<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lister A</submitter><funding>Cancer Research UK</funding><funding>Medical Research Council</funding><funding>National Institute for Health Research (NIHR)</funding><pagination>37</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3098205</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Nrf2 is a key transcriptional regulator of a battery of genes that facilitate phase II/III drug metabolism and defence against oxidative stress. Nrf2 is largely regulated by Keap1, which directs Nrf2 for proteasomal degradation. The Nrf2/Keap1 system is dysregulated in lung, head and neck, and breast cancers and this affects cellular proliferation and response to therapy. Here, we have investigated the integrity of the Nrf2/Keap1 system in pancreatic cancer.&lt;h4>Results&lt;/h4>Keap1, Nrf2 and the Nrf2 target genes AKR1c1 and GCLC were detected in a panel of five pancreatic cancer cell lines. Mutation analysis of NRF2 exon 2 and KEAP1 exons 2-6 in these cell lines identified no mutations in NRF2 and only synonomous mutations in KEAP1. RNAi depletion of Nrf2 caused a decrease </pubmed_abstract><journal>Molecular cancer</journal><pubmed_title>Nrf2 is overexpressed in pancreatic cancer: implications for cell proliferation and therapy.</pubmed_title><pmcid>PMC3098205</pmcid><funding_grant_id>G0700654</funding_grant_id><funding_grant_id>NF-SI-0510-10126</funding_grant_id><funding_grant_id>C6665/A7348</funding_grant_id><pubmed_authors>Costello E</pubmed_authors><pubmed_authors>Neoptolemos JP</pubmed_authors><pubmed_authors>Kitteringham NR</pubmed_authors><pubmed_authors>Lloyd B</pubmed_authors><pubmed_authors>Campbell F</pubmed_authors><pubmed_authors>Goldring CE</pubmed_authors><pubmed_authors>Owen A</pubmed_authors><pubmed_authors>Nedjadi T</pubmed_authors><pubmed_authors>Lister A</pubmed_authors><pubmed_authors>Copple IM</pubmed_authors><pubmed_authors>Williams S</pubmed_authors><pubmed_authors>Park BK</pubmed_authors></additional><is_claimable>false</is_claimable><name>Nrf2 is overexpressed in pancreatic cancer: implications for cell proliferation and therapy.</name><description>&lt;h4>Background&lt;/h4>Nrf2 is a key transcriptional regulator of a battery of genes that facilitate phase II/III drug metabolism and defence against oxidative stress. Nrf2 is largely regulated by Keap1, which directs Nrf2 for proteasomal degradation. The Nrf2/Keap1 system is dysregulated in lung, head and neck, and breast cancers and this affects cellular proliferation and response to therapy. Here, we have investigated the integrity of the Nrf2/Keap1 system in pancreatic cancer.&lt;h4>Results&lt;/h4>Keap1, Nrf2 and the Nrf2 target genes AKR1c1 and GCLC were detected in a panel of five pancreatic cancer cell lines. Mutation analysis of NRF2 exon 2 and KEAP1 exons 2-6 in these cell lines identified no mutations in NRF2 and only synonomous mutations in KEAP1. RNAi depletion of Nrf2 caused a decrease </description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Apr</publication><modification>2026-04-07T15:15:57.011Z</modification><creation>2019-03-27T00:41:47Z</creation></dates><accession>S-EPMC3098205</accession><cross_references><pubmed>21489257</pubmed><doi>10.1186/1476-4598-10-37</doi></cross_references></HashMap>