{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T18:38:45Z","timestamp":1790707125678,"version":"4.1.0"},"reference-count":49,"publisher":"National Academy of Sciences","issue":"12","license":[{"start":{"date-parts":[[2020,9,10]],"date-time":"2020-09-10T00:00:00Z","timestamp":1599696000000},"content-version":"vor","delay-in-days":184,"URL":"https:\/\/www.pnas.org\/site\/aboutpnas\/licenses.xhtml"}],"funder":[{"DOI":"10.13039\/100009863","name":"Neuroendocrine Tumor Research Foundation","doi-asserted-by":"publisher","award":["NA"],"award-info":[{"award-number":["NA"]}],"id":[{"id":"10.13039\/100009863","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000054","name":"HHS | NIH | National Cancer Institute","doi-asserted-by":"publisher","award":["CA208463"],"award-info":[{"award-number":["CA208463"]}],"id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000024","name":"Gouvernement du Canada | Canadian Institutes of Health Research","doi-asserted-by":"publisher","award":["NA"],"award-info":[{"award-number":["NA"]}],"id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2020,3,24]]},"abstract":"<jats:p>\n                    A more comprehensive understanding of the molecular mechanisms underlying pancreatic diseases, including pancreatitis and cancer, is essential to improve clinical management. MEN1 has established roles in epigenetic regulation and tumor suppression in the endocrine pancreas; however, intriguing recent data suggest MEN1 may also function in the exocrine pancreas. Using physiologically relevant genetic mouse models, we provide direct evidence that Men1 is essential for exocrine pancreas homeostasis in response to inflammation and oncogenic stress. Men1 loss causes increased injury and impaired regeneration following acute caerulein-induced pancreatitis, leading to more severe damage, loss of the normal acinar compartment, and increased cytokeratin 19-positive metaplasias and immune cell infiltration. We further demonstrate the Men1 protein is stabilized in response to insult, and loss of Men1 is associated with the overexpression of proinflammatory Jund target genes, suggesting that loss of Men1-mediated repression of Jund activity is, at least in part, responsible for the impaired response. Finally, we demonstrate that\n                    <jats:italic>Men1<\/jats:italic>\n                    loss significantly accelerates mutant Kras-dependent oncogenesis. Combined, this work establishes Men1 as an important mediator of pancreas homeostasis in vivo.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1920017117","type":"journal-article","created":{"date-parts":[[2020,3,10]],"date-time":"2020-03-10T17:15:08Z","timestamp":1583860508000},"page":"6622-6629","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":19,"title":["Men1 maintains exocrine pancreas homeostasis in response to inflammation and oncogenic stress"],"prefix":"10.1073","volume":"117","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1940-5169","authenticated-orcid":false,"given":"Amanda R.","family":"Wasylishen","sequence":"first","affiliation":[{"name":"Department of Genetics, University of Texas MD Anderson Cancer Center, Houston, TX 77030;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chang","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Genetics, University of Texas MD Anderson Cancer Center, Houston, TX 77030;"},{"name":"Genetics and Epigenetics Program, The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences, Houston, TX 77030;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gilda P.","family":"Chau","sequence":"additional","affiliation":[{"name":"Department of Genetics, University of Texas MD Anderson Cancer Center, Houston, TX 77030;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuan","family":"Qi","sequence":"additional","affiliation":[{"name":"Department of Bioinformatics and Computational Biology, University of Texas MD Anderson Cancer Center, Houston, TX 77030;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoping","family":"Su","sequence":"additional","affiliation":[{"name":"Department of Bioinformatics and Computational Biology, University of Texas MD Anderson Cancer Center, Houston, TX 77030;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael P.","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Surgical Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeannelyn S.","family":"Estrella","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8985-4886","authenticated-orcid":false,"given":"Guillermina","family":"Lozano","sequence":"additional","affiliation":[{"name":"Department of Genetics, University of Texas MD Anderson Cancer Center, Houston, TX 77030;"},{"name":"Genetics and Epigenetics Program, The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences, Houston, TX 77030;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2020,3,10]]},"reference":[{"key":"e_1_3_4_1_2","first-page":"598","article-title":"Acute pancreatitis","volume":"376","author":"Forsmark ChE.","year":"2017","unstructured":"ChE. Forsmark, S. S. Vege, C. M. Wilcox, Acute pancreatitis. N. Engl. J. Med. 376, 598\u2013599 (2017).","journal-title":"N. Engl. J. Med."},{"key":"e_1_3_4_2_2","doi-asserted-by":"crossref","first-page":"479","DOI":"10.1038\/s41575-019-0158-2","article-title":"New insights into acute pancreatitis","volume":"16","author":"Lee P. J.","year":"2019","unstructured":"P. J. Lee, G. I. Papachristou, New insights into acute pancreatitis. Nat. Rev. Gastroenterol. Hepatol. 16, 479\u2013496 (2019).","journal-title":"Nat. Rev. Gastroenterol. Hepatol."},{"key":"e_1_3_4_3_2","doi-asserted-by":"crossref","first-page":"129","DOI":"10.1007\/978-3-0348-0837-8_6","article-title":"The role of inflammation in pancreatic cancer","volume":"816","author":"Hausmann S.","year":"2014","unstructured":"S. Hausmann, B. Kong, C. Michalski, M. Erkan, H. Friess, The role of inflammation in pancreatic cancer. Adv. Exp. Med. Biol. 816, 129\u2013151 (2014).","journal-title":"Adv. Exp. Med. Biol."},{"key":"e_1_3_4_4_2","volume-title":"GeneReviews","author":"Giusti F.","year":"1993","unstructured":"F. Giusti, F. Marini, M. L. Brandi, \u201cMultiple endocrine neoplasia type 1\u201d in GeneReviews, M. P. Adam ., Eds. (University of Washington, Seattle, WA, 1993)."},{"key":"e_1_3_4_5_2","doi-asserted-by":"crossref","first-page":"2","DOI":"10.1016\/j.mce.2013.08.002","article-title":"Multiple endocrine neoplasia type 1 (MEN1) and type 4 (MEN4)","volume":"386","author":"Thakker R. V.","year":"2014","unstructured":"R. V. Thakker, Multiple endocrine neoplasia type 1 (MEN1) and type 4 (MEN4). Mol. Cell. Endocrinol. 386, 2\u201315 (2014).","journal-title":"Mol. Cell. Endocrinol."},{"key":"e_1_3_4_6_2","doi-asserted-by":"crossref","first-page":"1199","DOI":"10.1126\/science.1200609","article-title":"DAXX\/ATRX, MEN1, and mTOR pathway genes are frequently altered in pancreatic neuroendocrine tumors","volume":"331","author":"Jiao Y.","year":"2011","unstructured":"Y. Jiao ., DAXX\/ATRX, MEN1, and mTOR pathway genes are frequently altered in pancreatic neuroendocrine tumors. Science 331, 1199\u20131203 (2011).","journal-title":"Science"},{"key":"e_1_3_4_7_2","doi-asserted-by":"crossref","first-page":"65","DOI":"10.1038\/nature21063","article-title":"Whole-genome landscape of pancreatic neuroendocrine tumours","volume":"543","author":"Scarpa A.","year":"2017","unstructured":"A. Scarpa .; Australian Pancreatic Cancer Genome Initiative, Whole-genome landscape of pancreatic neuroendocrine tumours. Nature 543, 65\u201371 (2017).","journal-title":"Nature"},{"key":"e_1_3_4_8_2","doi-asserted-by":"crossref","first-page":"E1774","DOI":"10.1210\/jc.2012-1743","article-title":"Identification of somatic mutations in parathyroid tumors using whole-exome sequencing","volume":"97","author":"Cromer M. K.","year":"2012","unstructured":"M. K. Cromer ., Identification of somatic mutations in parathyroid tumors using whole-exome sequencing. J. Clin. Endocrinol. Metab. 97, E1774\u2013E1781 (2012).","journal-title":"J. Clin. Endocrinol. Metab."},{"key":"e_1_3_4_9_2","doi-asserted-by":"crossref","first-page":"1118","DOI":"10.1073\/pnas.98.3.1118","article-title":"A mouse model of multiple endocrine neoplasia, type 1, develops multiple endocrine tumors","volume":"98","author":"Crabtree J. S.","year":"2001","unstructured":"J. S. Crabtree ., A mouse model of multiple endocrine neoplasia, type 1, develops multiple endocrine tumors. Proc. Natl. Acad. Sci. U.S.A. 98, 1118\u20131123 (2001).","journal-title":"Proc. Natl. Acad. Sci. U.S.A."},{"key":"e_1_3_4_10_2","doi-asserted-by":"crossref","first-page":"6075","DOI":"10.1128\/MCB.23.17.6075-6085.2003","article-title":"Of mice and MEN1: Insulinomas in a conditional mouse knockout","volume":"23","author":"Crabtree J. S.","year":"2003","unstructured":"J. S. Crabtree ., Of mice and MEN1: Insulinomas in a conditional mouse knockout. Mol. Cell. Biol. 23, 6075\u20136085 (2003).","journal-title":"Mol. Cell. Biol."},{"key":"e_1_3_4_11_2","doi-asserted-by":"crossref","first-page":"1954","DOI":"10.1053\/j.gastro.2010.01.046","article-title":"Alpha cell-specific Men1 ablation triggers the transdifferentiation of glucagon-expressing cells and insulinoma development","volume":"138","author":"Lu J.","year":"2010","unstructured":"J. Lu ., Alpha cell-specific Men1 ablation triggers the transdifferentiation of glucagon-expressing cells and insulinoma development. Gastroenterology 138, 1954\u20131965 (2010).","journal-title":"Gastroenterology"},{"key":"e_1_3_4_12_2","doi-asserted-by":"crossref","first-page":"4024","DOI":"10.1210\/en.2009-1251","article-title":"Multiple endocrine neoplasia type 1 deletion in pancreatic alpha-cells leads to development of insulinomas in mice","volume":"151","author":"Shen H. C.","year":"2010","unstructured":"H. C. Shen ., Multiple endocrine neoplasia type 1 deletion in pancreatic alpha-cells leads to development of insulinomas in mice. Endocrinology 151, 4024\u20134030 (2010).","journal-title":"Endocrinology"},{"key":"e_1_3_4_13_2","doi-asserted-by":"crossref","first-page":"1858","DOI":"10.1158\/0008-5472.CAN-08-3662","article-title":"Recapitulation of pancreatic neuroendocrine tumors in human multiple endocrine neoplasia type I syndrome via Pdx1-directed inactivation of Men1","volume":"69","author":"Shen H. C.","year":"2009","unstructured":"H. C. Shen ., Recapitulation of pancreatic neuroendocrine tumors in human multiple endocrine neoplasia type I syndrome via Pdx1-directed inactivation of Men1. Cancer Res. 69, 1858\u20131866 (2009).","journal-title":"Cancer Res."},{"key":"e_1_3_4_14_2","doi-asserted-by":"crossref","first-page":"587","DOI":"10.1016\/S1097-2765(04)00081-4","article-title":"Menin associates with a trithorax family histone methyltransferase complex and with the hoxc8 locus","volume":"13","author":"Hughes C. M.","year":"2004","unstructured":"C. M. Hughes ., Menin associates with a trithorax family histone methyltransferase complex and with the hoxc8 locus. Mol. Cell 13, 587\u2013597 (2004).","journal-title":"Mol. Cell"},{"key":"e_1_3_4_15_2","doi-asserted-by":"crossref","first-page":"749","DOI":"10.1073\/pnas.0408836102","article-title":"Menin and MLL cooperatively regulate expression of cyclin-dependent kinase inhibitors","volume":"102","author":"Milne T. A.","year":"2005","unstructured":"T. A. Milne ., Menin and MLL cooperatively regulate expression of cyclin-dependent kinase inhibitors. Proc. Natl. Acad. Sci. U.S.A. 102, 749\u2013754 (2005).","journal-title":"Proc. Natl. Acad. Sci. U.S.A."},{"key":"e_1_3_4_16_2","doi-asserted-by":"crossref","first-page":"6147","DOI":"10.1128\/MCB.20.16.6147-6158.2000","article-title":"Functional collaboration between different cyclin-dependent kinase inhibitors suppresses tumor growth with distinct tissue specificity","volume":"20","author":"Franklin D. S.","year":"2000","unstructured":"D. S. Franklin, V. L. Godfrey, D. A. O\u2019Brien, C. Deng, Y. Xiong, Functional collaboration between different cyclin-dependent kinase inhibitors suppresses tumor growth with distinct tissue specificity. Mol. Cell. Biol. 20, 6147\u20136158 (2000).","journal-title":"Mol. Cell. Biol."},{"key":"e_1_3_4_17_2","doi-asserted-by":"crossref","first-page":"5639","DOI":"10.1128\/MCB.24.13.5639-5649.2004","article-title":"Leukemia proto-oncoprotein MLL forms a SET1-like histone methyltransferase complex with menin to regulate Hox gene expression","volume":"24","author":"Yokoyama A.","year":"2004","unstructured":"A. Yokoyama ., Leukemia proto-oncoprotein MLL forms a SET1-like histone methyltransferase complex with menin to regulate Hox gene expression. Mol. Cell. Biol. 24, 5639\u20135649 (2004).","journal-title":"Mol. Cell. Biol."},{"key":"e_1_3_4_18_2","doi-asserted-by":"crossref","first-page":"1107","DOI":"10.1016\/S1097-2765(02)00741-4","article-title":"MLL targets SET domain methyltransferase activity to Hox gene promoters","volume":"10","author":"Milne T. A.","year":"2002","unstructured":"T. A. Milne ., MLL targets SET domain methyltransferase activity to Hox gene promoters. Mol. Cell 10, 1107\u20131117 (2002).","journal-title":"Mol. Cell"},{"key":"e_1_3_4_19_2","doi-asserted-by":"crossref","first-page":"207","DOI":"10.1016\/j.cell.2005.09.025","article-title":"The menin tumor suppressor protein is an essential oncogenic cofactor for MLL-associated leukemogenesis","volume":"123","author":"Yokoyama A.","year":"2005","unstructured":"A. Yokoyama ., The menin tumor suppressor protein is an essential oncogenic cofactor for MLL-associated leukemogenesis. Cell 123, 207\u2013218 (2005).","journal-title":"Cell"},{"key":"e_1_3_4_20_2","doi-asserted-by":"crossref","first-page":"143","DOI":"10.1016\/S0092-8674(00)80967-8","article-title":"Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription","volume":"96","author":"Agarwal S. K.","year":"1999","unstructured":"S. K. Agarwal ., Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription. Cell 96, 143\u2013152 (1999).","journal-title":"Cell"},{"key":"e_1_3_4_21_2","doi-asserted-by":"crossref","first-page":"725","DOI":"10.1097\/MPA.0b013e31827591e9","article-title":"Pancreatic adenocarcinoma in a patient with multiple endocrine neoplasia 1 syndrome","volume":"42","author":"Karpathakis A.","year":"2013","unstructured":"A. Karpathakis ., Pancreatic adenocarcinoma in a patient with multiple endocrine neoplasia 1 syndrome. Pancreas 42, 725\u2013726 (2013).","journal-title":"Pancreas"},{"key":"e_1_3_4_22_2","doi-asserted-by":"crossref","first-page":"383","DOI":"10.1002\/gcc.20650","article-title":"Decreased expression and promoter methylation of the menin tumor suppressor in pancreatic ductal adenocarcinoma","volume":"48","author":"Cavallari I.","year":"2009","unstructured":"I. Cavallari ., Decreased expression and promoter methylation of the menin tumor suppressor in pancreatic ductal adenocarcinoma. Genes Chromosomes Cancer 48, 383\u2013396 (2009).","journal-title":"Genes Chromosomes Cancer"},{"key":"e_1_3_4_23_2","doi-asserted-by":"crossref","first-page":"17060","DOI":"10.1038\/nrdp.2017.60","article-title":"Chronic pancreatitis","volume":"3","author":"Kleeff J.","year":"2017","unstructured":"J. Kleeff ., Chronic pancreatitis. Nat. Rev. Dis. Primers 3, 17060 (2017).","journal-title":"Nat. Rev. Dis. Primers"},{"key":"e_1_3_4_24_2","doi-asserted-by":"crossref","first-page":"561","DOI":"10.1016\/j.bbrc.2009.03.068","article-title":"Acute pancreatitis markedly accelerates pancreatic cancer progression in mice expressing oncogenic Kras","volume":"382","author":"Carri\u00e8re C.","year":"2009","unstructured":"C. Carri\u00e8re, A. L. Young, J. R. Gunn, D. S. Longnecker, M. Korc, Acute pancreatitis markedly accelerates pancreatic cancer progression in mice expressing oncogenic Kras. Biochem. Biophys. Res. Commun. 382, 561\u2013565 (2009).","journal-title":"Biochem. Biophys. Res. Commun."},{"key":"e_1_3_4_25_2","doi-asserted-by":"crossref","first-page":"291","DOI":"10.1016\/j.ccr.2007.01.012","article-title":"Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice","volume":"11","author":"Guerra C.","year":"2007","unstructured":"C. Guerra ., Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice. Cancer Cell 11, 291\u2013302 (2007).","journal-title":"Cancer Cell"},{"key":"e_1_3_4_26_2","doi-asserted-by":"crossref","first-page":"212","DOI":"10.5946\/ce.2014.47.3.212","article-title":"Experimental models of pancreatitis","volume":"47","author":"Hyun J. J.","year":"2014","unstructured":"J. J. Hyun, H. S. Lee, Experimental models of pancreatitis. Clin. Endosc. 47, 212\u2013216 (2014).","journal-title":"Clin. Endosc."},{"key":"e_1_3_4_27_2","doi-asserted-by":"crossref","first-page":"737","DOI":"10.1016\/j.ccr.2012.10.025","article-title":"Identification of Sox9-dependent acinar-to-ductal reprogramming as the principal mechanism for initiation of pancreatic ductal adenocarcinoma","volume":"22","author":"Kopp J. L.","year":"2012","unstructured":"J. L. Kopp ., Identification of Sox9-dependent acinar-to-ductal reprogramming as the principal mechanism for initiation of pancreatic ductal adenocarcinoma. Cancer Cell 22, 737\u2013750 (2012).","journal-title":"Cancer Cell"},{"key":"e_1_3_4_28_2","doi-asserted-by":"crossref","first-page":"508","DOI":"10.1172\/JCI40045","article-title":"Beta-catenin blocks Kras-dependent reprogramming of acini into pancreatic cancer precursor lesions in mice","volume":"120","author":"Morris J. P.","year":"2010","unstructured":"J. P. Morris, 4th, D. A. Cano, S. Sekine, S. C. Wang, M. Hebrok, Beta-catenin blocks Kras-dependent reprogramming of acini into pancreatic cancer precursor lesions in mice. J. Clin. Invest. 120, 508\u2013520 (2010).","journal-title":"J. Clin. Invest."},{"key":"e_1_3_4_29_2","volume-title":"Guide for the Care and Use of Laboratory Animals","author":"National Research Council","year":"2011","unstructured":"National Research Council, Guide for the Care and Use of Laboratory Animals (National Academies Press, Washington, DC, ed. 8, 2011).","edition":"8"},{"key":"e_1_3_4_30_2","doi-asserted-by":"crossref","first-page":"621","DOI":"10.1016\/j.ccr.2014.03.014","article-title":"Oncogenic Kras activates a hematopoietic-to-epithelial IL-17 signaling axis in preinvasive pancreatic neoplasia","volume":"25","author":"McAllister F.","year":"2014","unstructured":"F. McAllister ., Oncogenic Kras activates a hematopoietic-to-epithelial IL-17 signaling axis in preinvasive pancreatic neoplasia. Cancer Cell 25, 621\u2013637 (2014).","journal-title":"Cancer Cell"},{"key":"e_1_3_4_31_2","doi-asserted-by":"crossref","first-page":"523","DOI":"10.1093\/bioinformatics\/btt703","article-title":"Causal analysis approaches in ingenuity pathway analysis","volume":"30","author":"Kr\u00e4mer A.","year":"2014","unstructured":"A. Kr\u00e4mer, J. Green, J. Pollard, Jr., S. Tugendreich, Causal analysis approaches in ingenuity pathway analysis. Bioinformatics 30, 523\u2013530 (2014).","journal-title":"Bioinformatics"},{"key":"e_1_3_4_32_2","doi-asserted-by":"crossref","first-page":"533","DOI":"10.1038\/nature25751","article-title":"Transcriptional regulation by NR5A2 links differentiation and inflammation in the pancreas","volume":"554","author":"Cobo I.","year":"2018","unstructured":"I. Cobo ., Transcriptional regulation by NR5A2 links differentiation and inflammation in the pancreas. Nature 554, 533\u2013537 (2018).","journal-title":"Nature"},{"key":"e_1_3_4_33_2","doi-asserted-by":"crossref","first-page":"128","DOI":"10.1186\/1471-2105-14-128","article-title":"Enrichr: Interactive and collaborative HTML5 gene list enrichment analysis tool","volume":"14","author":"Chen E. Y.","year":"2013","unstructured":"E. Y. Chen ., Enrichr: Interactive and collaborative HTML5 gene list enrichment analysis tool. BMC Bioinformatics 14, 128 (2013).","journal-title":"BMC Bioinformatics"},{"key":"e_1_3_4_34_2","doi-asserted-by":"crossref","first-page":"W90","DOI":"10.1093\/nar\/gkw377","article-title":"Enrichr: A comprehensive gene set enrichment analysis web server 2016 update","volume":"44","author":"Kuleshov M. V.","year":"2016","unstructured":"M. V. Kuleshov ., Enrichr: A comprehensive gene set enrichment analysis web server 2016 update. Nucleic Acids Res. 44, W90\u2013W907 (2016).","journal-title":"Nucleic Acids Res."},{"key":"e_1_3_4_35_2","doi-asserted-by":"crossref","first-page":"2473","DOI":"10.1073\/pnas.1421601112","article-title":"Cholesterol uptake disruption, in association with chemotherapy, is a promising combined metabolic therapy for pancreatic adenocarcinoma","volume":"112","author":"Guillaumond F.","year":"2015","unstructured":"F. Guillaumond ., Cholesterol uptake disruption, in association with chemotherapy, is a promising combined metabolic therapy for pancreatic adenocarcinoma. Proc. Natl. Acad. Sci. U.S.A. 112, 2473\u20132478 (2015).","journal-title":"Proc. Natl. Acad. Sci. U.S.A."},{"key":"e_1_3_4_36_2","first-page":"2016","article-title":"Combined gene expression analysis of whole-tissue and microdissected pancreatic ductal adenocarcinoma identifies genes specifically overexpressed in tumor epithelia","volume":"55","author":"Badea L.","year":"2008","unstructured":"L. Badea, V. Herlea, S. O. Dima, T. Dumitrascu, I. Popescu, Combined gene expression analysis of whole-tissue and microdissected pancreatic ductal adenocarcinoma identifies genes specifically overexpressed in tumor epithelia. Hepatogastroenterology 55, 2016\u20132027 (2008).","journal-title":"Hepatogastroenterology"},{"key":"e_1_3_4_37_2","doi-asserted-by":"crossref","first-page":"439","DOI":"10.1101\/gad.181800.111","article-title":"EZH2 couples pancreatic regeneration to neoplastic progression","volume":"26","author":"Mallen-St Clair J.","year":"2012","unstructured":"J. Mallen-St Clair ., EZH2 couples pancreatic regeneration to neoplastic progression. Genes Dev. 26, 439\u2013444 (2012).","journal-title":"Genes Dev."},{"key":"e_1_3_4_38_2","doi-asserted-by":"crossref","first-page":"e07125","DOI":"10.7554\/eLife.07125","article-title":"The acinar differentiation determinant PTF1A inhibits initiation of pancreatic ductal adenocarcinoma","volume":"4","author":"Krah N. M.","year":"2015","unstructured":"N. M. Krah ., The acinar differentiation determinant PTF1A inhibits initiation of pancreatic ductal adenocarcinoma. eLife 4, e07125 (2015).","journal-title":"eLife"},{"key":"e_1_3_4_39_2","doi-asserted-by":"crossref","first-page":"647","DOI":"10.1136\/gutjnl-2012-304381","article-title":"Nr5a2 heterozygosity sensitises to, and cooperates with, inflammation in KRas(G12V)-driven pancreatic tumourigenesis","volume":"63","author":"Flandez M.","year":"2014","unstructured":"M. Flandez ., Nr5a2 heterozygosity sensitises to, and cooperates with, inflammation in KRas(G12V)-driven pancreatic tumourigenesis. Gut 63, 647\u2013655 (2014).","journal-title":"Gut"},{"key":"e_1_3_4_40_2","doi-asserted-by":"crossref","first-page":"145","DOI":"10.1002\/9780470942390.mo110217","article-title":"Health evaluation of experimental laboratory mice","volume":"2","author":"Burkholder T.","year":"2012","unstructured":"T. Burkholder, C. Foltz, E. Karlsson, C. G. Linton, J. M. Smith, Health evaluation of experimental laboratory mice. Curr. Protoc. Mouse Biol. 2, 145\u2013165 (2012).","journal-title":"Curr. Protoc. Mouse Biol."},{"key":"e_1_3_4_41_2","doi-asserted-by":"crossref","first-page":"eaan2507","DOI":"10.1126\/science.aan2507","article-title":"A pathology atlas of the human cancer transcriptome","volume":"357","author":"Uhlen M.","year":"2017","unstructured":"M. Uhlen ., A pathology atlas of the human cancer transcriptome. Science 357, eaan2507 (2017).","journal-title":"Science"},{"key":"e_1_3_4_42_2","doi-asserted-by":"crossref","first-page":"589","DOI":"10.1016\/j.ccell.2015.02.016","article-title":"Pharmacologic inhibition of the Menin-MLL interaction blocks progression of MLL leukemia in vivo","volume":"27","author":"Borkin D.","year":"2015","unstructured":"D. Borkin ., Pharmacologic inhibition of the Menin-MLL interaction blocks progression of MLL leukemia in vivo. Cancer Cell 27, 589\u2013602 (2015).","journal-title":"Cancer Cell"},{"key":"e_1_3_4_43_2","doi-asserted-by":"crossref","first-page":"542","DOI":"10.1038\/nature10806","article-title":"The same pocket in menin binds both MLL and JUND but has opposite effects on transcription","volume":"482","author":"Huang J.","year":"2012","unstructured":"J. Huang ., The same pocket in menin binds both MLL and JUND but has opposite effects on transcription. Nature 482, 542\u2013546 (2012).","journal-title":"Nature"},{"key":"e_1_3_4_44_2","doi-asserted-by":"crossref","first-page":"437","DOI":"10.1016\/S1535-6108(03)00309-X","article-title":"Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse","volume":"4","author":"Hingorani S. R.","year":"2003","unstructured":"S. R. Hingorani ., Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse. Cancer Cell 4, 437\u2013450 (2003).","journal-title":"Cancer Cell"},{"key":"e_1_3_4_45_2","doi-asserted-by":"crossref","first-page":"15","DOI":"10.1093\/bioinformatics\/bts635","article-title":"STAR: Ultrafast universal RNA-seq aligner","volume":"29","author":"Dobin A.","year":"2013","unstructured":"A. Dobin ., STAR: Ultrafast universal RNA-seq aligner. Bioinformatics 29, 15\u201321 (2013).","journal-title":"Bioinformatics"},{"key":"e_1_3_4_46_2","doi-asserted-by":"crossref","first-page":"2078","DOI":"10.1093\/bioinformatics\/btp352","article-title":"The sequence alignment\/map format and SAMtools","volume":"25","author":"Li H.","year":"2009","unstructured":"H. Li .; 1000 Genome Project Data Processing Subgroup, The sequence alignment\/map format and SAMtools. Bioinformatics 25, 2078\u20132079 (2009).","journal-title":"Bioinformatics"},{"key":"e_1_3_4_47_2","doi-asserted-by":"crossref","first-page":"1760","DOI":"10.1101\/gr.135350.111","article-title":"GENCODE: The reference human genome annotation for the ENCODE project","volume":"22","author":"Harrow J.","year":"2012","unstructured":"J. Harrow ., GENCODE: The reference human genome annotation for the ENCODE project. Genome Res. 22, 1760\u20131774 (2012).","journal-title":"Genome Res."},{"key":"e_1_3_4_48_2","doi-asserted-by":"crossref","first-page":"166","DOI":"10.1093\/bioinformatics\/btu638","article-title":"HTSeq\u2013A Python framework to work with high-throughput sequencing data","volume":"31","author":"Anders S.","year":"2015","unstructured":"S. Anders, P. T. Pyl, W. Huber, HTSeq\u2013A Python framework to work with high-throughput sequencing data. Bioinformatics 31, 166\u2013169 (2015).","journal-title":"Bioinformatics"},{"key":"e_1_3_4_49_2","doi-asserted-by":"crossref","first-page":"550","DOI":"10.1186\/s13059-014-0550-8","article-title":"Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2","volume":"15","author":"Love M. I.","year":"2014","unstructured":"M. I. Love, W. Huber, S. Anders, Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2. Genome Biol. 15, 550 (2014).","journal-title":"Genome Biol."}],"container-title":["Proceedings of the National Academy of Sciences"],"original-title":[],"language":"en","link":[{"URL":"http:\/\/www.pnas.org\/syndication\/doi\/10.1073\/pnas.1920017117","content-type":"unspecified","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/pnas.org\/doi\/pdf\/10.1073\/pnas.1920017117","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,6,7]],"date-time":"2022-06-07T17:02:39Z","timestamp":1654621359000},"score":1,"resource":{"primary":{"URL":"https:\/\/pnas.org\/doi\/full\/10.1073\/pnas.1920017117"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2020,3,10]]},"references-count":49,"journal-issue":{"issue":"12","published-print":{"date-parts":[[2020,3,24]]}},"alternative-id":["10.1073\/pnas.1920017117"],"URL":"https:\/\/doi.org\/10.1073\/pnas.1920017117","relation":{},"ISSN":["0027-8424","1091-6490"],"issn-type":[{"value":"0027-8424","type":"print"},{"value":"1091-6490","type":"electronic"}],"subject":[],"published":{"date-parts":[[2020,3,10]]},"assertion":[{"value":"2020-03-10","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}