[1] Banales JM, Cardinale V, Carpino G et al. Expert consensus document: Cholangiocarcinoma: current knowledge and future perspectives consensus statement from the European Network for the Study of Cholangiocarcinoma (ENS-CCA). Nat Rev Gastroenterol Hepatol 2016;13:261-280.
[2] Zou S, Li J, Zhou H, Freeh C et al. Mutational landscape of intrahepatic cholangiocarcinoma. Nat Commun 2014;5:5696.
[3] Arai Y, Totoki Y, Hosoda F et al. Fibroblast growth factor receptor 2 tyrosine kinase fusions define a unique molecular subtype of cholangiocarcinoma. Hepatology 2014;59:1427-1434.
[4] Mazzaferro V, El-Rayes BF, Droz Dit Busset M et al. Derazantinib (ARQ 087) in advanced or inoperable FGFR2 gene fusion-positive intrahepatic cholangiocarcinoma. Br J Cancer 2019;120:165-171.
[5] Javle M, Lowery M, Shroff RT et al. Phase II study of BGJ398 in patients with FGFR-altered advanced cholangiocarcinoma. J Clin Oncol 2018;36:276-282.
[6] Suzuki T, Yamamoto M. Stress-sensing mechanisms and the physiological roles of the Keapl-Nrf2 system during cellular stress. J Biol Chern 2017;292:16817-16824.
[7] Taguchi K, Motohashi H, Yamamoto M. Molecular mechanisms of the Keapl-Nrf2 pathway in stress response and cancer evolution. Genes Cells 2011;16:123-140.
[8] DeNicola GM, Karreth FA, Humpton TJ et al. Oncogene-induced Nrf2 transcription promotes ROS detoxification and tumorigenesis. Nature 2011;475:106-109.
[9] Shibata T, Kokubu A, Saito S et al. NRF2 mutation confers malignant potential and resistance to chemoradiation therapy in advanced esophageal squamous cancer. Neoplasia 2011;13:864-873.
[10] Goldstein LD, Lee J, Gnad F et al. Recurrent Loss of NFE2L2 exon 2 is a mechanism for Nrf2 pathway activation in human cancers. Cell Rep 2016;16:2605-2617.
[11] Frank R, Scheffler M, Merkelbach-Bruse S et al. Clinical and pathological characteristics of KEAP1- and NFE2L2-mutated non-small cell lung carcinoma (NSCLC). Clin Cancer Res 2018;24:3087-3096.
[12] Shibata T, Kokubu A, Gotoh M et al. Genetic alteration of Keapl confers Gastroenterology 2008;135:1358-1368.
[13] Guan L, Zhang L, Gong Z et al. FoxO3 inactivation promotes human cholangiocarcinoma tumorigenesis and chemoresistance through Keapl-Nrf2 signaling. Hepatology 2016;63:1914-1927.
[14] Maruyama A, Tsukamoto S, Nishikawa K et al. Nrf2 regulates the alternative first exons of CD36 in macrophages through specific antioxidant response elements. ArchBiochem Biophys 2008;477:139-145.
[15] Watai Y, Kobayashi A, Nagase H et al. Subcellular localization and cytoplasmic complex status of endogenous Keapl. Genes Cells 2007;12:1163-1178.
[16] Okawa H, Motohashi H, Kobayashi A et al. Hepatocyte-specific deletion of the keapl gene activates Nrf2 and confers potent resistance against acute drug toxicity. Biochem Biophys Res Commun 2006;339:79-88.
[17] Blake DJ, Singh A, Kombairaju P et al. Deletion of Keapl in the lung attenuates acute cigarette smoke-induced oxidative stress and inflammation. Am J Respir Cell Mol Biol 2010;42:524-536.
[18] Postic C, Magnuson MA. DNA excision in liver by an albumin-Cre transgene occurs progressively with age. Genesis 2000;26:149-150.
[19] Hingorani SR, Petricoin EF, Maitra A et al. Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse. Cancer Cell 2003;4:437-450.
[20] Jackson EL, Willis N, Mercer K et al. Analysis of lung tumor initiation and progression using conditional expression of oncogenic K-ras. Genes Dev 2001;15:3243-3248.
[21] Olive KP, Tuveson DA, Ruhe ZC et al. Mutant p53 gain of function in two mouse models of Li-Fraumeni syndrome. Cell 2004;119:847-860.
[22] Wang X, Spandidos A, Wang H et al. PrimerBank: a PCR primer database for quantitative gene expression analysis, 2012 update. Nucleic Acids Res 2012;40:D 1144-1149.
[23] Komatsu M, Kurokawa H, Waguri S et al. The selective autophagy substrate p62 activates the stress responsive transcription factor Nrf2 through inactivation of Keapl. Nat Cell Biol 2010;12:213-223.
[24] Umemura A, He F, Taniguchi K et al. p62, upregulated during preneoplasia, induces ofhepatocellular carcinogenesis by maintaining survival Cancer Cell 2016;29:935-948.stressed HCC-initiating cells.
[25] O'Dell MR, Huang JL, Whitney-Miller CL et al. Kras(G12D) and p53 mutation cause primary intrahepatic cholangiocarcinoma. Cancer Res 2012;72:1557-1567.
[26] Taguchi K, Hirano I, Itoh T et al. Nrf2 enhances cholangiocyte expansion in Pten- deficient livers. Mol Cell Biol 2014;34:900-913.
[27] Hingorani SR, Wang L, Multani AS et al. Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice. Cancer Cell 2005;7:469-483.
[28] Samatiwat P, Prawan A, Senggunprai L et al. Nrf2 inhibition sensitizes cholangiocarcinoma cells to cytotoxic and antiproliferative activities of chemotherapeutic agents. Tumour Biol 2016;37:11495-11507.
[29] Kongpetch S, Puapairoj A, Ong CK et al. Haem oxygenase 1 expression is associated with prognosis in cholangiocarcinoma patients and with drug sensitivity in xenografted mice.Cell Prolif 2016;49:90-101.
[30] Poncy A, Antoniou A, Cordi S et al. Transcription factors SOX4 and SOX9 cooperatively control development of bile ducts Dev Biol 2015;404:136-148.
[31] Hill MA, Alexander WB, Guo B et al. Kras and Tp53 mutations cause cholangiocyte- and hepatocyte-derived cholangiocarcinoma. Cancer Res 2018;78:4445-4451.
[32] Hamada S, Taguchi K, Masamune A et al. Nrf2 promotes mutant K-ras/p53-driven pancreatic carcinogenesis. Carcinogenesis. 2017;38:661-670.
[33] Hamada S, Shimosegawa T, Taguchi K et al. Simultaneous K-ras activation and Keapl deletion cause atrophy of pancreatic parenchyma. Am J Physiol Gastrointest Liver Physiol. 2018;314:G65-G74.
[34] Taguchi K, Yamamoto M. The KEAP1-NRF2 system in cancer. Front Oncol. 2017;7:85.
[35] Lister A, Nedjadi T, Kitteringham NR et al. Nrf2 is overexpressed in pancreatic cancer: implications for cell proliferation and therapy. Mol Cancer. 2011;10:37.
論文の公開元へ
