[
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            "creatorSummary": "Wang et al.",
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        },
        "data": {
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            "version": 3,
            "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"
                },
                {
                    "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": "25188109",
            "PMCID": "",
            "ISSN": "1465-3931",
            "archive": "",
            "archiveLocation": "",
            "shortTitle": "Hepatobiliary/Pancreas Pathology",
            "language": "eng",
            "libraryCatalog": "NCBI PubMed",
            "callNumber": "",
            "rights": "",
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            "tags": [],
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        "version": 3,
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            "creatorSummary": "Layfield et al.",
            "parsedDate": "2014",
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        "data": {
            "key": "PBR526KX",
            "version": 3,
            "itemType": "journalArticle",
            "title": "Utilization of ancillary studies in the cytologic diagnosis of biliary and pancreatic lesions: The Papanicolaou Society of Cytopathology Guidelines",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Lester J.",
                    "lastName": "Layfield"
                },
                {
                    "creatorType": "author",
                    "firstName": "Hormoz",
                    "lastName": "Ehya"
                },
                {
                    "creatorType": "author",
                    "firstName": "Armando C.",
                    "lastName": "Filie"
                },
                {
                    "creatorType": "author",
                    "firstName": "Ralph H.",
                    "lastName": "Hruban"
                },
                {
                    "creatorType": "author",
                    "firstName": "Nirag",
                    "lastName": "Jhala"
                },
                {
                    "creatorType": "author",
                    "firstName": "Loren",
                    "lastName": "Joseph"
                },
                {
                    "creatorType": "author",
                    "firstName": "Philippe",
                    "lastName": "Vielh"
                },
                {
                    "creatorType": "author",
                    "firstName": "Martha B.",
                    "lastName": "Pitman"
                }
            ],
            "abstractNote": "The Papanicolaou Society of Cytopathology has developed a set of guidelines for pancreatobiliary cytology including indications for endoscopic ultrasound guided fine needle aspiration, terminology and nomenclature of pancreatobiliary disease, ancillary testing and post-biopsy management. All documents are based on the expertise of the authors, a review of the literature, discussion of the draft document at several national and international meetings and synthesis of selected online comments of the draft document. This document presents the results of these discussions regarding the use of ancillary testing in the cytologic diagnosis of biliary and pancreatic lesions. Currently, fluorescence in-situ hybridization (FISH) appears to be the most clinically relevant ancillary technique for cytology of bile duct strictures. The addition of FISH analysis to routine cytologic evaluation appears to yield the highest sensitivity without loss in specificity. Loss of immunohistochemical staining for the protein product of the SMAD4 gene and positive staining for mesothelin support a diagnosis of ductal adenocarcinoma. Immunohistochemical markers for endocrine and exocrine differentiation are sufficient for a diagnosis of endocrine and acinar tumors. Nuclear staining for beta-catenin supports a diagnosis of solid-pseudopapillary neoplasm. Cyst fluid analysis for amylase and carcinoembryonic antigen aids in the pre-operative classification of pancreatic cysts. A number of gene mutations (KRAS, GNAS, von Hippel-Lindau, RNF43 and CTNNB1) may be of aid in the diagnosis of cystic neoplasms. Other ancillary techniques do not appear to improve diagnostic sensitivity sufficiently to justify their increased costs.",
            "publicationTitle": "CytoJournal",
            "publisher": "",
            "place": "",
            "date": "2014",
            "volume": "11",
            "issue": "Suppl 1",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "4",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "Cytojournal",
            "DOI": "10.4103/1742-6413.133352",
            "citationKey": "",
            "url": "",
            "accessDate": "",
            "PMID": "25191518",
            "PMCID": "PMC4153340",
            "ISSN": "1742-6413",
            "archive": "",
            "archiveLocation": "",
            "shortTitle": "Utilization of ancillary studies in the cytologic diagnosis of biliary and pancreatic lesions",
            "language": "eng",
            "libraryCatalog": "NCBI PubMed",
            "callNumber": "",
            "rights": "",
            "extra": "",
            "tags": [],
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            "dateModified": "2014-09-09T14:29:18Z"
        }
    },
    {
        "key": "JGGA38SN",
        "version": 3,
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        "meta": {
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            },
            "creatorSummary": "Timp et al.",
            "parsedDate": "2014",
            "numChildren": 1
        },
        "data": {
            "key": "JGGA38SN",
            "version": 3,
            "itemType": "journalArticle",
            "title": "Large hypomethylated blocks as a universal defining epigenetic alteration in human solid tumors",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Winston",
                    "lastName": "Timp"
                },
                {
                    "creatorType": "author",
                    "firstName": "Hector Corrada",
                    "lastName": "Bravo"
                },
                {
                    "creatorType": "author",
                    "firstName": "Oliver G.",
                    "lastName": "McDonald"
                },
                {
                    "creatorType": "author",
                    "firstName": "Michael",
                    "lastName": "Goggins"
                },
                {
                    "creatorType": "author",
                    "firstName": "Chris",
                    "lastName": "Umbricht"
                },
                {
                    "creatorType": "author",
                    "firstName": "Martha",
                    "lastName": "Zeiger"
                },
                {
                    "creatorType": "author",
                    "firstName": "Andrew P.",
                    "lastName": "Feinberg"
                },
                {
                    "creatorType": "author",
                    "firstName": "Rafael A.",
                    "lastName": "Irizarry"
                }
            ],
            "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",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "61",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "Genome Med",
            "DOI": "10.1186/s13073-014-0061-y",
            "citationKey": "",
            "url": "",
            "accessDate": "",
            "PMID": "25191524",
            "PMCID": "PMC4154522",
            "ISSN": "1756-994X",
            "archive": "",
            "archiveLocation": "",
            "shortTitle": "",
            "language": "eng",
            "libraryCatalog": "NCBI PubMed",
            "callNumber": "",
            "rights": "",
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            "dateAdded": "2014-09-09T14:29:18Z",
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        }
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    {
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                }
            },
            "creatorSummary": "Chung et al.",
            "parsedDate": "2014-09-01",
            "numChildren": 1
        },
        "data": {
            "key": "R4WW5C37",
            "version": 3,
            "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"
                },
                {
                    "creatorType": "author",
                    "firstName": "Andreas",
                    "lastName": "Panopoulos"
                },
                {
                    "creatorType": "author",
                    "firstName": "Ergeng",
                    "lastName": "Hao"
                },
                {
                    "creatorType": "author",
                    "firstName": "Robert",
                    "lastName": "Margolis"
                },
                {
                    "creatorType": "author",
                    "firstName": "Alexey",
                    "lastName": "Terskikh"
                },
                {
                    "creatorType": "author",
                    "firstName": "Fred",
                    "lastName": "Levine"
                }
            ],
            "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": "",
            "partTitle": "",
            "pages": "",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "Physiol Rep",
            "DOI": "10.14814/phy2.12131",
            "citationKey": "",
            "url": "",
            "accessDate": "",
            "PMID": "25194022",
            "PMCID": "",
            "ISSN": "2051-817X",
            "archive": "",
            "archiveLocation": "",
            "shortTitle": "",
            "language": "eng",
            "libraryCatalog": "NCBI PubMed",
            "callNumber": "",
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        }
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    {
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            },
            "creatorSummary": "Nakanuma",
            "parsedDate": "2014-10",
            "numChildren": 1
        },
        "data": {
            "key": "M9PMFCJ2",
            "version": 3,
            "itemType": "journalArticle",
            "title": "Hepatobiliary/Pancreas Pathology: SY11-2 RECENT PROGRESS IN BILIARY TRACT PATHOLOGY AND CHOLANGIOCARCINOMA",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Yasuni",
                    "lastName": "Nakanuma"
                }
            ],
            "abstractNote": "The biliary tract and pancreas develop from the foregut at almost same time, and the morphology of the biliary tract and pancreatic ducts share several features. In addition, there are peribiliary glands around the biliary tract, which occasionally contain pancreatic acini and enzymes. Some pancreatic and biliary tract diseases share similar pathological features. For example, IgG4-related disease affects the pancreas (autoimmune pancreatitis) and the biliary tract (IgG4-related sclerosing cholangitis), and peribiliary cysts and pancreatic damages in chronic alcoholics show similar histologies. Interestingly, perihilar cholangiocarcinoma and pancreatic duct adenocarcinoma, and their precursor lesions such as biliary intraepithelial neoplasm (BilIN) and pancreatic intraepithelial neoplasm (PanIN), show similar histologies and phenotypes, suggesting that these carcinoma and precursor lesions share similar developmental processes. Based on the similarities between the pancreas and biliary tract, we would like to propose that several biliary diseases have their counterparts in the pancreas (pancreatic diseases with pancreatic counterparts).",
            "publicationTitle": "Pathology",
            "publisher": "",
            "place": "",
            "date": "Oct 2014",
            "volume": "46 Suppl 2",
            "issue": "",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "S24-25",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "Pathology",
            "DOI": "10.1097/01.PAT.0000454134.12330.49",
            "citationKey": "",
            "url": "",
            "accessDate": "",
            "PMID": "25188108",
            "PMCID": "",
            "ISSN": "1465-3931",
            "archive": "",
            "archiveLocation": "",
            "shortTitle": "Hepatobiliary/Pancreas Pathology",
            "language": "eng",
            "libraryCatalog": "NCBI PubMed",
            "callNumber": "",
            "rights": "",
            "extra": "",
            "tags": [],
            "collections": [],
            "relations": {},
            "dateAdded": "2014-09-09T14:29:18Z",
            "dateModified": "2014-09-09T14:29:18Z"
        }
    },
    {
        "key": "Z997Z3FJ",
        "version": 3,
        "library": {
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            },
            "creatorSummary": "Arumugam et al.",
            "parsedDate": "2014-08-08",
            "numChildren": 1
        },
        "data": {
            "key": "Z997Z3FJ",
            "version": 3,
            "itemType": "journalArticle",
            "title": "Preliminary evaluation of 1'-[(18)F]fluoroethyl-β-d-lactose ([(18)F]FEL) for detection of pancreatic cancer in nude mouse orthotopic xenografts",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Thiruvengadam",
                    "lastName": "Arumugam"
                },
                {
                    "creatorType": "author",
                    "firstName": "Vincenzo",
                    "lastName": "Paolillo"
                },
                {
                    "creatorType": "author",
                    "firstName": "Daniel",
                    "lastName": "Young"
                },
                {
                    "creatorType": "author",
                    "firstName": "XiaoXia",
                    "lastName": "Wen"
                },
                {
                    "creatorType": "author",
                    "firstName": "Craig D.",
                    "lastName": "Logsdon"
                },
                {
                    "creatorType": "author",
                    "firstName": "Louis",
                    "lastName": "De Palatis"
                },
                {
                    "creatorType": "author",
                    "firstName": "Mian M.",
                    "lastName": "Alauddin"
                }
            ],
            "abstractNote": "INTRODUCTION: Early detection of pancreatic cancer could save many thousands of lives. Non-invasive diagnostic imaging, including PET with [(18)F]FDG, has inadequate resolution for detection of small (2-3mm) pancreatic tumours. We demonstrated the efficacy of PET imaging with an (18)F-labelled lactose derivative, [(18)F]FEDL, that targets HIP/PAP, a biomarker that is overexpressed in the peritumoural pancreas. We developed another analogue, 1-[(18)F]fluoroethyl lactose ([(18)F]FEL), which is simpler to synthesise, for the same application. We conducted a preliminary evaluation of the new probe and its efficacy in detecting orthotopic pancreatic carcinoma xenografts in mice.\nMETHODS: Xenografts were developed in nude mice by injecting L3.6pl/GL(+) pancreatic carcinoma cells into the pancreas of each mouse. Tumour growth was monitored by bioluminescence imaging (BLI); accuracy of BLI tumour size estimates was verified by MRI in two representative mice. When the tumour size reached approximately 2-3mm, the animals were injected with [(18)F]FEL (3.7MBq) and underwent static PET/CT scans. Blood samples were collected at 2, 5, 10, 20 and 60min after [(18)F]FEL injection to track blood clearance. Following imaging, animals were sacrificed and their organs and tumours/pancreatic tissue were collected and counted on a gamma counter. Pancreas, including tumour, was frozen, sliced and used for autoradiography and immunohistochemical analysis of HIP/PAP expression.\nRESULTS: Tumour growth was rapid, as observed by BLI and MRI. Blood clearance of [(18)F]FEL was bi-exponential, with half-lives of approximately 3.5min and 40min. Mean accumulation of [(18)F]FEL in the peritumoural pancreatic tissue was 1.29±0.295 %ID/g, and that in the normal pancreas of control animals was 0.090±0.101 %ID/g. [(18)F]FEL was cleared predominantly by the kidneys. Comparative analysis of autoradiographic images and immunostaining results demonstrated a correlation between [(18)F]FEL binding and HIP/PAP expression.\nCONCLUSION: [(18)F]FEL may be useful for non-invasive imaging of early-stage pancreatic tumours by PET. The results warrant further studies.",
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                    "lastName": "Brugge"
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