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            "title": "Large hypomethylated blocks as a universal defining epigenetic alteration in human solid tumors",
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                {
                    "creatorType": "author",
                    "firstName": "Winston",
                    "lastName": "Timp"
                },
                {
                    "creatorType": "author",
                    "firstName": "Hector Corrada",
                    "lastName": "Bravo"
                },
                {
                    "creatorType": "author",
                    "firstName": "Oliver G.",
                    "lastName": "McDonald"
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                {
                    "creatorType": "author",
                    "firstName": "Michael",
                    "lastName": "Goggins"
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                {
                    "creatorType": "author",
                    "firstName": "Chris",
                    "lastName": "Umbricht"
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                {
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                    "firstName": "Martha",
                    "lastName": "Zeiger"
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                    "firstName": "Andrew P.",
                    "lastName": "Feinberg"
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                    "firstName": "Rafael A.",
                    "lastName": "Irizarry"
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            "abstractNote": "BACKGROUND: One of the most provocative recent observations in cancer epigenetics is the discovery of large hypomethylated blocks, including single copy genes, in colorectal cancer, that correspond in location to heterochromatic LOCKs (large organized chromatin lysine-modifications) and LADs (lamin-associated domains).\nMETHODS: Here we performed a comprehensive genome-scale analysis of 10 breast, 28 colon, nine lung, 38 thyroid, 18 pancreas cancers, and five pancreas neuroendocrine tumors as well as matched normal tissue from most of these cases, as well as 51 premalignant lesions. We used a new statistical approach that allows the identification of large hypomethylated blocks on the Illumina HumanMethylation450 BeadChip platform.\nRESULTS: We find that hypomethylated blocks are a universal feature of common solid human cancer, and that they occur at the earliest stage of premalignant tumors and progress through clinical stages of thyroid and colon cancer development. We also find that the disrupted CpG islands widely reported previously, including hypermethylated island bodies and hypomethylated shores, are enriched in hypomethylated blocks, with flattening of the methylation signal within and flanking the islands. Finally, we found that genes showing higher between individual gene expression variability are enriched within these hypomethylated blocks.\nCONCLUSION: Thus hypomethylated blocks appear to be a universal defining epigenetic alteration in human cancer, at least for common solid tumors.",
            "publicationTitle": "Genome Medicine",
            "publisher": "",
            "place": "",
            "date": "2014",
            "volume": "6",
            "issue": "8",
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            "partTitle": "",
            "pages": "61",
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            "journalAbbreviation": "Genome Med",
            "DOI": "10.1186/s13073-014-0061-y",
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            "language": "eng",
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            "extra": "PMID: 25191524 \nPMCID: PMC4154522",
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            "parsedDate": "2014-09-01",
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            "version": 2,
            "itemType": "journalArticle",
            "title": "Maternal embryonic leucine zipper kinase regulates pancreatic ductal, but not β-cell, regeneration",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Cheng-Ho",
                    "lastName": "Chung"
                },
                {
                    "creatorType": "author",
                    "firstName": "Amber",
                    "lastName": "Miller"
                },
                {
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                    "firstName": "Andreas",
                    "lastName": "Panopoulos"
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                {
                    "creatorType": "author",
                    "firstName": "Ergeng",
                    "lastName": "Hao"
                },
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                    "firstName": "Robert",
                    "lastName": "Margolis"
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                    "firstName": "Alexey",
                    "lastName": "Terskikh"
                },
                {
                    "creatorType": "author",
                    "firstName": "Fred",
                    "lastName": "Levine"
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            ],
            "abstractNote": "The maternal embryonic leucine zipper kinase (MELK) is expressed in stem/progenitor cells in some adult tissues, where it has been implicated in diverse biological processes, including the control of cell proliferation. Here, we described studies on its role in adult pancreatic regeneration in response to injury induced by duct ligation and β-cell ablation. MELK expression was studied using transgenic mice expressing GFP under the control of the MELK promoter, and the role of MELK was studied using transgenic mice deleted in the MELK kinase domain. Pancreatic damage was initiated using duct ligation and chemical beta-cell ablation. By tracing MELK expression using a MELK promoter-GFP transgene, we determined that expression was extremely low in the normal pancreas. However, following duct ligation and β-cell ablation, it became highly expressed in pancreatic ductal cells while remaining weakly expressed in α-cells and β- cells. In a mutant mouse in which the MELK kinase domain was deleted, there was no effect on pancreatic development. There was no apparent effect on islet regeneration, either. However, following duct ligation there was a dramatic increase in the number of small ducts, but no change in the total number of duct cells or duct cell proliferation. In vitro studies indicated that this was likely due to a defect in cell migration. These results implicate MELK in the control of the response of the pancreas to injury, specifically controlling cell migration in normal and transformed pancreatic duct cells.",
            "publicationTitle": "Physiological Reports",
            "publisher": "",
            "place": "",
            "date": "Sep 1, 2014",
            "volume": "2",
            "issue": "9",
            "section": "",
            "partNumber": "",
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            "pages": "",
            "series": "",
            "seriesTitle": "",
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            "journalAbbreviation": "Physiol Rep",
            "DOI": "10.14814/phy2.12131",
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            "url": "",
            "accessDate": "",
            "PMID": "",
            "PMCID": "",
            "ISSN": "2051-817X",
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            "language": "eng",
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            "creatorSummary": "Wang et al.",
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            "version": 2,
            "itemType": "journalArticle",
            "title": "Hepatobiliary/Pancreas Pathology: SY11-3 PANCREATIC DUCTAL ADENOCARCINOMA: NEOADJUVANT THERAPIES AND PATHOLOGY",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Huamin",
                    "lastName": "Wang"
                },
                {
                    "creatorType": "author",
                    "firstName": "Jeannelyn S.",
                    "lastName": "Estrella"
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                    "creatorType": "author",
                    "firstName": "Deyali",
                    "lastName": "Chatterjee"
                },
                {
                    "creatorType": "author",
                    "firstName": "Matthew H.",
                    "lastName": "Katz"
                },
                {
                    "creatorType": "author",
                    "firstName": "Asif",
                    "lastName": "Rashid"
                },
                {
                    "creatorType": "author",
                    "firstName": "Hua",
                    "lastName": "Wang"
                },
                {
                    "creatorType": "author",
                    "firstName": "Robert A.",
                    "lastName": "Wolff"
                },
                {
                    "creatorType": "author",
                    "firstName": "Gauri R.",
                    "lastName": "Varadhachary"
                },
                {
                    "creatorType": "author",
                    "firstName": "Jeffrey E.",
                    "lastName": "Lee"
                },
                {
                    "creatorType": "author",
                    "firstName": "Peter W.",
                    "lastName": "Pisters"
                },
                {
                    "creatorType": "author",
                    "firstName": "James L.",
                    "lastName": "Abbruzzese"
                },
                {
                    "creatorType": "author",
                    "firstName": "Jason B.",
                    "lastName": "Fleming"
                }
            ],
            "abstractNote": "Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human malignancies with less than 5% five-year survival rate. Despite significant improvements in medical and surgical oncology and postoperative mortality rate, the overall survival for patients with pancreatic cancer has not changed significantly in the last four decades. Neoadjuvant chemoradiation therapy (NCT) is increasingly used to treat patients with potentially resectable PDAC, especially for patients with borderline resectable disease. However, analysis of prognostic factors is limited for patients with PDAC treated with NCT and pancreaticoduodenectomy. We systemically examined the pancreaticoduodenectomy specimens from 240 consecutive patients with PDAC who received NCT and pancreaticoduodenectomy between 1999 and 2007 at our institution. We found that posttreatment pathologic stage, pathologic tumor response grading, tumor involvement of the superior mesenteric/portal vein, tumor invasion into the muscular vessels, and perineural invasion are significant prognostic factors in our patient population. Therefore careful pathologic evaluation of the pancreatectomy specimens plays a key role in predicting prognosis of patients with PDAC who received NCT and pancreaticoduodenectomy.",
            "publicationTitle": "Pathology",
            "publisher": "",
            "place": "",
            "date": "Oct 2014",
            "volume": "46 Suppl 2",
            "issue": "",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "S25",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "Pathology",
            "DOI": "10.1097/01.PAT.0000454135.19954.47",
            "citationKey": "",
            "url": "",
            "accessDate": "",
            "PMID": "",
            "PMCID": "",
            "ISSN": "1465-3931",
            "archive": "",
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            "shortTitle": "Hepatobiliary/Pancreas Pathology",
            "language": "eng",
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