<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Krehl S</submitter><funding>NCI NIH HHS</funding><pagination>620-8</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3291858</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>33(3)</volume><pubmed_abstract>Chronic inflammation and selenium deficiency are considered as risk factors for colon cancer. The protective effect of selenium might be mediated by specific selenoproteins, such as glutathione peroxidases (GPx). GPx-1 and -2 double knockout, but not single knockout mice, spontaneously develop ileocolitis and intestinal cancer. Since GPx2 is induced by the chemopreventive sulforaphane (SFN) via the nuclear factor E2-related factor 2 (Nrf2)/Keap1 system, the susceptibility of GPx2-KO and wild-type (WT) mice to azoxymethane and dextran sulfate sodium (AOM/DSS)-induced colon carcinogenesis was tested under different selenium states and SFN applications. WT and GPx2-KO mice were grown on a selenium-poor, -adequate or -supranutritional diet. SFN application started either 1 week before (SFN4) o</pubmed_abstract><journal>Carcinogenesis</journal><pubmed_title>Glutathione peroxidase-2 and selenium decreased inflammation and tumors in a mouse model of inflammation-associated carcinogenesis whereas sulforaphane effects differed with selenium supply.</pubmed_title><pmcid>PMC3291858</pmcid><funding_grant_id>R01 CA114569</funding_grant_id><pubmed_authors>Loewinger M</pubmed_authors><pubmed_authors>Banning A</pubmed_authors><pubmed_authors>Brauer MN</pubmed_authors><pubmed_authors>Chu FF</pubmed_authors><pubmed_authors>Esworthy RS</pubmed_authors><pubmed_authors>Florian S</pubmed_authors><pubmed_authors>Brigelius-Flohe R</pubmed_authors><pubmed_authors>Wessjohann LA</pubmed_authors><pubmed_authors>Kipp AP</pubmed_authors><pubmed_authors>Iori R</pubmed_authors><pubmed_authors>Krehl S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Glutathione peroxidase-2 and selenium decreased inflammation and tumors in a mouse model of inflammation-associated carcinogenesis whereas sulforaphane effects differed with selenium supply.</name><description>Chronic inflammation and selenium deficiency are considered as risk factors for colon cancer. The protective effect of selenium might be mediated by specific selenoproteins, such as glutathione peroxidases (GPx). GPx-1 and -2 double knockout, but not single knockout mice, spontaneously develop ileocolitis and intestinal cancer. Since GPx2 is induced by the chemopreventive sulforaphane (SFN) via the nuclear factor E2-related factor 2 (Nrf2)/Keap1 system, the susceptibility of GPx2-KO and wild-type (WT) mice to azoxymethane and dextran sulfate sodium (AOM/DSS)-induced colon carcinogenesis was tested under different selenium states and SFN applications. WT and GPx2-KO mice were grown on a selenium-poor, -adequate or -supranutritional diet. SFN application started either 1 week before (SFN4) o</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Mar</publication><modification>2025-04-04T14:12:38.025Z</modification><creation>2019-03-27T00:49:43Z</creation></dates><accession>S-EPMC3291858</accession><cross_references><pubmed>22180572</pubmed><doi>10.1093/carcin/bgr288</doi></cross_references></HashMap>