Carcinogenesis 2017 06;38(6):661-670
Division of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1, Seiryo-machi, Aoba-ku, Sendai, Miyagi, 980-8574, Japan.
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Am J Physiol Gastrointest Liver Physiol 2018 01 28;314(1):G65-G74. Epub 2017 Sep 28.
Division of Gastroenterology, Tohoku University Graduate School of Medicine , Sendai , Japan.
The Kelch-like ECH-associated protein 1 (Keap1)-NF-E2-related factor 2 (Nrf2) system has a wide variety of effects in addition to the oxidative stress response, such as growth promotion and chemoresistance of cancer cells. Nrf2 is constitutively activated in most cancer cells. However, the activation of Nrf2 together with oncogenic mutations does not always result in cancer promotion. Read More
J Pathol 2016 Feb 30;238(3):423-33. Epub 2015 Nov 30.
Department of Molecular and Clinical Cancer Medicine, University of Liverpool, UK.
The cellular defence protein Nrf2 is a mediator of oncogenesis in pancreatic ductal adenocarcinoma (PDAC) and other cancers. However, the control of Nrf2 expression and activity in cancer is not fully understood. We previously reported the absence of Keap1, a pivotal regulator of Nrf2, in ∼70% of PDAC cases. Read More
BMC Cancer 2016 Feb 25;16:155. Epub 2016 Feb 25.
Group Inflammatory Carcinogenesis, Institute for Experimental Cancer Research, Christian-Albrechts-University Kiel, Arnold-Heller-Str. 3, Building 17, 24105, Kiel, Germany.
Background: Nuclear factor E2 related factor-2 (Nrf2) is an oxidative stress inducible transcription factor being essential in regulating cell homeostasis. Thus, acute induction of Nrf2 in epithelial cells exposed to inflammation confers protection from oxidative cell damage and mutagenesis supporting an anti-tumorigenic role for Nrf2. However, pancreatic ductal adenocarcinoma (PDAC) is characterized by persistent Nrf2 activity conferring therapy resistance which points to a pro-tumorigenic role of Nrf2. Read More
Gastroenterology 2014 Nov 12;147(5):1119-33.e4. Epub 2014 Aug 12.
Stem Cells and Cancer Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain; Centre for Stem Cells in Cancer & Ageing, Barts Cancer Institute, Queen Mary University of London, UK. Electronic address:
Background & Aims: Although smoking is a leading risk factor for pancreatic ductal adenocarcinoma (PDAC), little is known about the mechanisms by which smoking promotes initiation or progression of PDAC.
Methods: We studied the effects of nicotine administration on pancreatic cancer development in Kras(+/LSLG12Vgeo);Elas-tTA/tetO-Cre (Ela-KRAS) mice, Kras(+/LSLG12D);Trp53+/LSLR172H;Pdx-1-Cre (KPC) mice (which express constitutively active forms of KRAS), and C57/B6 mice. Mice were given nicotine for up to 86 weeks to produce blood levels comparable with those of intermediate smokers. Read More