseandselenoproteinkgenesandseleniumstatusmodulateriskofprostatecancer AT johnhesketh polymorphismsinthioredoxinreductaseandselenoproteinkgenesandseleniumstatusmodulateriskofprostatecancer
_version_	1718422092866650112

Polymorphisms in thioredoxin reductase and selenoprotein K genes and selenium status modulate risk of prostate cancer.

Ejemplares similares