at northwestern memorial hospital convention center 251 ......pancreatitis i mecklenburg conference...

38TH ANNUAL MEETING OF THE AMERICAN PANCREATIC ASSOCIATION

AMERICAN PANCREATIC ASSOCIATION GOVERNING BOARDAMERICAN PANCREATIC ASSOCIATION GOVERNING BOARDAMERICAN PANCREATIC ASSOCIATION GOVERNING BOARDAMERICAN PANCREATIC ASSOCIATION GOVERNING BOARDAMERICAN PANCREATIC ASSOCIATION GOVERNING BOARDRaul A. Urrutia, MD, President

Craig D. Logsdon, PhD, President-ElectChristopher E. Forsmark, MD, Past-President

Ashok K. Saluja, PhD, Secretary-TreasurerAndrew Warshaw, MD, Councilor

Suresh Chari, MD, CouncilorDiane Simeone, MD, Councilor

Address Correspondences to:Address Correspondences to:Address Correspondences to:Address Correspondences to:Address Correspondences to:The APA OfficeAmerican Pancreatic AssociationPO Box 14906Minneapolis, MN 55414Phone: (612) 626-9797Fax: (612) 624-8909Email: [email protected]

Ashok K. Saluja, PhDAshok K. Saluja, PhDAshok K. Saluja, PhDAshok K. Saluja, PhDAshok K. Saluja, PhDAPA Secretary-TreasurerAPA Secretary-TreasurerAPA Secretary-TreasurerAPA Secretary-TreasurerAPA Secretary-Treasurer

Professor & Vice ChairDepartment of Surgery

University of Minnesota420 Delaware Street, SE, MMC 290

Minneapolis, MN 55455Phone: (612) 624-8108

Fax: (612) 624-8909Email: [email protected]

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At Northwestern Memorial Hospital Convention CenterAt Northwestern Memorial Hospital Convention CenterAt Northwestern Memorial Hospital Convention CenterAt Northwestern Memorial Hospital Convention CenterAt Northwestern Memorial Hospital Convention Center251 East Huron Street, Chicago, IL

MAIN OFFICESMAIN OFFICESMAIN OFFICESMAIN OFFICESMAIN OFFICES


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POSTER SESSION IPOSTER SESSION IPOSTER SESSION IPOSTER SESSION IPOSTER SESSION IKRUMLOVSKY ATRIUM

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ORAL SESSION 1:ORAL SESSION 1:ORAL SESSION 1:ORAL SESSION 1:ORAL SESSION 1:BASIC SCIENCESBASIC SCIENCESBASIC SCIENCESBASIC SCIENCESBASIC SCIENCES

MECKLENBURGCONFERENCE

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POSTER SESSION IIPOSTER SESSION IIPOSTER SESSION IIPOSTER SESSION IIPOSTER SESSION IIKRUMLOVSKY ATRIUM

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APA/LUSTGARTENAPA/LUSTGARTENAPA/LUSTGARTENAPA/LUSTGARTENAPA/LUSTGARTENSYMPOSIUMSYMPOSIUMSYMPOSIUMSYMPOSIUMSYMPOSIUM

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ATIC CANCER”7:30AM-4PM

DETAILS CAN BE FOUNDIN THE PROGRAM FOR

THE SYMPOSIUM

APA/LUSTGARTEN SYMPOSIUMAPA/LUSTGARTEN SYMPOSIUMAPA/LUSTGARTEN SYMPOSIUMAPA/LUSTGARTEN SYMPOSIUMAPA/LUSTGARTEN SYMPOSIUM“PANCREATIC CANCER 2007: STEM CELLS INTHE PANCREAS AND PANCREATIC CANCER”

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8:00AM8:00AM8:00AM8:00AM8:00AM

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Continental Breakfast & RegistrationContinental Breakfast & RegistrationContinental Breakfast & RegistrationContinental Breakfast & RegistrationContinental Breakfast & RegistrationKrumlovsky Atrium

MOLECULAR MECHANISMS OF KWASHIORKOR-IN-MOLECULAR MECHANISMS OF KWASHIORKOR-IN-MOLECULAR MECHANISMS OF KWASHIORKOR-IN-MOLECULAR MECHANISMS OF KWASHIORKOR-IN-MOLECULAR MECHANISMS OF KWASHIORKOR-IN-DUCED EXOCRINE PANCREAS DYSFUNCTION.DUCED EXOCRINE PANCREAS DYSFUNCTION.DUCED EXOCRINE PANCREAS DYSFUNCTION.DUCED EXOCRINE PANCREAS DYSFUNCTION.DUCED EXOCRINE PANCREAS DYSFUNCTION. SJ Crozier,LE Ginsburg, LG D’Alecy, SA Ernst, JA Williams. Departments ofMolecular & Integrative Physiology and Cell & DevelopmentalBiology, The University of Michigan, Ann Arbor, MI.

PROFILING GLYCAN STRUCTURES ON MUCINS IN THEPROFILING GLYCAN STRUCTURES ON MUCINS IN THEPROFILING GLYCAN STRUCTURES ON MUCINS IN THEPROFILING GLYCAN STRUCTURES ON MUCINS IN THEPROFILING GLYCAN STRUCTURES ON MUCINS IN THESERA OF PANCREATIC CANCER PATIENTS USINGSERA OF PANCREATIC CANCER PATIENTS USINGSERA OF PANCREATIC CANCER PATIENTS USINGSERA OF PANCREATIC CANCER PATIENTS USINGSERA OF PANCREATIC CANCER PATIENTS USINGANTIBODY ARRAYS: CANCER-ASSOCIATED VARIATIONANTIBODY ARRAYS: CANCER-ASSOCIATED VARIATIONANTIBODY ARRAYS: CANCER-ASSOCIATED VARIATIONANTIBODY ARRAYS: CANCER-ASSOCIATED VARIATIONANTIBODY ARRAYS: CANCER-ASSOCIATED VARIATIONAND POTENTIAL DISEASE MARKERS.AND POTENTIAL DISEASE MARKERS.AND POTENTIAL DISEASE MARKERS.AND POTENTIAL DISEASE MARKERS.AND POTENTIAL DISEASE MARKERS. T Yue, S Chen, IGoldstein, MA Hollingsworth, D Simeone, RE Brand, BB Haab.Van Andel Research Institute, Grand Rapids, MI, University ofMichigan Medical School, Ann Arbor, MI, University of NebraskaMedical Center, Omaha, NE, Evanston Northwestern Healthcare,Evanston, IL.

DIFERENTIAL EFFECTS OF BILE ACIDS ON PANCREATICDIFERENTIAL EFFECTS OF BILE ACIDS ON PANCREATICDIFERENTIAL EFFECTS OF BILE ACIDS ON PANCREATICDIFERENTIAL EFFECTS OF BILE ACIDS ON PANCREATICDIFERENTIAL EFFECTS OF BILE ACIDS ON PANCREATICDUCTAL BICARBONATE SECRETIONDUCTAL BICARBONATE SECRETIONDUCTAL BICARBONATE SECRETIONDUCTAL BICARBONATE SECRETIONDUCTAL BICARBONATE SECRETION. P Hegyi, V Venglovecz,B Ozsvari, T Takacs, J Lonovics, A Varro, Z Rakonczay. FirstDepartment of Medicine, Department of Pharmacology andPharmacotherapy. University of Szeged, Szeged, Hungary.

TRIPTOLIDE INHIBITS TUMOR GROWTH AND LOCAL-TRIPTOLIDE INHIBITS TUMOR GROWTH AND LOCAL-TRIPTOLIDE INHIBITS TUMOR GROWTH AND LOCAL-TRIPTOLIDE INHIBITS TUMOR GROWTH AND LOCAL-TRIPTOLIDE INHIBITS TUMOR GROWTH AND LOCAL-REGIONAL SPREAD IN VIVO VIA INCREASED APOPTOSISREGIONAL SPREAD IN VIVO VIA INCREASED APOPTOSISREGIONAL SPREAD IN VIVO VIA INCREASED APOPTOSISREGIONAL SPREAD IN VIVO VIA INCREASED APOPTOSISREGIONAL SPREAD IN VIVO VIA INCREASED APOPTOSISAND DECREASED HEAT SHOCK PROTEIN 70 (HSP70).AND DECREASED HEAT SHOCK PROTEIN 70 (HSP70).AND DECREASED HEAT SHOCK PROTEIN 70 (HSP70).AND DECREASED HEAT SHOCK PROTEIN 70 (HSP70).AND DECREASED HEAT SHOCK PROTEIN 70 (HSP70).PA Phillips, V Dudeja, D Borja-Cacho, J McCarroll, R Dawra, WGrizzle, S Vickers, A Saluja. Department of Surgery, Universityof Minnesota, Minneapolis, MN.

Oral Session 1: Basic SciencesOral Session 1: Basic SciencesOral Session 1: Basic SciencesOral Session 1: Basic SciencesOral Session 1: Basic SciencesMecklenburg Conference RoomModerators: Vijay Singh, MD & Herbert Gaisano, MD

44444 THURSDAY, NOVEMBER 1, 2007THURSDAY, NOVEMBER 1, 2007THURSDAY, NOVEMBER 1, 2007THURSDAY, NOVEMBER 1, 2007THURSDAY, NOVEMBER 1, 2007



9:00AM9:00AM9:00AM9:00AM9:00AM

9:15AM9:15AM9:15AM9:15AM9:15AM

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RefreshmentsRefreshmentsRefreshmentsRefreshmentsRefreshmentsKrumlovsky Atrium

TISSUE TRANSGLUTAMINASE DOWNREGULATIONTISSUE TRANSGLUTAMINASE DOWNREGULATIONTISSUE TRANSGLUTAMINASE DOWNREGULATIONTISSUE TRANSGLUTAMINASE DOWNREGULATIONTISSUE TRANSGLUTAMINASE DOWNREGULATIONPOTENTIATES GEMCITABINE EFFICACY AND BLOCKSPOTENTIATES GEMCITABINE EFFICACY AND BLOCKSPOTENTIATES GEMCITABINE EFFICACY AND BLOCKSPOTENTIATES GEMCITABINE EFFICACY AND BLOCKSPOTENTIATES GEMCITABINE EFFICACY AND BLOCKSPANCREATIC CANCER GROWTH AND METASTASIS PANCREATIC CANCER GROWTH AND METASTASIS PANCREATIC CANCER GROWTH AND METASTASIS PANCREATIC CANCER GROWTH AND METASTASIS PANCREATIC CANCER GROWTH AND METASTASIS INININININVIVOVIVOVIVOVIVOVIVO. S Guha, S Verma, A Kunnumakkara, P Diagaradjane, SKrishnan, J Gelovani, B Aggarwal, G Lopez-Bernstein, K Mehta.Departments of Gastroenterology, Hepatology, and Nutrition,Experimental Therapeutics, Radiation Oncology, ExperimentalDiagnostic Imaging, University of Texas M. D. Anderson CancerCenter, Houston, Texas.

SYNAPTOTAGMIN 1, THE NEURONAL CALCIUM SENSINGSYNAPTOTAGMIN 1, THE NEURONAL CALCIUM SENSINGSYNAPTOTAGMIN 1, THE NEURONAL CALCIUM SENSINGSYNAPTOTAGMIN 1, THE NEURONAL CALCIUM SENSINGSYNAPTOTAGMIN 1, THE NEURONAL CALCIUM SENSINGPROTEIN FOR EXOCYTOSIS AND COMPLEXIN 2 AREPROTEIN FOR EXOCYTOSIS AND COMPLEXIN 2 AREPROTEIN FOR EXOCYTOSIS AND COMPLEXIN 2 AREPROTEIN FOR EXOCYTOSIS AND COMPLEXIN 2 AREPROTEIN FOR EXOCYTOSIS AND COMPLEXIN 2 AREPRESENT IN ACINAR CELLS AND MODULATE CALCIUM-PRESENT IN ACINAR CELLS AND MODULATE CALCIUM-PRESENT IN ACINAR CELLS AND MODULATE CALCIUM-PRESENT IN ACINAR CELLS AND MODULATE CALCIUM-PRESENT IN ACINAR CELLS AND MODULATE CALCIUM-DEPENDENT EXOCYTOSISDEPENDENT EXOCYTOSISDEPENDENT EXOCYTOSISDEPENDENT EXOCYTOSISDEPENDENT EXOCYTOSIS. MA Falkowski, DDH Thomas, CLMartin, MD Baumler, GE Groblewski. Department of NutritionalSciences, University of Wisconsin, Madison, WI.

AN ACTIVE AKT IS REQUIRED FOR THE HEDGEHOG-AN ACTIVE AKT IS REQUIRED FOR THE HEDGEHOG-AN ACTIVE AKT IS REQUIRED FOR THE HEDGEHOG-AN ACTIVE AKT IS REQUIRED FOR THE HEDGEHOG-AN ACTIVE AKT IS REQUIRED FOR THE HEDGEHOG-MEDIATED SURVIVAL OF PANCREATIC CANCER CELLSMEDIATED SURVIVAL OF PANCREATIC CANCER CELLSMEDIATED SURVIVAL OF PANCREATIC CANCER CELLSMEDIATED SURVIVAL OF PANCREATIC CANCER CELLSMEDIATED SURVIVAL OF PANCREATIC CANCER CELLS.GL Lund, JJ Han, C Lokko, ME Fernandez-Zapico.Gastroenterology Research Unit, Mayo Clinic College ofMedicine, Rochester, MN.

HP1 HP1 HP1 HP1 HP1 ã HAS A SIGNIFICANT IMPACT ON CELL CYCLE HAS A SIGNIFICANT IMPACT ON CELL CYCLE HAS A SIGNIFICANT IMPACT ON CELL CYCLE HAS A SIGNIFICANT IMPACT ON CELL CYCLE HAS A SIGNIFICANT IMPACT ON CELL CYCLEPROGRESSION THROUGH THE REGULATION OF G2/M,PROGRESSION THROUGH THE REGULATION OF G2/M,PROGRESSION THROUGH THE REGULATION OF G2/M,PROGRESSION THROUGH THE REGULATION OF G2/M,PROGRESSION THROUGH THE REGULATION OF G2/M,CENTROSOME BIOLOGY AND, CHROMOSOMAL STABILITYCENTROSOME BIOLOGY AND, CHROMOSOMAL STABILITYCENTROSOME BIOLOGY AND, CHROMOSOMAL STABILITYCENTROSOME BIOLOGY AND, CHROMOSOMAL STABILITYCENTROSOME BIOLOGY AND, CHROMOSOMAL STABILITYIN PANCREATIC CANCER CELLSIN PANCREATIC CANCER CELLSIN PANCREATIC CANCER CELLSIN PANCREATIC CANCER CELLSIN PANCREATIC CANCER CELLS..... G Lomberk, D Bensi, TChristensen, J Salisbury, R Urrutia. GI Research Unit. Mayo Clinic,Rochester, MN.

THURSDAY, NOVEMBER 1, 2007THURSDAY, NOVEMBER 1, 2007THURSDAY, NOVEMBER 1, 2007THURSDAY, NOVEMBER 1, 2007THURSDAY, NOVEMBER 1, 2007 55555

10:15 AM - 11:45 PM10:15 AM - 11:45 PM10:15 AM - 11:45 PM10:15 AM - 11:45 PM10:15 AM - 11:45 PMOral Session 2: Pancreatic Cancer IOral Session 2: Pancreatic Cancer IOral Session 2: Pancreatic Cancer IOral Session 2: Pancreatic Cancer IOral Session 2: Pancreatic Cancer IMecklenburg Conference Room

Moderators: Claus Schäfer, MD & Paul Grippo, PhD


10:15AM10:15AM10:15AM10:15AM10:15AM

10:30AM10:30AM10:30AM10:30AM10:30AM

10:45AM10:45AM10:45AM10:45AM10:45AM

11:00AM11:00AM11:00AM11:00AM11:00AM

PILOT STUDY DETERMINING THE FEASIBILITY OFPILOT STUDY DETERMINING THE FEASIBILITY OFPILOT STUDY DETERMINING THE FEASIBILITY OFPILOT STUDY DETERMINING THE FEASIBILITY OFPILOT STUDY DETERMINING THE FEASIBILITY OFDIAGNOSING PANCREATIC CANCER USING SINGLE CELLDIAGNOSING PANCREATIC CANCER USING SINGLE CELLDIAGNOSING PANCREATIC CANCER USING SINGLE CELLDIAGNOSING PANCREATIC CANCER USING SINGLE CELLDIAGNOSING PANCREATIC CANCER USING SINGLE CELLPARTIAL WAVE SPECTROSCOPY OF THE DUODENALPARTIAL WAVE SPECTROSCOPY OF THE DUODENALPARTIAL WAVE SPECTROSCOPY OF THE DUODENALPARTIAL WAVE SPECTROSCOPY OF THE DUODENALPARTIAL WAVE SPECTROSCOPY OF THE DUODENALMUCOSA.MUCOSA.MUCOSA.MUCOSA.MUCOSA. H Subramanian, R Brand, P Pradhan, N Deep, V Parikh,N Hasabou, D Polidoro, C Sturgis, V Backman. BiomedicalEngineering Department, Northwestern University, Evanston,IL, Evanston Northwestern Healthcare, Evanston, IL.

HSP70 INHIBITS APOPTOSIS IN PANCREATIC CANCERHSP70 INHIBITS APOPTOSIS IN PANCREATIC CANCERHSP70 INHIBITS APOPTOSIS IN PANCREATIC CANCERHSP70 INHIBITS APOPTOSIS IN PANCREATIC CANCERHSP70 INHIBITS APOPTOSIS IN PANCREATIC CANCERCELLS BY TWO INDEPENDENT MECHANISMS:CELLS BY TWO INDEPENDENT MECHANISMS:CELLS BY TWO INDEPENDENT MECHANISMS:CELLS BY TWO INDEPENDENT MECHANISMS:CELLS BY TWO INDEPENDENT MECHANISMS:ATTENUATING CYTOSOLIC CAATTENUATING CYTOSOLIC CAATTENUATING CYTOSOLIC CAATTENUATING CYTOSOLIC CAATTENUATING CYTOSOLIC CA2+2+2+2+2+ AND STABILIZING AND STABILIZING AND STABILIZING AND STABILIZING AND STABILIZINGLYSOSOMES.LYSOSOMES.LYSOSOMES.LYSOSOMES.LYSOSOMES. V Dudeja, P Phillips, R Dawra, S Vickers, A Saluja.Department of Surgery, University of Minnesota, Minneapolis,MN.

ASYMPTOMATIC HYPERAMYLASEMIA AND/ORASYMPTOMATIC HYPERAMYLASEMIA AND/ORASYMPTOMATIC HYPERAMYLASEMIA AND/ORASYMPTOMATIC HYPERAMYLASEMIA AND/ORASYMPTOMATIC HYPERAMYLASEMIA AND/ORSPONTANEOUS DEVELOPMENT OF MURINE PANCREATICSPONTANEOUS DEVELOPMENT OF MURINE PANCREATICSPONTANEOUS DEVELOPMENT OF MURINE PANCREATICSPONTANEOUS DEVELOPMENT OF MURINE PANCREATICSPONTANEOUS DEVELOPMENT OF MURINE PANCREATICINTRAEPITHELIAL NEOPLASIA (MPANIN) IN ELA-INTRAEPITHELIAL NEOPLASIA (MPANIN) IN ELA-INTRAEPITHELIAL NEOPLASIA (MPANIN) IN ELA-INTRAEPITHELIAL NEOPLASIA (MPANIN) IN ELA-INTRAEPITHELIAL NEOPLASIA (MPANIN) IN ELA-CREERT2; LSL-KRASCREERT2; LSL-KRASCREERT2; LSL-KRASCREERT2; LSL-KRASCREERT2; LSL-KRASG12DG12DG12DG12DG12D MICE: INSIGHTS INTO CELLULAR MICE: INSIGHTS INTO CELLULAR MICE: INSIGHTS INTO CELLULAR MICE: INSIGHTS INTO CELLULAR MICE: INSIGHTS INTO CELLULARORIGINS OF PANCREATIC CANCER. ORIGINS OF PANCREATIC CANCER. ORIGINS OF PANCREATIC CANCER. ORIGINS OF PANCREATIC CANCER. ORIGINS OF PANCREATIC CANCER. N Habbe, RA Meguid,V Fendrich, G Feldmann, RH Hruban, SD Leach, A Maitra.Departments of Pathology and Surgery, The Sol GoldmanPancreatic Cancer Research Center, Johns Hopkins UniversitySchool of Medicine, Baltimore, MD.

CONCOMITANT ACTIVATION OF KRAS AND EGFRCONCOMITANT ACTIVATION OF KRAS AND EGFRCONCOMITANT ACTIVATION OF KRAS AND EGFRCONCOMITANT ACTIVATION OF KRAS AND EGFRCONCOMITANT ACTIVATION OF KRAS AND EGFRSIGNALING IN MURINE PANCREATIC CARCINOGENESIS.SIGNALING IN MURINE PANCREATIC CARCINOGENESIS.SIGNALING IN MURINE PANCREATIC CARCINOGENESIS.SIGNALING IN MURINE PANCREATIC CARCINOGENESIS.SIGNALING IN MURINE PANCREATIC CARCINOGENESIS.JT Siveke, H Einwaechter, I Wasilewitsch, B Sipos, G Kloeppel, RSchmid. Technical University of Munich, Germany, Universityof Schleswig-Holstein, Kiel, Germany.

NEUROPILIN-1 ASSOCIATION WITH c-MET INNEUROPILIN-1 ASSOCIATION WITH c-MET INNEUROPILIN-1 ASSOCIATION WITH c-MET INNEUROPILIN-1 ASSOCIATION WITH c-MET INNEUROPILIN-1 ASSOCIATION WITH c-MET INPANCREATIC CANCER CELLS ENHANCES HEPATOCYTEPANCREATIC CANCER CELLS ENHANCES HEPATOCYTEPANCREATIC CANCER CELLS ENHANCES HEPATOCYTEPANCREATIC CANCER CELLS ENHANCES HEPATOCYTEPANCREATIC CANCER CELLS ENHANCES HEPATOCYTEGROWTH FACTOR-MEDIATED CELL INVASION.GROWTH FACTOR-MEDIATED CELL INVASION.GROWTH FACTOR-MEDIATED CELL INVASION.GROWTH FACTOR-MEDIATED CELL INVASION.GROWTH FACTOR-MEDIATED CELL INVASION. A.Matsushita, T. Götze, M. Kawamoto, K. Cho, Y. Nakamura, T.Aimoto, E. Uchida, T. Ishiwata, Z. Naito, T. Tajiri, M Korc.Department of Surgery, Department of Integrative Pathology,Nippon Medical School, Tokyo, Japan, Departments of Medicine,and Pharmacology and Toxicology, Dartmouth Medical School,Hanover, NH.


11:15AM11:15AM11:15AM11:15AM11:15AM


11:30AM11:30AM11:30AM11:30AM11:30AM

11:45 AM - 12:30 PM11:45 AM - 12:30 PM11:45 AM - 12:30 PM11:45 AM - 12:30 PM11:45 AM - 12:30 PM

12:30 PM - 1:30 PM12:30 PM - 1:30 PM12:30 PM - 1:30 PM12:30 PM - 1:30 PM12:30 PM - 1:30 PM

Frank P. Brooks Memorial Basic ScienceFrank P. Brooks Memorial Basic ScienceFrank P. Brooks Memorial Basic ScienceFrank P. Brooks Memorial Basic ScienceFrank P. Brooks Memorial Basic ScienceState-of-the-Art LectureState-of-the-Art LectureState-of-the-Art LectureState-of-the-Art LectureState-of-the-Art LectureIntroduction: Raul Urrutia, MDJ. Silvio Gutkind, Ph.DJ. Silvio Gutkind, Ph.DJ. Silvio Gutkind, Ph.DJ. Silvio Gutkind, Ph.DJ. Silvio Gutkind, Ph.DChief, Oral and Pharyngeal Cancer Branch, DIRChief, Cell Growth Regulation Section and Molecular CarcinogenesisUnit, OPCB, DIRNational Institutes of Health

“““““G Protein-regulated Signaling Networks and Cancer: What HaveG Protein-regulated Signaling Networks and Cancer: What HaveG Protein-regulated Signaling Networks and Cancer: What HaveG Protein-regulated Signaling Networks and Cancer: What HaveG Protein-regulated Signaling Networks and Cancer: What HaveWe Learned?We Learned?We Learned?We Learned?We Learned?”””””

Complementary Luncheon &Complementary Luncheon &Complementary Luncheon &Complementary Luncheon &Complementary Luncheon &Poster ReviewPoster ReviewPoster ReviewPoster ReviewPoster ReviewKrumlovsky Atrium


EVALUATING THE IMPACT OF A MULTIDISCIPLINARYEVALUATING THE IMPACT OF A MULTIDISCIPLINARYEVALUATING THE IMPACT OF A MULTIDISCIPLINARYEVALUATING THE IMPACT OF A MULTIDISCIPLINARYEVALUATING THE IMPACT OF A MULTIDISCIPLINARYSINGLE DAY CLINIC ON THE MANAGEMENT OFSINGLE DAY CLINIC ON THE MANAGEMENT OFSINGLE DAY CLINIC ON THE MANAGEMENT OFSINGLE DAY CLINIC ON THE MANAGEMENT OFSINGLE DAY CLINIC ON THE MANAGEMENT OFPANCREATIC CANCER.PANCREATIC CANCER.PANCREATIC CANCER.PANCREATIC CANCER.PANCREATIC CANCER. KR Voong, JM Herman, J Colemann, DLaheru, R Schulick, K Campbell, T Pawlik, E Fishman, F Asrari, MMakary, S Ali, R Donehower, D Frassica, RH Hruban. TheDepartments of Radiation Oncology & Molecular RadiationSciences, Medical Oncology, Surgery, Pathology, Radiology; TheSol Goldman Pancreatic Cancer Research Center, Johns HopkinsHospital, Baltimore, MD.

1:30 PM - 3:30 PM1:30 PM - 3:30 PM1:30 PM - 3:30 PM1:30 PM - 3:30 PM1:30 PM - 3:30 PMOral Session 3: Pancreatitis IOral Session 3: Pancreatitis IOral Session 3: Pancreatitis IOral Session 3: Pancreatitis IOral Session 3: Pancreatitis IMecklenberg Conference RoomModerators: Christopher E. Forsmark, MD & Sohail Z. Husain, MD

MITOCHONDRIAL CAMITOCHONDRIAL CAMITOCHONDRIAL CAMITOCHONDRIAL CAMITOCHONDRIAL CA2+2+2+2+2+ OVERLOAD IS THE PRINCIPAL OVERLOAD IS THE PRINCIPAL OVERLOAD IS THE PRINCIPAL OVERLOAD IS THE PRINCIPAL OVERLOAD IS THE PRINCIPALMECHANISM OF INJURY TO PANCREATIC ACINAR CELLSMECHANISM OF INJURY TO PANCREATIC ACINAR CELLSMECHANISM OF INJURY TO PANCREATIC ACINAR CELLSMECHANISM OF INJURY TO PANCREATIC ACINAR CELLSMECHANISM OF INJURY TO PANCREATIC ACINAR CELLSFROM BILE SALTS. FROM BILE SALTS. FROM BILE SALTS. FROM BILE SALTS. FROM BILE SALTS. JA Murphy, DN Criddle, NP Neoptolemos,OV Gerasimenko, AV Tepikin, OH Petersen, R Sutton. MRC Group,Physiological Laboratory, Division of Surgery and Oncology,University of Liverpool, UK.

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PANCREATECTOMY (P) AND ISLET AUTO-PANCREATECTOMY (P) AND ISLET AUTO-PANCREATECTOMY (P) AND ISLET AUTO-PANCREATECTOMY (P) AND ISLET AUTO-PANCREATECTOMY (P) AND ISLET AUTO-TRANSPLANTATION (IAT) FOR CHRONIC PANCREATITISTRANSPLANTATION (IAT) FOR CHRONIC PANCREATITISTRANSPLANTATION (IAT) FOR CHRONIC PANCREATITISTRANSPLANTATION (IAT) FOR CHRONIC PANCREATITISTRANSPLANTATION (IAT) FOR CHRONIC PANCREATITIS(CP).(CP).(CP).(CP).(CP). AM Carlson, JJ Blondet, A Gruessner, MD Bellin, B Hering,G Beilman, AM Moran, DER Sutherland. Departments of Surgeryand Pediatrics, University of Minnesota, Minneapolis, MN.

PANCREATIC ACINAR CELL DAMAGE RESULTING FROMPANCREATIC ACINAR CELL DAMAGE RESULTING FROMPANCREATIC ACINAR CELL DAMAGE RESULTING FROMPANCREATIC ACINAR CELL DAMAGE RESULTING FROMPANCREATIC ACINAR CELL DAMAGE RESULTING FROMSUPRA-STIMULATION IS REGULATED BY SRC-MEDIATEDSUPRA-STIMULATION IS REGULATED BY SRC-MEDIATEDSUPRA-STIMULATION IS REGULATED BY SRC-MEDIATEDSUPRA-STIMULATION IS REGULATED BY SRC-MEDIATEDSUPRA-STIMULATION IS REGULATED BY SRC-MEDIATEDCORTACTIN-ACTIN DYNAMICS.CORTACTIN-ACTIN DYNAMICS.CORTACTIN-ACTIN DYNAMICS.CORTACTIN-ACTIN DYNAMICS.CORTACTIN-ACTIN DYNAMICS. VP Singh, MA McNiven.Department of Gastroenterology and Hepatology, Mayo ClinicCollege of Medicine, Rochester, MN.

THE NATURAL HISTORY OF ACUTE PANCREATITIS: ATHE NATURAL HISTORY OF ACUTE PANCREATITIS: ATHE NATURAL HISTORY OF ACUTE PANCREATITIS: ATHE NATURAL HISTORY OF ACUTE PANCREATITIS: ATHE NATURAL HISTORY OF ACUTE PANCREATITIS: ALONG-TERM POPULATION-BASED STUDY. LONG-TERM POPULATION-BASED STUDY. LONG-TERM POPULATION-BASED STUDY. LONG-TERM POPULATION-BASED STUDY. LONG-TERM POPULATION-BASED STUDY. PG Lankisch,N Breuer, A Bruns, B Weber-Dany, AB Lowenfels, P Maisonneuve.Municipal Clinic of Lueneburg, Germany, New York MedicalCollege, Valhalla, NY, USA, European Institute of Oncology,Milan, Italy.

INCREASED EXPRESSION OF HEAT SHOCK PROTEIN 70INCREASED EXPRESSION OF HEAT SHOCK PROTEIN 70INCREASED EXPRESSION OF HEAT SHOCK PROTEIN 70INCREASED EXPRESSION OF HEAT SHOCK PROTEIN 70INCREASED EXPRESSION OF HEAT SHOCK PROTEIN 70LEADS TO STABILIZATION OF PANCREATIC ACINARLEADS TO STABILIZATION OF PANCREATIC ACINARLEADS TO STABILIZATION OF PANCREATIC ACINARLEADS TO STABILIZATION OF PANCREATIC ACINARLEADS TO STABILIZATION OF PANCREATIC ACINARLYSOSOMES IN RATS IN VITRO.LYSOSOMES IN RATS IN VITRO.LYSOSOMES IN RATS IN VITRO.LYSOSOMES IN RATS IN VITRO.LYSOSOMES IN RATS IN VITRO. R. Talukdar, R. Dawra, V.Dudeja, D. Borja, P. Zwolak, Y. Yokoyama, R. Chugh, S. Vickers,A. Saluja. Department of Surgery, University of Minnesota,Minneapolis, MN.

THE IMPACT OF LEUKOCYTES ON EARLY AND LATETHE IMPACT OF LEUKOCYTES ON EARLY AND LATETHE IMPACT OF LEUKOCYTES ON EARLY AND LATETHE IMPACT OF LEUKOCYTES ON EARLY AND LATETHE IMPACT OF LEUKOCYTES ON EARLY AND LATEPROTEASE ACTIVATION IN EXPERIMENTALPROTEASE ACTIVATION IN EXPERIMENTALPROTEASE ACTIVATION IN EXPERIMENTALPROTEASE ACTIVATION IN EXPERIMENTALPROTEASE ACTIVATION IN EXPERIMENTALPANCREATITIS.PANCREATITIS.PANCREATITIS.PANCREATITIS.PANCREATITIS. J Mayerle, M Sendler, A Dummer, B Brandt-Nedelev, K Scharffetter-Kochanek, FU Weiss, W Halangk, MMLerch. Department of Medicine A, Ernst-Moritz-Arndt-University Greifswald, Germany, Division of ExperimentalSurgery, Otto-von-Guericke University Magdeburg, Germany,Department of Dermatology and Allergology, University of Ulm,Germany.

DESCRIBING CT FINDINGS IN SEVERE ACUTEDESCRIBING CT FINDINGS IN SEVERE ACUTEDESCRIBING CT FINDINGS IN SEVERE ACUTEDESCRIBING CT FINDINGS IN SEVERE ACUTEDESCRIBING CT FINDINGS IN SEVERE ACUTEPANCREATITIS USING MORPHOLOGIC TERMS: ANPANCREATITIS USING MORPHOLOGIC TERMS: ANPANCREATITIS USING MORPHOLOGIC TERMS: ANPANCREATITIS USING MORPHOLOGIC TERMS: ANPANCREATITIS USING MORPHOLOGIC TERMS: ANINTERNATIONAL INTEROBSERVER AGREEMENT STUDY.INTERNATIONAL INTEROBSERVER AGREEMENT STUDY.INTERNATIONAL INTEROBSERVER AGREEMENT STUDY.INTERNATIONAL INTEROBSERVER AGREEMENT STUDY.INTERNATIONAL INTEROBSERVER AGREEMENT STUDY.HC van Santvoort, TL Bollen, MG Besselink, KD Horvath, PCFreeny, HG Gooszen, The International Reviewer Group. Surgery,University Medical Center Utrecht, Radiology, St AntoniusHospital, Nieuwegein, The Netherlands, Surgery, Radiology,University of Washington Medical Center, Seattle.


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Refreshments Refreshments Refreshments Refreshments Refreshments & & & & & Poster DiscussionPoster DiscussionPoster DiscussionPoster DiscussionPoster DiscussionKrumlovsky Atrium

Clinical Controversies in PancreatologyClinical Controversies in PancreatologyClinical Controversies in PancreatologyClinical Controversies in PancreatologyClinical Controversies in Pancreatology“Should patients with a strong family history of“Should patients with a strong family history of“Should patients with a strong family history of“Should patients with a strong family history of“Should patients with a strong family history ofpancreatic cancer be screened on a periodic basis forpancreatic cancer be screened on a periodic basis forpancreatic cancer be screened on a periodic basis forpancreatic cancer be screened on a periodic basis forpancreatic cancer be screened on a periodic basis forcancer of the pancreas?”cancer of the pancreas?”cancer of the pancreas?”cancer of the pancreas?”cancer of the pancreas?”

Will iam Steinberg, MDWill iam Steinberg, MDWill iam Steinberg, MDWill iam Steinberg, MDWill iam Steinberg, MDDepartment of Medicine, George Washington University MedicalCenterWashington, DCIntroduction

Marcia Irene Canto, MD, MHSMarcia Irene Canto, MD, MHSMarcia Irene Canto, MD, MHSMarcia Irene Canto, MD, MHSMarcia Irene Canto, MD, MHSDivision of Gastroenterology & Hepatology, Johns Hopkins UniversityBaltimore, MDPatients with a strong family history should be screened on a periodicbasis for cancer of the pancreas

Michael J. Levy, MDMichael J. Levy, MDMichael J. Levy, MDMichael J. Levy, MDMichael J. Levy, MDDepartment of Internal Medicine, Mayo ClinicRochester, MNPatients with a strong family history should not be screened on aperiodic basis for cancer of the pancreas

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Questions and AnswersQuestions and AnswersQuestions and AnswersQuestions and AnswersQuestions and Answers


DIFFERENTIAL ANTI-INFLAMMATORY PROPERTIES OFDIFFERENTIAL ANTI-INFLAMMATORY PROPERTIES OFDIFFERENTIAL ANTI-INFLAMMATORY PROPERTIES OFDIFFERENTIAL ANTI-INFLAMMATORY PROPERTIES OFDIFFERENTIAL ANTI-INFLAMMATORY PROPERTIES OFPEROXISOME PROLIFERATOR-ACTIVATED RECEPTORSPEROXISOME PROLIFERATOR-ACTIVATED RECEPTORSPEROXISOME PROLIFERATOR-ACTIVATED RECEPTORSPEROXISOME PROLIFERATOR-ACTIVATED RECEPTORSPEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS(PPAR) Á AND Ã IN CERULEIN-INDUCED PANCREATITIS.(PPAR) Á AND Ã IN CERULEIN-INDUCED PANCREATITIS.(PPAR) Á AND Ã IN CERULEIN-INDUCED PANCREATITIS.(PPAR) Á AND Ã IN CERULEIN-INDUCED PANCREATITIS.(PPAR) Á AND Ã IN CERULEIN-INDUCED PANCREATITIS.T. Griesbacher, V. Pommer, R. Schuligoi, B. Tiran, B.A. Peskar.Inst. Exp. Clin. Pharmacology, and Clin. Dept. Med. Chem. Lab.Diagnostics, Medical University of Graz, Austria.


8:00 AM - 6:00 PM8:00 AM - 6:00 PM8:00 AM - 6:00 PM8:00 AM - 6:00 PM8:00 AM - 6:00 PM

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POSTER SESSION IPOSTER SESSION IPOSTER SESSION IPOSTER SESSION IPOSTER SESSION IKrumlovsky AtriumBOARD#BOARD#BOARD#BOARD#BOARD# TITLETITLETITLETITLETITLE

TRANSCRIPTIONAL PROFILE OF CALCINEURIN-NFATTRANSCRIPTIONAL PROFILE OF CALCINEURIN-NFATTRANSCRIPTIONAL PROFILE OF CALCINEURIN-NFATTRANSCRIPTIONAL PROFILE OF CALCINEURIN-NFATTRANSCRIPTIONAL PROFILE OF CALCINEURIN-NFATSIGNALING IN CCK-INDUCED PANCREATIC GROWTH.SIGNALING IN CCK-INDUCED PANCREATIC GROWTH.SIGNALING IN CCK-INDUCED PANCREATIC GROWTH.SIGNALING IN CCK-INDUCED PANCREATIC GROWTH.SIGNALING IN CCK-INDUCED PANCREATIC GROWTH.GT Gurda, JA Williams. Molecular & Integrative Physiology, TheUniversity of Michigan, Ann Arbor, MI.VAV1 SIGNALING: A NOVEL REGULATOR OF GLI TRAN-VAV1 SIGNALING: A NOVEL REGULATOR OF GLI TRAN-VAV1 SIGNALING: A NOVEL REGULATOR OF GLI TRAN-VAV1 SIGNALING: A NOVEL REGULATOR OF GLI TRAN-VAV1 SIGNALING: A NOVEL REGULATOR OF GLI TRAN-SCRIPTIONAL ACTIVITY IN PANCREATIC CANCER.SCRIPTIONAL ACTIVITY IN PANCREATIC CANCER.SCRIPTIONAL ACTIVITY IN PANCREATIC CANCER.SCRIPTIONAL ACTIVITY IN PANCREATIC CANCER.SCRIPTIONAL ACTIVITY IN PANCREATIC CANCER. LJPeña-Sanchez, JJ Han, S Bangarulingam, DD Billadeau, MEFernandez-Zapico. Gastroenterology Research Unit, MayoClinic College of Medicine, Rochester, MN.SUPPRESSOR OF FUSED PROMOTES GLI ONCOGENICSUPPRESSOR OF FUSED PROMOTES GLI ONCOGENICSUPPRESSOR OF FUSED PROMOTES GLI ONCOGENICSUPPRESSOR OF FUSED PROMOTES GLI ONCOGENICSUPPRESSOR OF FUSED PROMOTES GLI ONCOGENICACTIVITY IN PANCREATIC CANCER. ACTIVITY IN PANCREATIC CANCER. ACTIVITY IN PANCREATIC CANCER. ACTIVITY IN PANCREATIC CANCER. ACTIVITY IN PANCREATIC CANCER. JJ Han, ME Fernandez-Zapico. Gastroenterology Research Unit, Mayo Clinic Collegeof Medicine, Rochester, MN.A NEW MOLECULAR MODEL FOR REGULATION OF THEA NEW MOLECULAR MODEL FOR REGULATION OF THEA NEW MOLECULAR MODEL FOR REGULATION OF THEA NEW MOLECULAR MODEL FOR REGULATION OF THEA NEW MOLECULAR MODEL FOR REGULATION OF THETGFTGFTGFTGFTGFB RECEPTOR II PROMOTER VIA INTERACTION WITHRECEPTOR II PROMOTER VIA INTERACTION WITHRECEPTOR II PROMOTER VIA INTERACTION WITHRECEPTOR II PROMOTER VIA INTERACTION WITHRECEPTOR II PROMOTER VIA INTERACTION WITHTHE LONG-TERM CHROMATIN REPRESSOR PROTEIN,THE LONG-TERM CHROMATIN REPRESSOR PROTEIN,THE LONG-TERM CHROMATIN REPRESSOR PROTEIN,THE LONG-TERM CHROMATIN REPRESSOR PROTEIN,THE LONG-TERM CHROMATIN REPRESSOR PROTEIN,HP1 WITH THE TUMOR SUPPRESSOR KLF11.HP1 WITH THE TUMOR SUPPRESSOR KLF11.HP1 WITH THE TUMOR SUPPRESSOR KLF11.HP1 WITH THE TUMOR SUPPRESSOR KLF11.HP1 WITH THE TUMOR SUPPRESSOR KLF11. G Lomberk,JS Zhang, MJ Truty, R Urrutia. GI Research Unit and CancerCenter Program. Mayo Clinic, Rochester, MN.


5:30 PM - 6:30 PM5:30 PM - 6:30 PM5:30 PM - 6:30 PM5:30 PM - 6:30 PM5:30 PM - 6:30 PMWine & Cheese ReceptionWine & Cheese ReceptionWine & Cheese ReceptionWine & Cheese ReceptionWine & Cheese ReceptionKrumlovsky Atrium

6:30 PM - 7:15 PM6:30 PM - 7:15 PM6:30 PM - 7:15 PM6:30 PM - 7:15 PM6:30 PM - 7:15 PMRolfe Foundation Lecture on Pancreatic CancerRolfe Foundation Lecture on Pancreatic CancerRolfe Foundation Lecture on Pancreatic CancerRolfe Foundation Lecture on Pancreatic CancerRolfe Foundation Lecture on Pancreatic CancerMarsha L. Frazier, Ph.DAssociate Professor of SurgeryMD Anderson Cancer CenterUniversity of Texas

“““““Pancreatic Cancer Risk and Early DetectionPancreatic Cancer Risk and Early DetectionPancreatic Cancer Risk and Early DetectionPancreatic Cancer Risk and Early DetectionPancreatic Cancer Risk and Early Detection”””””







BOARD#BOARD#BOARD#BOARD#BOARD# TITLETITLETITLETITLETITLERISK OF PANCREATIC CANCER FOLLOWING BREASTRISK OF PANCREATIC CANCER FOLLOWING BREASTRISK OF PANCREATIC CANCER FOLLOWING BREASTRISK OF PANCREATIC CANCER FOLLOWING BREASTRISK OF PANCREATIC CANCER FOLLOWING BREASTCANCER: FOLLOW-UP OF 16,016 PATIENTS TREATEDCANCER: FOLLOW-UP OF 16,016 PATIENTS TREATEDCANCER: FOLLOW-UP OF 16,016 PATIENTS TREATEDCANCER: FOLLOW-UP OF 16,016 PATIENTS TREATEDCANCER: FOLLOW-UP OF 16,016 PATIENTS TREATEDIN A SINGLE INSTITUTION.IN A SINGLE INSTITUTION.IN A SINGLE INSTITUTION.IN A SINGLE INSTITUTION.IN A SINGLE INSTITUTION. P Maisonneuve, N Rotmensz, MColleoni, A Luini, G Viale, B Santillo, A Lowenfels. European In-stitute of Oncology, Milan, Italy, Department of Surgery, NewYork Medical College, NY.IMPROVED CONTEMPORARY SURGICAL MANAGEMENTIMPROVED CONTEMPORARY SURGICAL MANAGEMENTIMPROVED CONTEMPORARY SURGICAL MANAGEMENTIMPROVED CONTEMPORARY SURGICAL MANAGEMENTIMPROVED CONTEMPORARY SURGICAL MANAGEMENTOF INSULINOMA: A 25-YEAR EXPERIENCE AT THE MAS-OF INSULINOMA: A 25-YEAR EXPERIENCE AT THE MAS-OF INSULINOMA: A 25-YEAR EXPERIENCE AT THE MAS-OF INSULINOMA: A 25-YEAR EXPERIENCE AT THE MAS-OF INSULINOMA: A 25-YEAR EXPERIENCE AT THE MAS-SACHUSETTS GENERAL HOSPITAL.SACHUSETTS GENERAL HOSPITAL.SACHUSETTS GENERAL HOSPITAL.SACHUSETTS GENERAL HOSPITAL.SACHUSETTS GENERAL HOSPITAL. M Nikfarjam, A Warshaw,L Axelrod, V Deshpande, S Thayer, C Ferrone, C Fernández-delCastillo. Department of Surgery, Medicine, Pathology, Massa-chusetts General Hospital, Boston, MA.DEVELOPMENT OF METAPLASTIC PRECURSOR LESIONSDEVELOPMENT OF METAPLASTIC PRECURSOR LESIONSDEVELOPMENT OF METAPLASTIC PRECURSOR LESIONSDEVELOPMENT OF METAPLASTIC PRECURSOR LESIONSDEVELOPMENT OF METAPLASTIC PRECURSOR LESIONSIN MURINE PANCREAS FOLLOWING MUTANT KRAS EX-IN MURINE PANCREAS FOLLOWING MUTANT KRAS EX-IN MURINE PANCREAS FOLLOWING MUTANT KRAS EX-IN MURINE PANCREAS FOLLOWING MUTANT KRAS EX-IN MURINE PANCREAS FOLLOWING MUTANT KRAS EX-PRESSION IN ADULT PDX1-POSITIVE CELLS.PRESSION IN ADULT PDX1-POSITIVE CELLS.PRESSION IN ADULT PDX1-POSITIVE CELLS.PRESSION IN ADULT PDX1-POSITIVE CELLS.PRESSION IN ADULT PDX1-POSITIVE CELLS. UW Burley III,K Adrian, MR Barron, C Pelham, TE Adrian, RH Bell Jr, RJMacDonald, GY Yang, PJ Grippo. Departments of Surgery andPathology, Northwestern University, Chicago, IL; Departmentof Physiology, UAE University, Al Ain, UAE; American Board ofSurgery, Philadelphia, PA; Department of Molecular Biology, UT-Southwestern, Dallas, TX.TARGETED NANOPARTICLES FOR IMAGING INCIPIENTTARGETED NANOPARTICLES FOR IMAGING INCIPIENTTARGETED NANOPARTICLES FOR IMAGING INCIPIENTTARGETED NANOPARTICLES FOR IMAGING INCIPIENTTARGETED NANOPARTICLES FOR IMAGING INCIPIENTPANCREATIC DUCTAL ADENOCARINOMA.PANCREATIC DUCTAL ADENOCARINOMA.PANCREATIC DUCTAL ADENOCARINOMA.PANCREATIC DUCTAL ADENOCARINOMA.PANCREATIC DUCTAL ADENOCARINOMA. K Kelly, NBardeesy, R Anbazhagan, S Gurumurthy, J Berger, H Alencar, UMahmood, R Weissleder. Center for Molecular Imaging Research,Massachusetts General Hospital and Harvard Medical School,Charlestown, MA, Center for Systems Biology, MassachusettsGeneral Hospital, Boston MA, MGH Cancer Center, Massachu-setts General Hospital and Harvard Medical School, Boston, MA.CLINICAL OUTCOME OF LAPAROSCOPIC DISTALCLINICAL OUTCOME OF LAPAROSCOPIC DISTALCLINICAL OUTCOME OF LAPAROSCOPIC DISTALCLINICAL OUTCOME OF LAPAROSCOPIC DISTALCLINICAL OUTCOME OF LAPAROSCOPIC DISTALPANCREATECTOMY: A CASE-CONTROL COMPARISONPANCREATECTOMY: A CASE-CONTROL COMPARISONPANCREATECTOMY: A CASE-CONTROL COMPARISONPANCREATECTOMY: A CASE-CONTROL COMPARISONPANCREATECTOMY: A CASE-CONTROL COMPARISONOF LAPAROSCOPIC VS OPENOF LAPAROSCOPIC VS OPENOF LAPAROSCOPIC VS OPENOF LAPAROSCOPIC VS OPENOF LAPAROSCOPIC VS OPEN. Y Nakamura, E Uchida, TAimoto, A Matsushita, K Cho, M Kawamoto, T Tajiri. Departmentof Surgery, Nippon Medical School, Tokyo, Japan.TRAIL DECREASES THE EXPRESSION OF HSP70 PROTEINTRAIL DECREASES THE EXPRESSION OF HSP70 PROTEINTRAIL DECREASES THE EXPRESSION OF HSP70 PROTEINTRAIL DECREASES THE EXPRESSION OF HSP70 PROTEINTRAIL DECREASES THE EXPRESSION OF HSP70 PROTEINLEVELS IN PANCREATIC CANCER CELLSLEVELS IN PANCREATIC CANCER CELLSLEVELS IN PANCREATIC CANCER CELLSLEVELS IN PANCREATIC CANCER CELLSLEVELS IN PANCREATIC CANCER CELLS. D Borja-Cacho,PA Phillips, V Dudeja, R Dawra, P Zwolak, J McCarroll, JS Ankeny,R Talukdar, R Chugh, S Vickers, A Saluja. Department of Sur-gery, University of Minnesota, Minneapolis, MN.YAP PART OF THE HIPPO PATHWAY IS OVEREXPRESSEDYAP PART OF THE HIPPO PATHWAY IS OVEREXPRESSEDYAP PART OF THE HIPPO PATHWAY IS OVEREXPRESSEDYAP PART OF THE HIPPO PATHWAY IS OVEREXPRESSEDYAP PART OF THE HIPPO PATHWAY IS OVEREXPRESSEDIN PANCREATIC CANCER. IN PANCREATIC CANCER. IN PANCREATIC CANCER. IN PANCREATIC CANCER. IN PANCREATIC CANCER. T Grote, S Gaiser, H Wang, G Halder,C Logsdon. Department of Cancer Biology, Pathology, Biochem-istry and Molecular Biology and GI Medical Oncology, Universityof Texas, M.D. Anderson Cancer Center, Houston, TX.










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BOARD#BOARD#BOARD#BOARD#BOARD# TITLETITLETITLETITLETITLEDIFFERENTIAL ROLES OF PROTEIN KINASE C ISOFORMSDIFFERENTIAL ROLES OF PROTEIN KINASE C ISOFORMSDIFFERENTIAL ROLES OF PROTEIN KINASE C ISOFORMSDIFFERENTIAL ROLES OF PROTEIN KINASE C ISOFORMSDIFFERENTIAL ROLES OF PROTEIN KINASE C ISOFORMSIN ACUTE PANCREATITIS. IN ACUTE PANCREATITIS. IN ACUTE PANCREATITIS. IN ACUTE PANCREATITIS. IN ACUTE PANCREATITIS. S. Osgood, T.R Kolodecik, J. Reeve,S.J. Pandol, F.S. Gorelick, EC Thrower. Department of InternalMedicine, Section of Digestive Diseases, Department of CellBiology, Veterans Administration Connecticut Healthcare, WestHaven, and Yale University School of Medicine, New Haven, CT,VA Greater Los Angeles Health Care System and the Universityof California Los Angeles, CA.EXPRESSION OF ENDOCRINE GLAND-VASCULAR EN-EXPRESSION OF ENDOCRINE GLAND-VASCULAR EN-EXPRESSION OF ENDOCRINE GLAND-VASCULAR EN-EXPRESSION OF ENDOCRINE GLAND-VASCULAR EN-EXPRESSION OF ENDOCRINE GLAND-VASCULAR EN-DOTHELIAL GROWTH FACTOR IN THE RAT PANCREAS.DOTHELIAL GROWTH FACTOR IN THE RAT PANCREAS.DOTHELIAL GROWTH FACTOR IN THE RAT PANCREAS.DOTHELIAL GROWTH FACTOR IN THE RAT PANCREAS.DOTHELIAL GROWTH FACTOR IN THE RAT PANCREAS.A Morales-Miranda, S Morimoto, L Díaz-Nieto, G Robles-Díaz,V Díaz-Sánchez. Department of Reproductive Biology, InstitutoNacional de Ciencias Médicas y Nutrición Salvador Zubirán.Department of Experimental Medicine, Faculty of Medicine-UNAM. MEXFAM A.C. Mexico.PROTEINASE-ACTIVATED RECEPTOR-2 (PAR-2) DEFI-PROTEINASE-ACTIVATED RECEPTOR-2 (PAR-2) DEFI-PROTEINASE-ACTIVATED RECEPTOR-2 (PAR-2) DEFI-PROTEINASE-ACTIVATED RECEPTOR-2 (PAR-2) DEFI-PROTEINASE-ACTIVATED RECEPTOR-2 (PAR-2) DEFI-CIENT MICE ARE PROTECTED AGAINST TAUROCHO-CIENT MICE ARE PROTECTED AGAINST TAUROCHO-CIENT MICE ARE PROTECTED AGAINST TAUROCHO-CIENT MICE ARE PROTECTED AGAINST TAUROCHO-CIENT MICE ARE PROTECTED AGAINST TAUROCHO-LATE INDUCED ACUTE PANCREATITIS. LATE INDUCED ACUTE PANCREATITIS. LATE INDUCED ACUTE PANCREATITIS. LATE INDUCED ACUTE PANCREATITIS. LATE INDUCED ACUTE PANCREATITIS. J Laukkarinen, ERWeiss, G Perides, ML Steer. Dept. of Surgery,Tufts-New En-gland Medical Center, Boston, MA and Dept. of Gastroenterol-ogy & Alimentary Tract Surgery, Tampere University Hospital,Tampere, Finland.COCOCOCOCO22222 ABDOMINAL INSUFFLATION PRETREATMENT DE- ABDOMINAL INSUFFLATION PRETREATMENT DE- ABDOMINAL INSUFFLATION PRETREATMENT DE- ABDOMINAL INSUFFLATION PRETREATMENT DE- ABDOMINAL INSUFFLATION PRETREATMENT DE-CREASES SYSTEMIC INFLAMMATORY RESPONSE IN EX-CREASES SYSTEMIC INFLAMMATORY RESPONSE IN EX-CREASES SYSTEMIC INFLAMMATORY RESPONSE IN EX-CREASES SYSTEMIC INFLAMMATORY RESPONSE IN EX-CREASES SYSTEMIC INFLAMMATORY RESPONSE IN EX-PERIMENTAL ACUTE PANCREATITIS. PERIMENTAL ACUTE PANCREATITIS. PERIMENTAL ACUTE PANCREATITIS. PERIMENTAL ACUTE PANCREATITIS. PERIMENTAL ACUTE PANCREATITIS. MCC Machado, AMMCoelho, SN Sampietre, NAT Molan, MAC Machado, T Bacchella.Department of Gastroenterology, University of Sao Paulo, SaoPaulo, Brazil.ZENTASEZENTASEZENTASEZENTASEZENTASE, A NOVEL PANCREATIC ENZYME PRODUCT, A NOVEL PANCREATIC ENZYME PRODUCT, A NOVEL PANCREATIC ENZYME PRODUCT, A NOVEL PANCREATIC ENZYME PRODUCT, A NOVEL PANCREATIC ENZYME PRODUCT(PEP),(PEP),(PEP),(PEP),(PEP), IS SAFE AND EFFECTIVE IN MILD, MODERATE, IS SAFE AND EFFECTIVE IN MILD, MODERATE, IS SAFE AND EFFECTIVE IN MILD, MODERATE, IS SAFE AND EFFECTIVE IN MILD, MODERATE, IS SAFE AND EFFECTIVE IN MILD, MODERATE,AND AGGRESSIVE EXOCRINE PANCREATIC INSUFFI-AND AGGRESSIVE EXOCRINE PANCREATIC INSUFFI-AND AGGRESSIVE EXOCRINE PANCREATIC INSUFFI-AND AGGRESSIVE EXOCRINE PANCREATIC INSUFFI-AND AGGRESSIVE EXOCRINE PANCREATIC INSUFFI-CIENCY (EPI).CIENCY (EPI).CIENCY (EPI).CIENCY (EPI).CIENCY (EPI). JE Heubi, SR Boas, K Blake, SZ Nasr, MS Woo, GRGraff, KA Hardy, R Amaro-Galvez, M Latino, C Lee. CincinnatiChildren’s Hospital Medical Center, Cincinnati, OH, ChicagoCF Care, Glenview, IL, Nemours, Jacksonville, FL, Michigan U.,Ann Arbor, MI, Children’s H., Los Angeles, CA, Penn State H.,Hershey, PA, Children’s H., Oakland, CA, Texas U., Tyler, TX,Eurand, Milan, Italy, Eurand, Vandalia, OH.THE ROLE OF ERM PROTEIN MOESIN IN PHENOTYPETHE ROLE OF ERM PROTEIN MOESIN IN PHENOTYPETHE ROLE OF ERM PROTEIN MOESIN IN PHENOTYPETHE ROLE OF ERM PROTEIN MOESIN IN PHENOTYPETHE ROLE OF ERM PROTEIN MOESIN IN PHENOTYPEDIFFERENTIATION OF PANCREATIC CANCER.DIFFERENTIATION OF PANCREATIC CANCER.DIFFERENTIATION OF PANCREATIC CANCER.DIFFERENTIATION OF PANCREATIC CANCER.DIFFERENTIATION OF PANCREATIC CANCER. I. Abiatari,T. De Oliveira, H. Friess, J. Kleeff. Department of General Sur-gery, Technical University of Munich, Germany.










BOARD#BOARD#BOARD#BOARD#BOARD# TITLETITLETITLETITLETITLEP21 AND P27 POLYMORPHISMS COOPERATIVELY CON-P21 AND P27 POLYMORPHISMS COOPERATIVELY CON-P21 AND P27 POLYMORPHISMS COOPERATIVELY CON-P21 AND P27 POLYMORPHISMS COOPERATIVELY CON-P21 AND P27 POLYMORPHISMS COOPERATIVELY CON-TRIBUTE TO AN EARLIER AGE AT DIAGNOSIS OF PAN-TRIBUTE TO AN EARLIER AGE AT DIAGNOSIS OF PAN-TRIBUTE TO AN EARLIER AGE AT DIAGNOSIS OF PAN-TRIBUTE TO AN EARLIER AGE AT DIAGNOSIS OF PAN-TRIBUTE TO AN EARLIER AGE AT DIAGNOSIS OF PAN-CREATIC CANCER.CREATIC CANCER.CREATIC CANCER.CREATIC CANCER.CREATIC CANCER. J. Chen, A. M. Killary, S. Sen, C. I. Amos, D.B. Evans, M. L. Frazier. Departments of Epidemiology, CancerGenetics, Molecular Pathology, Surgical Oncology, The Univer-sity of Texas M. D. Anderson Cancer Center, Houston, Texas;Program in Human and Molecular Genetics, The University ofTexas Graduate School of Biomedical Sciences, Houston, TX.MESOTHELIN IS A MALIGNANT FACTOR AND THERA-MESOTHELIN IS A MALIGNANT FACTOR AND THERA-MESOTHELIN IS A MALIGNANT FACTOR AND THERA-MESOTHELIN IS A MALIGNANT FACTOR AND THERA-MESOTHELIN IS A MALIGNANT FACTOR AND THERA-PEUTIC VACCINE TARGET FOR PANCREATIC CANCER.PEUTIC VACCINE TARGET FOR PANCREATIC CANCER.PEUTIC VACCINE TARGET FOR PANCREATIC CANCER.PEUTIC VACCINE TARGET FOR PANCREATIC CANCER.PEUTIC VACCINE TARGET FOR PANCREATIC CANCER. MLi, U Bharadwaj, R Zhang, S Zhang, H Mu, C Chen, Q Yao. Molecu-lar Surgeon Research Center, Michael E. DeBakey Department ofSurgery, Baylor College of Medicine, Houston, TX.IgE IgE IgE IgE IgE ANTI-PANCREATIC CANCER ANTIBODIES FROM PAN-ANTI-PANCREATIC CANCER ANTIBODIES FROM PAN-ANTI-PANCREATIC CANCER ANTIBODIES FROM PAN-ANTI-PANCREATIC CANCER ANTIBODIES FROM PAN-ANTI-PANCREATIC CANCER ANTIBODIES FROM PAN-CREATIC CANCER PATIENTS MEDIATE ANTIBODY DE-CREATIC CANCER PATIENTS MEDIATE ANTIBODY DE-CREATIC CANCER PATIENTS MEDIATE ANTIBODY DE-CREATIC CANCER PATIENTS MEDIATE ANTIBODY DE-CREATIC CANCER PATIENTS MEDIATE ANTIBODY DE-PENDENT CELLULAR CYTOTOXICITY (ADCC) AGAINSTPENDENT CELLULAR CYTOTOXICITY (ADCC) AGAINSTPENDENT CELLULAR CYTOTOXICITY (ADCC) AGAINSTPENDENT CELLULAR CYTOTOXICITY (ADCC) AGAINSTPENDENT CELLULAR CYTOTOXICITY (ADCC) AGAINSTPANCREATIC CANCER CELLS.PANCREATIC CANCER CELLS.PANCREATIC CANCER CELLS.PANCREATIC CANCER CELLS.PANCREATIC CANCER CELLS. SL Fu, D Viterbo, Y Lin CMueller, J Pierre, T Smith-Norowitz, W Bowne, MR Pincus, MEZenilman, MH Bluth. Departments of Surgery, Pediatrics, Pa-thology, SUNY Downstate Medical Center, Brooklyn, NY.GENETICALLY DESIGNING A MORE POTENT ANTI-PAN-GENETICALLY DESIGNING A MORE POTENT ANTI-PAN-GENETICALLY DESIGNING A MORE POTENT ANTI-PAN-GENETICALLY DESIGNING A MORE POTENT ANTI-PAN-GENETICALLY DESIGNING A MORE POTENT ANTI-PAN-CREATIC CANCER AGENT BY SIMULTANEOUSLYCREATIC CANCER AGENT BY SIMULTANEOUSLYCREATIC CANCER AGENT BY SIMULTANEOUSLYCREATIC CANCER AGENT BY SIMULTANEOUSLYCREATIC CANCER AGENT BY SIMULTANEOUSLYCOTARGETING HUMAN IL-13 AND EGF RECEPTORS INCOTARGETING HUMAN IL-13 AND EGF RECEPTORS INCOTARGETING HUMAN IL-13 AND EGF RECEPTORS INCOTARGETING HUMAN IL-13 AND EGF RECEPTORS INCOTARGETING HUMAN IL-13 AND EGF RECEPTORS INA MOUSE XENOGRAFT MODEL.A MOUSE XENOGRAFT MODEL.A MOUSE XENOGRAFT MODEL.A MOUSE XENOGRAFT MODEL.A MOUSE XENOGRAFT MODEL. DA Vallera, A Saluja, SMVickers, DJ Buchsbaum, B Stish. University of Minnesota CancerCenter, Section on Molecular Cancer Therapeutics, Departmentsof Therapeutic Radiology-Radiation Oncology and Surgery, Min-neapolis, MN, Department of Radiation Oncology, University ofAlabama at Birmingham, Birmingham, AL.COMBINED EFFECT OF GEMCITABINE AND GSK3b IN-COMBINED EFFECT OF GEMCITABINE AND GSK3b IN-COMBINED EFFECT OF GEMCITABINE AND GSK3b IN-COMBINED EFFECT OF GEMCITABINE AND GSK3b IN-COMBINED EFFECT OF GEMCITABINE AND GSK3b IN-HIBITOR AGAINST HUMAN PANCREATIC CANCER: GSK3bHIBITOR AGAINST HUMAN PANCREATIC CANCER: GSK3bHIBITOR AGAINST HUMAN PANCREATIC CANCER: GSK3bHIBITOR AGAINST HUMAN PANCREATIC CANCER: GSK3bHIBITOR AGAINST HUMAN PANCREATIC CANCER: GSK3bAS A NEW THERAPEUTIC MOLECULAR TARGET.AS A NEW THERAPEUTIC MOLECULAR TARGET.AS A NEW THERAPEUTIC MOLECULAR TARGET.AS A NEW THERAPEUTIC MOLECULAR TARGET.AS A NEW THERAPEUTIC MOLECULAR TARGET. TShimasaki, Y Ishigaki, X Zhao, N Tomosugi, T Tanaka, W Mai, KKawakami, T Minamoto, Y Motoo. Kanazawa Medical University /Medical Oncology, Kanazawa Medical University Medical Re-search Institute, Kanazawa Medical University /Oncologic Pa-thology, Kanazawa University /Cancer Research Institute/Divi-sion of Translational and Clinical Oncology, Japan.PROBIOTICS REDUCE OXIDATIVE STRESS IN THE EARLYPROBIOTICS REDUCE OXIDATIVE STRESS IN THE EARLYPROBIOTICS REDUCE OXIDATIVE STRESS IN THE EARLYPROBIOTICS REDUCE OXIDATIVE STRESS IN THE EARLYPROBIOTICS REDUCE OXIDATIVE STRESS IN THE EARLYPHASE OF ACUTE PANCREATITIS.PHASE OF ACUTE PANCREATITIS.PHASE OF ACUTE PANCREATITIS.PHASE OF ACUTE PANCREATITIS.PHASE OF ACUTE PANCREATITIS. F Lutgendorff, LMTrulsson, LP van Minnen, GT Rijkers, HM Timmerman, HGGooszen, JD Söderholm, LMA Akkermans, PA Sandström. De-partment of Surgery, University Hospital, Linköping, Sweden;Department of Surgery, University Medical Center, Utrecht, TheNetherlands.








DOMINANT NEGATIVE MUTATION OF CYSTEINE STRINGDOMINANT NEGATIVE MUTATION OF CYSTEINE STRINGDOMINANT NEGATIVE MUTATION OF CYSTEINE STRINGDOMINANT NEGATIVE MUTATION OF CYSTEINE STRINGDOMINANT NEGATIVE MUTATION OF CYSTEINE STRINGPROTEIN (CSP) J-DOMAIN INHIBITS HSP70PROTEIN (CSP) J-DOMAIN INHIBITS HSP70PROTEIN (CSP) J-DOMAIN INHIBITS HSP70PROTEIN (CSP) J-DOMAIN INHIBITS HSP70PROTEIN (CSP) J-DOMAIN INHIBITS HSP70COCHAPERONE FUNCTION AND DEFINES A ROLE FORCOCHAPERONE FUNCTION AND DEFINES A ROLE FORCOCHAPERONE FUNCTION AND DEFINES A ROLE FORCOCHAPERONE FUNCTION AND DEFINES A ROLE FORCOCHAPERONE FUNCTION AND DEFINES A ROLE FORTHESE MOLECULES IN ACINAR CELL CATHESE MOLECULES IN ACINAR CELL CATHESE MOLECULES IN ACINAR CELL CATHESE MOLECULES IN ACINAR CELL CATHESE MOLECULES IN ACINAR CELL CA2+2+2+2+2+-STIMULATED-STIMULATED-STIMULATED-STIMULATED-STIMULATEDSECRETION. SECRETION. SECRETION. SECRETION. SECRETION. MD Baumler, N Weng, DDH Thomas, JE Braun, GEGroblewski. Department of Nutritional Sciences, University ofWisconsin, Madison, Department of Physiology, University ofCalgary, Alberta, CanadaACTIVATOR PROTEIN-1 HAS AN ESSENTIAL ROLE INACTIVATOR PROTEIN-1 HAS AN ESSENTIAL ROLE INACTIVATOR PROTEIN-1 HAS AN ESSENTIAL ROLE INACTIVATOR PROTEIN-1 HAS AN ESSENTIAL ROLE INACTIVATOR PROTEIN-1 HAS AN ESSENTIAL ROLE INPANCREATIC CANCER CELLS AND IS REGULATED BY APANCREATIC CANCER CELLS AND IS REGULATED BY APANCREATIC CANCER CELLS AND IS REGULATED BY APANCREATIC CANCER CELLS AND IS REGULATED BY APANCREATIC CANCER CELLS AND IS REGULATED BY ANOVEL AKT-MEDIATED MECHANISMNOVEL AKT-MEDIATED MECHANISMNOVEL AKT-MEDIATED MECHANISMNOVEL AKT-MEDIATED MECHANISMNOVEL AKT-MEDIATED MECHANISM. S Shin, T Asano, YYao, JL Abbruzzese, SAG Reddy. Department of Gastrointesti-nal Medical Oncology, The University of Texas M. D. AndersonCancer Center, Houston, TX.ANIMAL SURVIVAL IN SEVERE ACUTE PANCREATITIS ISANIMAL SURVIVAL IN SEVERE ACUTE PANCREATITIS ISANIMAL SURVIVAL IN SEVERE ACUTE PANCREATITIS ISANIMAL SURVIVAL IN SEVERE ACUTE PANCREATITIS ISANIMAL SURVIVAL IN SEVERE ACUTE PANCREATITIS ISDEPENDENT ON T-CELL ACTIVITY.DEPENDENT ON T-CELL ACTIVITY.DEPENDENT ON T-CELL ACTIVITY.DEPENDENT ON T-CELL ACTIVITY.DEPENDENT ON T-CELL ACTIVITY. J Mayerle, A Dummer,M Sendler, J Kalkowski, C Sünder, FU Weiss, BM Bröker, MMLerch. Department of Medicine A, Department of Immunol-ogy, Ernst-Moritz-Arndt-University Greifswald, Germany.THE GALANIN ANTAGONIST C7 BUT NOT M35 ANDTHE GALANIN ANTAGONIST C7 BUT NOT M35 ANDTHE GALANIN ANTAGONIST C7 BUT NOT M35 ANDTHE GALANIN ANTAGONIST C7 BUT NOT M35 ANDTHE GALANIN ANTAGONIST C7 BUT NOT M35 ANDGALANTIDE EXACERBATES CAERULEIN-INDUCEDGALANTIDE EXACERBATES CAERULEIN-INDUCEDGALANTIDE EXACERBATES CAERULEIN-INDUCEDGALANTIDE EXACERBATES CAERULEIN-INDUCEDGALANTIDE EXACERBATES CAERULEIN-INDUCEDACUTE PANCREATITIS IN MICE.ACUTE PANCREATITIS IN MICE.ACUTE PANCREATITIS IN MICE.ACUTE PANCREATITIS IN MICE.ACUTE PANCREATITIS IN MICE. M Bhandari, M Kawamoto,AC Thomas, CJ Carati, AC Schloithe, J Toouli, GTP Saccone.Departments of General and Digestive Surgery, AnatomicalPathology, and Anatomy and Histology, Flinders Medical Cen-tre, Flinders University, Adelaide, South Australia, Australia.TREATMENT OF NECROTIZING PANCREATITIS FROMTREATMENT OF NECROTIZING PANCREATITIS FROMTREATMENT OF NECROTIZING PANCREATITIS FROMTREATMENT OF NECROTIZING PANCREATITIS FROMTREATMENT OF NECROTIZING PANCREATITIS FROMTHE SURGEON’S POINT OF VIEW – WHAT HAS CHANGEDTHE SURGEON’S POINT OF VIEW – WHAT HAS CHANGEDTHE SURGEON’S POINT OF VIEW – WHAT HAS CHANGEDTHE SURGEON’S POINT OF VIEW – WHAT HAS CHANGEDTHE SURGEON’S POINT OF VIEW – WHAT HAS CHANGEDDURING THE PAST 10 YEARS? DURING THE PAST 10 YEARS? DURING THE PAST 10 YEARS? DURING THE PAST 10 YEARS? DURING THE PAST 10 YEARS? R Isenmann, I Goelz, D Henne-Bruns. Department of Abdominal and Transplant Surgery,University of Ulm, Ulm, Germany.FIBER MODIFICATION AUGMENTS ANTITUMOR EFFECTFIBER MODIFICATION AUGMENTS ANTITUMOR EFFECTFIBER MODIFICATION AUGMENTS ANTITUMOR EFFECTFIBER MODIFICATION AUGMENTS ANTITUMOR EFFECTFIBER MODIFICATION AUGMENTS ANTITUMOR EFFECTOF CONDITIONALLY REPLICATIVE ADENOVIRUS UPONOF CONDITIONALLY REPLICATIVE ADENOVIRUS UPONOF CONDITIONALLY REPLICATIVE ADENOVIRUS UPONOF CONDITIONALLY REPLICATIVE ADENOVIRUS UPONOF CONDITIONALLY REPLICATIVE ADENOVIRUS UPONSYSTEMIC ADMINISTRATION IN ORTHOTOPIC PANCRE-SYSTEMIC ADMINISTRATION IN ORTHOTOPIC PANCRE-SYSTEMIC ADMINISTRATION IN ORTHOTOPIC PANCRE-SYSTEMIC ADMINISTRATION IN ORTHOTOPIC PANCRE-SYSTEMIC ADMINISTRATION IN ORTHOTOPIC PANCRE-ATIC CANCER MODEL.ATIC CANCER MODEL.ATIC CANCER MODEL.ATIC CANCER MODEL.ATIC CANCER MODEL. J Davydova, PJ Ramirez, SM Vickers,M Yamamoto. Department of Surgery, University of Minne-sota, Minneapolis, MN, Gene Therapy Center, University of Ala-bama, Birmingham, AL.TUBERCULOSIS INFECTION DURING CHRONIC PANCRE-TUBERCULOSIS INFECTION DURING CHRONIC PANCRE-TUBERCULOSIS INFECTION DURING CHRONIC PANCRE-TUBERCULOSIS INFECTION DURING CHRONIC PANCRE-TUBERCULOSIS INFECTION DURING CHRONIC PANCRE-ATITIS: INCIDENCE AND RISK FACTORS.ATITIS: INCIDENCE AND RISK FACTORS.ATITIS: INCIDENCE AND RISK FACTORS.ATITIS: INCIDENCE AND RISK FACTORS.ATITIS: INCIDENCE AND RISK FACTORS. ST Barbu, MCazacu. IV-th Surgical Clinic, University of Medicine and Phar-macy “Iuliu Hatieganu” Cluj-Napoca, Romania.


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BOARD#BOARD#BOARD#BOARD#BOARD# TITLETITLETITLETITLETITLETHE EZH2 HISTONE METHYLTRANSFERASE CONTRIBUTESTHE EZH2 HISTONE METHYLTRANSFERASE CONTRIBUTESTHE EZH2 HISTONE METHYLTRANSFERASE CONTRIBUTESTHE EZH2 HISTONE METHYLTRANSFERASE CONTRIBUTESTHE EZH2 HISTONE METHYLTRANSFERASE CONTRIBUTESTO PANCREATIC CANCER CELL PROLIFERATIONTO PANCREATIC CANCER CELL PROLIFERATIONTO PANCREATIC CANCER CELL PROLIFERATIONTO PANCREATIC CANCER CELL PROLIFERATIONTO PANCREATIC CANCER CELL PROLIFERATIONTHROUGH EPIGENETIC SILENCING OF CDK INHIBITORTHROUGH EPIGENETIC SILENCING OF CDK INHIBITORTHROUGH EPIGENETIC SILENCING OF CDK INHIBITORTHROUGH EPIGENETIC SILENCING OF CDK INHIBITORTHROUGH EPIGENETIC SILENCING OF CDK INHIBITORGENES.GENES.GENES.GENES.GENES. AV Ougolkov, ME Fernandez-Zapico, DD Billadeau. Di-visions of Oncology Research and Gastroenterology ResearchUnit, Mayo Clinic College of Medicine, Rochester, MN.HSP70 STABILIZES THE LYSOSOMES BY TRANSPORTINGHSP70 STABILIZES THE LYSOSOMES BY TRANSPORTINGHSP70 STABILIZES THE LYSOSOMES BY TRANSPORTINGHSP70 STABILIZES THE LYSOSOMES BY TRANSPORTINGHSP70 STABILIZES THE LYSOSOMES BY TRANSPORTINGMUC1 TO THE LYSOSOMES.MUC1 TO THE LYSOSOMES.MUC1 TO THE LYSOSOMES.MUC1 TO THE LYSOSOMES.MUC1 TO THE LYSOSOMES. V Dudeja, R Chugh, Y Yokoyama,R Talukdar, D Borja-Cacho, P Zwolak, R Dawra, S Vickers, A Saluja.Department of Surgery, University of Minnesota, Minneapolis,MN.Ly-6CLy-6CLy-6CLy-6CLy-6Chihihihihi INFLAMMATORY MONOCYTES GOVERN THEINFLAMMATORY MONOCYTES GOVERN THEINFLAMMATORY MONOCYTES GOVERN THEINFLAMMATORY MONOCYTES GOVERN THEINFLAMMATORY MONOCYTES GOVERN THESEVERITY OF CAERULEIN- AND TAUROCHOLATE-IN-SEVERITY OF CAERULEIN- AND TAUROCHOLATE-IN-SEVERITY OF CAERULEIN- AND TAUROCHOLATE-IN-SEVERITY OF CAERULEIN- AND TAUROCHOLATE-IN-SEVERITY OF CAERULEIN- AND TAUROCHOLATE-IN-DUCED ACUTE PANCREATITIS IN MICE.DUCED ACUTE PANCREATITIS IN MICE.DUCED ACUTE PANCREATITIS IN MICE.DUCED ACUTE PANCREATITIS IN MICE.DUCED ACUTE PANCREATITIS IN MICE. G Perides, JLaukkarinen, ER Weiss, J Duffield, ML Steer. Depts. of Surgery,Tufts-New England Medical Center, Boston, MA, Tampere Uni-versity Hospital, Tampere, Finland and Department of Medi-cine, Brigham and Women’s Hospital, Boston, MA.ISOLATION OF QUIESCENT (NORMAL) HUMAN PANCRE-ISOLATION OF QUIESCENT (NORMAL) HUMAN PANCRE-ISOLATION OF QUIESCENT (NORMAL) HUMAN PANCRE-ISOLATION OF QUIESCENT (NORMAL) HUMAN PANCRE-ISOLATION OF QUIESCENT (NORMAL) HUMAN PANCRE-ATIC STELLATE CELLS (HPSCS): A USEFUL IN VITROATIC STELLATE CELLS (HPSCS): A USEFUL IN VITROATIC STELLATE CELLS (HPSCS): A USEFUL IN VITROATIC STELLATE CELLS (HPSCS): A USEFUL IN VITROATIC STELLATE CELLS (HPSCS): A USEFUL IN VITROTOOL FOR STUDIES OF HPSC BIOLOGY.TOOL FOR STUDIES OF HPSC BIOLOGY.TOOL FOR STUDIES OF HPSC BIOLOGY.TOOL FOR STUDIES OF HPSC BIOLOGY.TOOL FOR STUDIES OF HPSC BIOLOGY. A Vonlaufen, Z Xu,L Yang, Biankin, N Parker, R Pirola, J Wilson, M Apte. PancreaticResearch Group, University of New South Wales, Sydney, Aus-tralia.MOLECULAR ANALYSIS OF HEREDITARY PANCREATITISMOLECULAR ANALYSIS OF HEREDITARY PANCREATITISMOLECULAR ANALYSIS OF HEREDITARY PANCREATITISMOLECULAR ANALYSIS OF HEREDITARY PANCREATITISMOLECULAR ANALYSIS OF HEREDITARY PANCREATITISASSOCIATED PRSS1 MUTATIONS.ASSOCIATED PRSS1 MUTATIONS.ASSOCIATED PRSS1 MUTATIONS.ASSOCIATED PRSS1 MUTATIONS.ASSOCIATED PRSS1 MUTATIONS. J Schnekenburger, BNeumann, V Schick, W Domschke, WE Schmidt, P Felderbauer.Department of Medicine B, University Hospital Münster, Univer-sity Hospital Bochum, Germany.ADMISSION APACHE II FOR PREDICTION OF IN-HOSPI-ADMISSION APACHE II FOR PREDICTION OF IN-HOSPI-ADMISSION APACHE II FOR PREDICTION OF IN-HOSPI-ADMISSION APACHE II FOR PREDICTION OF IN-HOSPI-ADMISSION APACHE II FOR PREDICTION OF IN-HOSPI-TAL MORTALITY IN ACUTE PANCREATITISTAL MORTALITY IN ACUTE PANCREATITISTAL MORTALITY IN ACUTE PANCREATITISTAL MORTALITY IN ACUTE PANCREATITISTAL MORTALITY IN ACUTE PANCREATITIS. BU Wu, RSJohannes, X Sun, PA Banks. Division of Gastroenterology, Cen-ter for Pancreatic Disease, Brigham & Women’s Hospital, Bos-ton, MA; Cardinal Health-MediQual, Marlborough, MA.EFFICACY OF A SOFT FLUTED SILICONE DRAIN (BLAKEEFFICACY OF A SOFT FLUTED SILICONE DRAIN (BLAKEEFFICACY OF A SOFT FLUTED SILICONE DRAIN (BLAKEEFFICACY OF A SOFT FLUTED SILICONE DRAIN (BLAKEEFFICACY OF A SOFT FLUTED SILICONE DRAIN (BLAKEDRAINDRAINDRAINDRAINDRAINRRRRR) ON PANCREATIC FISTULA AFTER) ON PANCREATIC FISTULA AFTER) ON PANCREATIC FISTULA AFTER) ON PANCREATIC FISTULA AFTER) ON PANCREATIC FISTULA AFTERPANCREATICODUODENECTOMY. CLINICAL RESEARCHPANCREATICODUODENECTOMY. CLINICAL RESEARCHPANCREATICODUODENECTOMY. CLINICAL RESEARCHPANCREATICODUODENECTOMY. CLINICAL RESEARCHPANCREATICODUODENECTOMY. CLINICAL RESEARCHAND BASIC EXPERIMENT.AND BASIC EXPERIMENT.AND BASIC EXPERIMENT.AND BASIC EXPERIMENT.AND BASIC EXPERIMENT. T Aimoto, E Uchida, Y Nakamura,A Matsushita, A Katsuno, K Chou, M Kawamoto, T Tajiri. Depart-ment of Surgery, Nippon Medical School, Tokyo, Japan.ISCHEMIC ACUTE PANCREATITIS: CLINICAL FEATURES<ISCHEMIC ACUTE PANCREATITIS: CLINICAL FEATURES<ISCHEMIC ACUTE PANCREATITIS: CLINICAL FEATURES<ISCHEMIC ACUTE PANCREATITIS: CLINICAL FEATURES<ISCHEMIC ACUTE PANCREATITIS: CLINICAL FEATURES<DIAGNOSIS< THERAPY AND OUTCOME.DIAGNOSIS< THERAPY AND OUTCOME.DIAGNOSIS< THERAPY AND OUTCOME.DIAGNOSIS< THERAPY AND OUTCOME.DIAGNOSIS< THERAPY AND OUTCOME. Th. Hackert, W.Hartwig, L. Schneider, O. Strobel, M.W. Büchler, J. Werner. Dept.of Surgery, University of Heidelberg, Germany.










BOARD#BOARD#BOARD#BOARD#BOARD# TITLETITLETITLETITLETITLEA CRITICAL ROLE FOR MACROPHAGES IN PREVENTINGA CRITICAL ROLE FOR MACROPHAGES IN PREVENTINGA CRITICAL ROLE FOR MACROPHAGES IN PREVENTINGA CRITICAL ROLE FOR MACROPHAGES IN PREVENTINGA CRITICAL ROLE FOR MACROPHAGES IN PREVENTINGPANCREATITIS ASSOCIATED DIABETES.PANCREATITIS ASSOCIATED DIABETES.PANCREATITIS ASSOCIATED DIABETES.PANCREATITIS ASSOCIATED DIABETES.PANCREATITIS ASSOCIATED DIABETES. JS Tessem, H Pelli,X Dai, X Zong, ER Stanley, J Jensen, JN Jensen, J DeGregori. Pro-gram in Molecular Biology, University of Colorado Health Sci-ences Center, Aurora, CO; Department of Developmental andMolecular Biology, Albert Einstein College of Medicine, Bronx,NY; Barbara Davis Center for Childhood Diabetes, Universityof Colorado Health Sciences Center, Aurora, CO.CXCL8/IL-8 AND CXCL12/SDF-1A COOPERATIVELYCXCL8/IL-8 AND CXCL12/SDF-1A COOPERATIVELYCXCL8/IL-8 AND CXCL12/SDF-1A COOPERATIVELYCXCL8/IL-8 AND CXCL12/SDF-1A COOPERATIVELYCXCL8/IL-8 AND CXCL12/SDF-1A COOPERATIVELYPROMOTE INVASION AND ANGIOGENESIS OF PANCRE-PROMOTE INVASION AND ANGIOGENESIS OF PANCRE-PROMOTE INVASION AND ANGIOGENESIS OF PANCRE-PROMOTE INVASION AND ANGIOGENESIS OF PANCRE-PROMOTE INVASION AND ANGIOGENESIS OF PANCRE-ATIC CANCER. ATIC CANCER. ATIC CANCER. ATIC CANCER. ATIC CANCER. Y Matsuo, N Ochi, H Takeyama, H Sawai, YOkada, T Manabe, S Guha. Department of GI Surgery, NagoyaCity University, Nagoya, Japan and Department of Gastroen-terology, Hepatology and Nutrition, UT MD Anderson CancerCenter, Houston, TX.IMPORTANCE OF REACTIVE OXYGEN SPECIES GENERA-IMPORTANCE OF REACTIVE OXYGEN SPECIES GENERA-IMPORTANCE OF REACTIVE OXYGEN SPECIES GENERA-IMPORTANCE OF REACTIVE OXYGEN SPECIES GENERA-IMPORTANCE OF REACTIVE OXYGEN SPECIES GENERA-TION BY BILE ACIDS AND NON-OXIDATIVE ETHANOLTION BY BILE ACIDS AND NON-OXIDATIVE ETHANOLTION BY BILE ACIDS AND NON-OXIDATIVE ETHANOLTION BY BILE ACIDS AND NON-OXIDATIVE ETHANOLTION BY BILE ACIDS AND NON-OXIDATIVE ETHANOLMETABOLITES TO PANCREATIC ACINAR CELL FATE.METABOLITES TO PANCREATIC ACINAR CELL FATE.METABOLITES TO PANCREATIC ACINAR CELL FATE.METABOLITES TO PANCREATIC ACINAR CELL FATE.METABOLITES TO PANCREATIC ACINAR CELL FATE.Criddle DN, Booth D, Jaffar M, Gerasmenko OV, Tepikin AV,Petersen OH, Sutton R. Physiological Laboratory; Division ofSurgery and Oncology, University of Liverpool; Morvus Tech-nology Ltd. UK.CHARACTERIZATION OF A NOVEL MODEL OF SEVERECHARACTERIZATION OF A NOVEL MODEL OF SEVERECHARACTERIZATION OF A NOVEL MODEL OF SEVERECHARACTERIZATION OF A NOVEL MODEL OF SEVERECHARACTERIZATION OF A NOVEL MODEL OF SEVEREACUTE PANCREATITIS IN MICEACUTE PANCREATITIS IN MICEACUTE PANCREATITIS IN MICEACUTE PANCREATITIS IN MICEACUTE PANCREATITIS IN MICE. W Hartwig, E Schimmel, FFortunato, F Bergmann, T Hackert, P Strobel, L Schneider, MWBüchler, J Werner. Department of General, Visceral, and Trans-plant Surgery, Department of Pathology, University of Heidel-berg, Germany.INTERLEUKIN-13 EXERTS AUTOCRINE GROWTH PRO-INTERLEUKIN-13 EXERTS AUTOCRINE GROWTH PRO-INTERLEUKIN-13 EXERTS AUTOCRINE GROWTH PRO-INTERLEUKIN-13 EXERTS AUTOCRINE GROWTH PRO-INTERLEUKIN-13 EXERTS AUTOCRINE GROWTH PRO-MOTING EFFECTS IN HUMAN PANCREATIC CANCER ANDMOTING EFFECTS IN HUMAN PANCREATIC CANCER ANDMOTING EFFECTS IN HUMAN PANCREATIC CANCER ANDMOTING EFFECTS IN HUMAN PANCREATIC CANCER ANDMOTING EFFECTS IN HUMAN PANCREATIC CANCER ANDITS EXPRESSION CORRELATES WITH A PROPENSITY FORITS EXPRESSION CORRELATES WITH A PROPENSITY FORITS EXPRESSION CORRELATES WITH A PROPENSITY FORITS EXPRESSION CORRELATES WITH A PROPENSITY FORITS EXPRESSION CORRELATES WITH A PROPENSITY FORLYMPH NODE METASTASES.LYMPH NODE METASTASES.LYMPH NODE METASTASES.LYMPH NODE METASTASES.LYMPH NODE METASTASES. A Formentini, O Prokopchuk, JSträter, J Kleeff, G Leder, D Henne-Bruns, M Korc, M Kornmann.Department of General, Visceral and Transplantation Surgery,Department of Pathology, University of Ulm, Ulm, Germany;Department of General Surgery, University of Heidelberg,Heidelberg, Germany; Departments of Medicine, Pharmacol-ogy and Toxicology, Dartmouth Hitchcock Medical Center andDartmouth Medical School, Hanover, NH.









BOARD#BOARD#BOARD#BOARD#BOARD# TITLETITLETITLETITLETITLEEPS8 IS INCREASED IN PANCREATIC CANCER AND RE-EPS8 IS INCREASED IN PANCREATIC CANCER AND RE-EPS8 IS INCREASED IN PANCREATIC CANCER AND RE-EPS8 IS INCREASED IN PANCREATIC CANCER AND RE-EPS8 IS INCREASED IN PANCREATIC CANCER AND RE-QUIRED FOR DYNAMIC ACTIN-BASED CELL PROTRU-QUIRED FOR DYNAMIC ACTIN-BASED CELL PROTRU-QUIRED FOR DYNAMIC ACTIN-BASED CELL PROTRU-QUIRED FOR DYNAMIC ACTIN-BASED CELL PROTRU-QUIRED FOR DYNAMIC ACTIN-BASED CELL PROTRU-SIONS AND INTERCELLULAR CYTOSKELETAL ORGANI-SIONS AND INTERCELLULAR CYTOSKELETAL ORGANI-SIONS AND INTERCELLULAR CYTOSKELETAL ORGANI-SIONS AND INTERCELLULAR CYTOSKELETAL ORGANI-SIONS AND INTERCELLULAR CYTOSKELETAL ORGANI-ZATION.ZATION.ZATION.ZATION.ZATION. T Welsch, K Endlich, T Giese, MW Büchler, J Schmidt.Dept. of General, Visceral and Transplantation Surgery, Univer-sity of Heidelberg, Germany, Dept. of Anatomy and Cell Biology,University of Greifswald, Germany, Dept. of Immunology, Uni-versity of Heidelberg, Germany.KERATINOCYTE GROWTH FACTOR AND ITS RECEPTORKERATINOCYTE GROWTH FACTOR AND ITS RECEPTORKERATINOCYTE GROWTH FACTOR AND ITS RECEPTORKERATINOCYTE GROWTH FACTOR AND ITS RECEPTORKERATINOCYTE GROWTH FACTOR AND ITS RECEPTORCORRELATE WITH VENOUS INVASION VIA MATRIXCORRELATE WITH VENOUS INVASION VIA MATRIXCORRELATE WITH VENOUS INVASION VIA MATRIXCORRELATE WITH VENOUS INVASION VIA MATRIXCORRELATE WITH VENOUS INVASION VIA MATRIXMETALLOPROTEINASE-9 (MMP-9) IN PANCREATIC CAN-METALLOPROTEINASE-9 (MMP-9) IN PANCREATIC CAN-METALLOPROTEINASE-9 (MMP-9) IN PANCREATIC CAN-METALLOPROTEINASE-9 (MMP-9) IN PANCREATIC CAN-METALLOPROTEINASE-9 (MMP-9) IN PANCREATIC CAN-CER.CER.CER.CER.CER. K Cho, T Ishiwata, E Uchida, T Aimoto, Y Nakamura, AMatsushita, A Katsuno, M Kawamoto, N Nakazawa, Z Naito, TTajiri. Surgery for Organ and Biological Regulation (Depart-ment of Surgery), Graduate School of Medicine, Nippon MedicalSchool, Department of Pathology, Integrative Oncological Pa-thology, Nippon Medical School, Tokyo, Japan.GROWTH INHIBITORY EFFECTS OF GEMCITABINE AREGROWTH INHIBITORY EFFECTS OF GEMCITABINE AREGROWTH INHIBITORY EFFECTS OF GEMCITABINE AREGROWTH INHIBITORY EFFECTS OF GEMCITABINE AREGROWTH INHIBITORY EFFECTS OF GEMCITABINE AREAUGMENTED BY THE FLAVONOID APIGENIN IN HUMANAUGMENTED BY THE FLAVONOID APIGENIN IN HUMANAUGMENTED BY THE FLAVONOID APIGENIN IN HUMANAUGMENTED BY THE FLAVONOID APIGENIN IN HUMANAUGMENTED BY THE FLAVONOID APIGENIN IN HUMANPANCREATIC CANCER CELLS. PANCREATIC CANCER CELLS. PANCREATIC CANCER CELLS. PANCREATIC CANCER CELLS. PANCREATIC CANCER CELLS. BM Milam, LG Melstrom, MJStrouch, JJ McGill, MR Salabat, DB Van Beek, DM Heiferman, MJHeiferman, XZ Ding, TA Adrian, DJ Bentrem. Northwestern Me-morial Hospital and Lurie Comprehensive Cancer Center, Chi-cago, IL.TIME TRENDS IN INCIDENCE OF ACUTE PANCREATITISTIME TRENDS IN INCIDENCE OF ACUTE PANCREATITISTIME TRENDS IN INCIDENCE OF ACUTE PANCREATITISTIME TRENDS IN INCIDENCE OF ACUTE PANCREATITISTIME TRENDS IN INCIDENCE OF ACUTE PANCREATITISIN LÜNEBURG: A POPULATION-BASED STUDYIN LÜNEBURG: A POPULATION-BASED STUDYIN LÜNEBURG: A POPULATION-BASED STUDYIN LÜNEBURG: A POPULATION-BASED STUDYIN LÜNEBURG: A POPULATION-BASED STUDY..... PGLankisch, M Karimi, A Bruns, P Maisonneuve, AB Lowenfels. Mu-nicipal Clinic of Lueneburg, Germany; European Institute of On-cology, Milan, Italy; New York Medical College, Valhalla, NY.PROTECTIVE ROLE OF THE ANGIOTENSIN II TYPE2 RE-PROTECTIVE ROLE OF THE ANGIOTENSIN II TYPE2 RE-PROTECTIVE ROLE OF THE ANGIOTENSIN II TYPE2 RE-PROTECTIVE ROLE OF THE ANGIOTENSIN II TYPE2 RE-PROTECTIVE ROLE OF THE ANGIOTENSIN II TYPE2 RE-CEPTOR SIGNALING PATHWAY IN A MOUSE MODEL OFCEPTOR SIGNALING PATHWAY IN A MOUSE MODEL OFCEPTOR SIGNALING PATHWAY IN A MOUSE MODEL OFCEPTOR SIGNALING PATHWAY IN A MOUSE MODEL OFCEPTOR SIGNALING PATHWAY IN A MOUSE MODEL OFPANCREATITIS. PANCREATITIS. PANCREATITIS. PANCREATITIS. PANCREATITIS. B. Ulmasov, Z. Xu, T. Inagami, BA.Neuschwander-Tetri. Department of Internal Medicine, SaintLouis University School of Medicine ,St. Louis, MO; Departmentof General Surgery, The First Affiliated Hospital of Nanjing Medi-cal University, Nanjing, China; Department of Biochemistry,Vanderbilt University School of Medicine, Nashville, TN.SECRETAGOGUES DIFFERENTIALLY ACTIVATE ENDO-SECRETAGOGUES DIFFERENTIALLY ACTIVATE ENDO-SECRETAGOGUES DIFFERENTIALLY ACTIVATE ENDO-SECRETAGOGUES DIFFERENTIALLY ACTIVATE ENDO-SECRETAGOGUES DIFFERENTIALLY ACTIVATE ENDO-PLASMIC RETICULUM STRESS RESPONSES IN PANCRE-PLASMIC RETICULUM STRESS RESPONSES IN PANCRE-PLASMIC RETICULUM STRESS RESPONSES IN PANCRE-PLASMIC RETICULUM STRESS RESPONSES IN PANCRE-PLASMIC RETICULUM STRESS RESPONSES IN PANCRE-ATIC ACINI. ATIC ACINI. ATIC ACINI. ATIC ACINI. ATIC ACINI. CH Kubisch, CD Logsdon. Department of InternalMedicine II, Ludwig-Maximilians-University of Munich, Germany,Department. of Cancer Biology and GI Medical Oncology, TheUniversity of Texas M. D. Anderson Cancer Center, Houston,TX.







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ELEVATED PLASMA C-PEPTIDE AND LOW PANCREATICELEVATED PLASMA C-PEPTIDE AND LOW PANCREATICELEVATED PLASMA C-PEPTIDE AND LOW PANCREATICELEVATED PLASMA C-PEPTIDE AND LOW PANCREATICELEVATED PLASMA C-PEPTIDE AND LOW PANCREATICAMYLASE IN ELDERLY HIP FRACTURE PATIENTS WITHAMYLASE IN ELDERLY HIP FRACTURE PATIENTS WITHAMYLASE IN ELDERLY HIP FRACTURE PATIENTS WITHAMYLASE IN ELDERLY HIP FRACTURE PATIENTS WITHAMYLASE IN ELDERLY HIP FRACTURE PATIENTS WITHOSTEOPOROSIS. OSTEOPOROSIS. OSTEOPOROSIS. OSTEOPOROSIS. OSTEOPOROSIS. K Cho. Geriatric Department, KarolinskaUniversity Hospital, Neurobiology Institution, Karolinska Uni-versity, Huddinge, Sweden.TW-37, A NONPEPTIDIC SMALL-MOLECULE INHIBITORTW-37, A NONPEPTIDIC SMALL-MOLECULE INHIBITORTW-37, A NONPEPTIDIC SMALL-MOLECULE INHIBITORTW-37, A NONPEPTIDIC SMALL-MOLECULE INHIBITORTW-37, A NONPEPTIDIC SMALL-MOLECULE INHIBITOROF BCL-2, INHIBITS INVASION AND ANGIOGENESIS INOF BCL-2, INHIBITS INVASION AND ANGIOGENESIS INOF BCL-2, INHIBITS INVASION AND ANGIOGENESIS INOF BCL-2, INHIBITS INVASION AND ANGIOGENESIS INOF BCL-2, INHIBITS INVASION AND ANGIOGENESIS INPANCREATIC CANCERPANCREATIC CANCERPANCREATIC CANCERPANCREATIC CANCERPANCREATIC CANCER. Z Wang, W Song, A Aboukameel, GWang, S Wang, FH Sarkar, RM Mohammad. Department of In-ternal Medicine, Division of Hematology and Oncology,Karmanos Cancer Institute, Wayne State University,Detroit,Michigan Department of Pathology, Karmanos CancerInstitute, Wayne State University, Detroit, Michigan Depart-ment of Internal Medicine, Pharmacology and Medicinal Chem-istry, University of Michigan Comprehensive Cancer Center,University of Michigan, Ann Arbor, MI.HUMAN ENT1 IS PREDICTIVE OF RESPONSE IN PATIENTSHUMAN ENT1 IS PREDICTIVE OF RESPONSE IN PATIENTSHUMAN ENT1 IS PREDICTIVE OF RESPONSE IN PATIENTSHUMAN ENT1 IS PREDICTIVE OF RESPONSE IN PATIENTSHUMAN ENT1 IS PREDICTIVE OF RESPONSE IN PATIENTSWITH PANCREATIC CANCER TREATED WITHWITH PANCREATIC CANCER TREATED WITHWITH PANCREATIC CANCER TREATED WITHWITH PANCREATIC CANCER TREATED WITHWITH PANCREATIC CANCER TREATED WITHGEMCITABINE: RESULTS FROM THE RTOG 9704 PRO-GEMCITABINE: RESULTS FROM THE RTOG 9704 PRO-GEMCITABINE: RESULTS FROM THE RTOG 9704 PRO-GEMCITABINE: RESULTS FROM THE RTOG 9704 PRO-GEMCITABINE: RESULTS FROM THE RTOG 9704 PRO-SPECTIVE RANDOMIZED TRIALSPECTIVE RANDOMIZED TRIALSPECTIVE RANDOMIZED TRIALSPECTIVE RANDOMIZED TRIALSPECTIVE RANDOMIZED TRIAL. . . . . J Farrell, M Garcia, R Lai, AAmmar, W Regine, R Abrams, A Bowen Benson, J Macdonald,CE Cass, H Elsaleh, J Mackey. Division of Digestive Diseases,UCLA School of Medicine, Los Angeles, CA, RTOG Phiadelphia,PA Cross Cancer Institute, University of Alberta, University ofMaryland Medical Systems, Baltimore, MD, Rush UniversityMedical Center, Chicago Il, Northwestern University, Chicago,IL, St. Vincent’s CCC, New York, NY, The Australian NationalUniversity, Canberra, ACT Australia.ANALYSIS OF SELECTED CYTOKINES GENES POLYMOR-ANALYSIS OF SELECTED CYTOKINES GENES POLYMOR-ANALYSIS OF SELECTED CYTOKINES GENES POLYMOR-ANALYSIS OF SELECTED CYTOKINES GENES POLYMOR-ANALYSIS OF SELECTED CYTOKINES GENES POLYMOR-PHISMS IN PANCREATIC CANCER AND CHRONIC PAN-PHISMS IN PANCREATIC CANCER AND CHRONIC PAN-PHISMS IN PANCREATIC CANCER AND CHRONIC PAN-PHISMS IN PANCREATIC CANCER AND CHRONIC PAN-PHISMS IN PANCREATIC CANCER AND CHRONIC PAN-CREATITIS.CREATITIS.CREATITIS.CREATITIS.CREATITIS. R Talar-Wojnarowska, A Gasiorowska, B Smolarz,B Romanowicz-Makowska, A Kulig, E Malecka-Panas. Depart-ment of Digestive Tract Diseases, Medical University of Lodz,Poland, Laboratory of Molecular Genetics, Institute of PolishMother’s Memorial Hospital, Lodz, Poland.INTRADUCTAL PAPILLARY MUCINOUS NEOPLASMINTRADUCTAL PAPILLARY MUCINOUS NEOPLASMINTRADUCTAL PAPILLARY MUCINOUS NEOPLASMINTRADUCTAL PAPILLARY MUCINOUS NEOPLASMINTRADUCTAL PAPILLARY MUCINOUS NEOPLASM(IPMN): AN INFECTIOUS ETIOLOGY? A PILOT STUDY.(IPMN): AN INFECTIOUS ETIOLOGY? A PILOT STUDY.(IPMN): AN INFECTIOUS ETIOLOGY? A PILOT STUDY.(IPMN): AN INFECTIOUS ETIOLOGY? A PILOT STUDY.(IPMN): AN INFECTIOUS ETIOLOGY? A PILOT STUDY.MD Bishop, SA Gross, M Krishna, RV Lloyd. Gastroenterologyand Hepatology, Pathology, Mayo Clinic, Jacksonville, Pathol-ogy, Mayo Clinic, Rochester, MN.











BOARD#BOARD#BOARD#BOARD#BOARD# TITLETITLETITLETITLETITLELOSS OF CRBP1 EXPRESSION, A KEY COMPONENT OFLOSS OF CRBP1 EXPRESSION, A KEY COMPONENT OFLOSS OF CRBP1 EXPRESSION, A KEY COMPONENT OFLOSS OF CRBP1 EXPRESSION, A KEY COMPONENT OFLOSS OF CRBP1 EXPRESSION, A KEY COMPONENT OFRETINOIC ACID SIGNALLING, IS A COMMON AND EARLYRETINOIC ACID SIGNALLING, IS A COMMON AND EARLYRETINOIC ACID SIGNALLING, IS A COMMON AND EARLYRETINOIC ACID SIGNALLING, IS A COMMON AND EARLYRETINOIC ACID SIGNALLING, IS A COMMON AND EARLYEVENT IN PANCREATIC CANCER. EVENT IN PANCREATIC CANCER. EVENT IN PANCREATIC CANCER. EVENT IN PANCREATIC CANCER. EVENT IN PANCREATIC CANCER. E.K. Colvin, J.M. Susanto,S.A. O’Toole, J.G. Kench, A. Mawson, V. Ong, M. Pinese, C.J. Scarlett,A.V. Biankin. Cancer Research Program, Garvan Institute ofMedical Research, Darlinghurst, NSW, Australia.ONCOGENIC NFATC2 IS A KEY DOWNSTREAM TRAN-ONCOGENIC NFATC2 IS A KEY DOWNSTREAM TRAN-ONCOGENIC NFATC2 IS A KEY DOWNSTREAM TRAN-ONCOGENIC NFATC2 IS A KEY DOWNSTREAM TRAN-ONCOGENIC NFATC2 IS A KEY DOWNSTREAM TRAN-SCRIPTION FACTOR IN K-RAS INDUCED PANCREATICSCRIPTION FACTOR IN K-RAS INDUCED PANCREATICSCRIPTION FACTOR IN K-RAS INDUCED PANCREATICSCRIPTION FACTOR IN K-RAS INDUCED PANCREATICSCRIPTION FACTOR IN K-RAS INDUCED PANCREATICCANCER CELL PROLIFERATIONCANCER CELL PROLIFERATIONCANCER CELL PROLIFERATIONCANCER CELL PROLIFERATIONCANCER CELL PROLIFERATION. J Motzer, T Linhart, A König,T Gress, V Ellenrieder. Department of Gastroenterology, Uni-versity of Marburg, Germany.COMPARISON OF SECRETIN AND CHOLECYSTOKININCOMPARISON OF SECRETIN AND CHOLECYSTOKININCOMPARISON OF SECRETIN AND CHOLECYSTOKININCOMPARISON OF SECRETIN AND CHOLECYSTOKININCOMPARISON OF SECRETIN AND CHOLECYSTOKININ(CCK) ENDOSCOPIC PANCREATIC FUNCTION TESTS(CCK) ENDOSCOPIC PANCREATIC FUNCTION TESTS(CCK) ENDOSCOPIC PANCREATIC FUNCTION TESTS(CCK) ENDOSCOPIC PANCREATIC FUNCTION TESTS(CCK) ENDOSCOPIC PANCREATIC FUNCTION TESTS(ePFT) FOR EVALUATION OF CHRONIC PANCREATITIS(ePFT) FOR EVALUATION OF CHRONIC PANCREATITIS(ePFT) FOR EVALUATION OF CHRONIC PANCREATITIS(ePFT) FOR EVALUATION OF CHRONIC PANCREATITIS(ePFT) FOR EVALUATION OF CHRONIC PANCREATITIS(CP)(CP)(CP)(CP)(CP). T Stevens, DL Conwell, F Van Lente, L Kirchner, E Purich.Cleveland Clinic Foundation, Cleveland, OH.ADJUVANT CHEMORADIATION PROVIDES BENEFIT FORADJUVANT CHEMORADIATION PROVIDES BENEFIT FORADJUVANT CHEMORADIATION PROVIDES BENEFIT FORADJUVANT CHEMORADIATION PROVIDES BENEFIT FORADJUVANT CHEMORADIATION PROVIDES BENEFIT FORPATIENTS WITH ADVANCED INVASIVE INTRADUCTALPATIENTS WITH ADVANCED INVASIVE INTRADUCTALPATIENTS WITH ADVANCED INVASIVE INTRADUCTALPATIENTS WITH ADVANCED INVASIVE INTRADUCTALPATIENTS WITH ADVANCED INVASIVE INTRADUCTALPAPILLARY MUCINOUS NEOPLASM.PAPILLARY MUCINOUS NEOPLASM.PAPILLARY MUCINOUS NEOPLASM.PAPILLARY MUCINOUS NEOPLASM.PAPILLARY MUCINOUS NEOPLASM. BM Alexander, CFernandez Del-Castillo, LA Kachnic, A Niemierko, KR Kozak, LSBlaszkowsky, AL Warshaw, CG Willett, DP Ryan, JW Clark, TS Hong.Massachusetts General Hospital, Harvard Medical School, Bos-ton, MA; Duke University Medical Center, Durham, NC.A NOVEL NON-TOXIC MULTI-TARGETED APPROACHA NOVEL NON-TOXIC MULTI-TARGETED APPROACHA NOVEL NON-TOXIC MULTI-TARGETED APPROACHA NOVEL NON-TOXIC MULTI-TARGETED APPROACHA NOVEL NON-TOXIC MULTI-TARGETED APPROACHFOR PANCREATIC CANCER THERAPY.FOR PANCREATIC CANCER THERAPY.FOR PANCREATIC CANCER THERAPY.FOR PANCREATIC CANCER THERAPY.FOR PANCREATIC CANCER THERAPY. F Sarkar, S Banerjee,Z Wang, Y Li, J Abbruzzese. Karmanos Cancer Institute, WayneState University, Detroit MI and MD Anderson Cancer Center,Houston TX.Bcl-xL AND Bcl-2 PROSURVIVAL PROTEINS PROTECTBcl-xL AND Bcl-2 PROSURVIVAL PROTEINS PROTECTBcl-xL AND Bcl-2 PROSURVIVAL PROTEINS PROTECTBcl-xL AND Bcl-2 PROSURVIVAL PROTEINS PROTECTBcl-xL AND Bcl-2 PROSURVIVAL PROTEINS PROTECTAGAINST NECROSIS IN PANCREATITIS.AGAINST NECROSIS IN PANCREATITIS.AGAINST NECROSIS IN PANCREATITIS.AGAINST NECROSIS IN PANCREATITIS.AGAINST NECROSIS IN PANCREATITIS. IV Odinokova, KFSung, K Hermann, OA Mareninova, I Gukovsky, AS Gukovskaya.Veterans Affairs Greater Los Angeles Healthcare System andDepartment of Medicine, David Geffen School of Medicine, Uni-versity of California at Los Angeles, CA.EFFECT OF RENIN-ANGIOTENSIN SYSTEM ON REGULA-EFFECT OF RENIN-ANGIOTENSIN SYSTEM ON REGULA-EFFECT OF RENIN-ANGIOTENSIN SYSTEM ON REGULA-EFFECT OF RENIN-ANGIOTENSIN SYSTEM ON REGULA-EFFECT OF RENIN-ANGIOTENSIN SYSTEM ON REGULA-TION OF PANCREATIC SECRETION IN CONSCIOUS RATS.TION OF PANCREATIC SECRETION IN CONSCIOUS RATS.TION OF PANCREATIC SECRETION IN CONSCIOUS RATS.TION OF PANCREATIC SECRETION IN CONSCIOUS RATS.TION OF PANCREATIC SECRETION IN CONSCIOUS RATS.M Yamamoto, M Otani, L Wei, M Otsuki. Department of Gastro-enterology and Metabolism, University of Occupational andEnvironmental Health, Japan, School of Medicine, Kitakyushu,Japan.






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TRIPTOLIDE INHIBITS HEAT SHOCK PROTEIN 70 (HSP70)TRIPTOLIDE INHIBITS HEAT SHOCK PROTEIN 70 (HSP70)TRIPTOLIDE INHIBITS HEAT SHOCK PROTEIN 70 (HSP70)TRIPTOLIDE INHIBITS HEAT SHOCK PROTEIN 70 (HSP70)TRIPTOLIDE INHIBITS HEAT SHOCK PROTEIN 70 (HSP70)EXPRESSION BY INHIBITING DNA BINDING OF HEATEXPRESSION BY INHIBITING DNA BINDING OF HEATEXPRESSION BY INHIBITING DNA BINDING OF HEATEXPRESSION BY INHIBITING DNA BINDING OF HEATEXPRESSION BY INHIBITING DNA BINDING OF HEATSHOCK FACTOR-1.SHOCK FACTOR-1.SHOCK FACTOR-1.SHOCK FACTOR-1.SHOCK FACTOR-1. V Dudeja, R Chugh, Y Yokoyama, RTalukdar, D Borja-Cacho, P Zwolak, R Dawra, S Vickers, A Saluja.Department of Surgery, University of Minnesota, Minneapolis,MN.HAMSTER PANCREATIC CANCER MODEL FOR EXPERI-HAMSTER PANCREATIC CANCER MODEL FOR EXPERI-HAMSTER PANCREATIC CANCER MODEL FOR EXPERI-HAMSTER PANCREATIC CANCER MODEL FOR EXPERI-HAMSTER PANCREATIC CANCER MODEL FOR EXPERI-MENTAL THERAPEUTIC TRIALSMENTAL THERAPEUTIC TRIALSMENTAL THERAPEUTIC TRIALSMENTAL THERAPEUTIC TRIALSMENTAL THERAPEUTIC TRIALS. E Uchida, T Aimoto, YNakamura, K Cho, M Hiroi, M Kawamoto, T Tajiri, T Ishiwata, ZNaito. Dept. of Surgery, Dept. of Pathology, Nippon MedicalSchool, Tokyo, Japan.A RARE CASE OF SMALL SOLID-PSEUDOPAPILLARYA RARE CASE OF SMALL SOLID-PSEUDOPAPILLARYA RARE CASE OF SMALL SOLID-PSEUDOPAPILLARYA RARE CASE OF SMALL SOLID-PSEUDOPAPILLARYA RARE CASE OF SMALL SOLID-PSEUDOPAPILLARYNEOPLASM OF THE PANCREAS WITHOUT CYSTIC FOR-NEOPLASM OF THE PANCREAS WITHOUT CYSTIC FOR-NEOPLASM OF THE PANCREAS WITHOUT CYSTIC FOR-NEOPLASM OF THE PANCREAS WITHOUT CYSTIC FOR-NEOPLASM OF THE PANCREAS WITHOUT CYSTIC FOR-MATION, DIAGNOSED BY EUS-FNA.MATION, DIAGNOSED BY EUS-FNA.MATION, DIAGNOSED BY EUS-FNA.MATION, DIAGNOSED BY EUS-FNA.MATION, DIAGNOSED BY EUS-FNA. Y Takayama, KShimizu, D Suzuki, M Ohashi, H Oyama, T Hatori, K Shiratori.Depts. of Medicine and Surgery, Institute of Gastroenterology,Tokyo Women’s Medical University, Tokyo, Japan.PROBIOTICS MAINTAIN MUCOSAL BARRIER INTEGRITYPROBIOTICS MAINTAIN MUCOSAL BARRIER INTEGRITYPROBIOTICS MAINTAIN MUCOSAL BARRIER INTEGRITYPROBIOTICS MAINTAIN MUCOSAL BARRIER INTEGRITYPROBIOTICS MAINTAIN MUCOSAL BARRIER INTEGRITYIN EXPERIMENTAL ACUTE PANCREATITIS VIAIN EXPERIMENTAL ACUTE PANCREATITIS VIAIN EXPERIMENTAL ACUTE PANCREATITIS VIAIN EXPERIMENTAL ACUTE PANCREATITIS VIAIN EXPERIMENTAL ACUTE PANCREATITIS VIASTABILISATION OF TIGHT JUNCTIONS AND ENHANCE-STABILISATION OF TIGHT JUNCTIONS AND ENHANCE-STABILISATION OF TIGHT JUNCTIONS AND ENHANCE-STABILISATION OF TIGHT JUNCTIONS AND ENHANCE-STABILISATION OF TIGHT JUNCTIONS AND ENHANCE-MENT OF MUCOSAL GLUTATHIONE.MENT OF MUCOSAL GLUTATHIONE.MENT OF MUCOSAL GLUTATHIONE.MENT OF MUCOSAL GLUTATHIONE.MENT OF MUCOSAL GLUTATHIONE. F Lutgendorff, PASandström, LM Trulsson, LP van Minnen, GT Rijkers, HMTimmerman, HG Gooszen, LMA Akkermans, JD Söderholm.Department of Surgery, University Hospital, Linköping, Swe-den, Department of Surgery, University Medical Center, Utrecht,The Netherlands.OPTIMIZED CONCEPT FOR THE TREATMENT OF ACUTEOPTIMIZED CONCEPT FOR THE TREATMENT OF ACUTEOPTIMIZED CONCEPT FOR THE TREATMENT OF ACUTEOPTIMIZED CONCEPT FOR THE TREATMENT OF ACUTEOPTIMIZED CONCEPT FOR THE TREATMENT OF ACUTEPANCREATITIS IN PATIENTS. PANCREATITIS IN PATIENTS. PANCREATITIS IN PATIENTS. PANCREATITIS IN PATIENTS. PANCREATITIS IN PATIENTS. G Alsfasser, F Schwandner,A Pertschy, J Witkowski, T Foitzik, E Klar. Dept of Surgery, Deptof Radiology, University of Rostock, Rostock, Germany.PANCREATIC STONE PROTEIN/ REGENERATINGPANCREATIC STONE PROTEIN/ REGENERATINGPANCREATIC STONE PROTEIN/ REGENERATINGPANCREATIC STONE PROTEIN/ REGENERATINGPANCREATIC STONE PROTEIN/ REGENERATINGPROTEIN ACTIVATES GRANULOCYTES AND IS HIGHLYPROTEIN ACTIVATES GRANULOCYTES AND IS HIGHLYPROTEIN ACTIVATES GRANULOCYTES AND IS HIGHLYPROTEIN ACTIVATES GRANULOCYTES AND IS HIGHLYPROTEIN ACTIVATES GRANULOCYTES AND IS HIGHLYINCREASED IN BLOOD DURING POST-TRAUMATICINCREASED IN BLOOD DURING POST-TRAUMATICINCREASED IN BLOOD DURING POST-TRAUMATICINCREASED IN BLOOD DURING POST-TRAUMATICINCREASED IN BLOOD DURING POST-TRAUMATICSEPSIS. SEPSIS. SEPSIS. SEPSIS. SEPSIS. M. Keel, L. Härter, Th. Reding, L.-K. Sun, M. Hersberger,B. Seifert, D. Bimmler, R. Graf. Division of Trauma Surgery,Dept. Visceral and Transplantation Surgery, Dept. ClinicalChemistry, Dept. Biostatistics, University of Zürich.

CONCLUSION OF THE FIRST DAYCONCLUSION OF THE FIRST DAYCONCLUSION OF THE FIRST DAYCONCLUSION OF THE FIRST DAYCONCLUSION OF THE FIRST DAY








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CCCCContinental Breakfast & Registrationontinental Breakfast & Registrationontinental Breakfast & Registrationontinental Breakfast & Registrationontinental Breakfast & RegistrationKrumlovsky Atrium

Moderators: Suresh T. Chari, MD & Julia V. Mayerle, MD

Oral Session 4: PANCREAOral Session 4: PANCREAOral Session 4: PANCREAOral Session 4: PANCREAOral Session 4: PANCREATIC CANCER IITIC CANCER IITIC CANCER IITIC CANCER IITIC CANCER IIMecklenburg Conference Room

EVALUATION OF THE CONSENSUS GUIDELINES FOR THEEVALUATION OF THE CONSENSUS GUIDELINES FOR THEEVALUATION OF THE CONSENSUS GUIDELINES FOR THEEVALUATION OF THE CONSENSUS GUIDELINES FOR THEEVALUATION OF THE CONSENSUS GUIDELINES FOR THEOPERATIVE MANAGEMENT OF SIDE BRANCH INTRADUC-OPERATIVE MANAGEMENT OF SIDE BRANCH INTRADUC-OPERATIVE MANAGEMENT OF SIDE BRANCH INTRADUC-OPERATIVE MANAGEMENT OF SIDE BRANCH INTRADUC-OPERATIVE MANAGEMENT OF SIDE BRANCH INTRADUC-TAL PAPILLARY MUCINOUS NEOPLASM OF PANCREAS.TAL PAPILLARY MUCINOUS NEOPLASM OF PANCREAS.TAL PAPILLARY MUCINOUS NEOPLASM OF PANCREAS.TAL PAPILLARY MUCINOUS NEOPLASM OF PANCREAS.TAL PAPILLARY MUCINOUS NEOPLASM OF PANCREAS. RTang, B Weinberg, D Dawson, V Chaudhari, S Raman, H Reber, OJHines, J Tomlinson, J Farrell. Division of Digestive Diseases, De-partment of Pathology, Department of Radiology, Departmentof Surgery UCLA School of Medicine, Los Angeles, CA.

TGFTGFTGFTGFTGFBR1R1R1R1R1 HAPLOINSUFFICIENCY INHIBITS THE DEVELOP-HAPLOINSUFFICIENCY INHIBITS THE DEVELOP-HAPLOINSUFFICIENCY INHIBITS THE DEVELOP-HAPLOINSUFFICIENCY INHIBITS THE DEVELOP-HAPLOINSUFFICIENCY INHIBITS THE DEVELOP-MENT OF MURINE MUTANT KRAS-INDUCED PANCREATICMENT OF MURINE MUTANT KRAS-INDUCED PANCREATICMENT OF MURINE MUTANT KRAS-INDUCED PANCREATICMENT OF MURINE MUTANT KRAS-INDUCED PANCREATICMENT OF MURINE MUTANT KRAS-INDUCED PANCREATICPRECANCER.PRECANCER.PRECANCER.PRECANCER.PRECANCER. K Adrian, MR Barron, DJ Bentrem, Y Xu, S Phukan,M Sadim, B Pasche, A Discristofano, PJ Grippo. Departments ofSurgery and Medicine, Northwestern University, Chicago, IL; FoxChase Cancer Center, Philadelphia, PA.

ATDC, A HIGHLY EXPRESSED PROTEIN IN PANCREATICATDC, A HIGHLY EXPRESSED PROTEIN IN PANCREATICATDC, A HIGHLY EXPRESSED PROTEIN IN PANCREATICATDC, A HIGHLY EXPRESSED PROTEIN IN PANCREATICATDC, A HIGHLY EXPRESSED PROTEIN IN PANCREATICCANCER, CONTRIBUTES TO TUMORIGENICITY BYCANCER, CONTRIBUTES TO TUMORIGENICITY BYCANCER, CONTRIBUTES TO TUMORIGENICITY BYCANCER, CONTRIBUTES TO TUMORIGENICITY BYCANCER, CONTRIBUTES TO TUMORIGENICITY BYUPREGULATING WNT/B-CATENIN SIGNALING.UPREGULATING WNT/B-CATENIN SIGNALING.UPREGULATING WNT/B-CATENIN SIGNALING.UPREGULATING WNT/B-CATENIN SIGNALING.UPREGULATING WNT/B-CATENIN SIGNALING. L Wang, CJLee, DG Heidt, ME Ljungman, DM Simeone. Depts. of Surgery,Molecular and Integrative Physiology, Radiation Oncology,University of Michigan, Ann Arbor, MI.

ACINAR CELL SPECIFIC TARGETING OF MUTANT KRASACINAR CELL SPECIFIC TARGETING OF MUTANT KRASACINAR CELL SPECIFIC TARGETING OF MUTANT KRASACINAR CELL SPECIFIC TARGETING OF MUTANT KRASACINAR CELL SPECIFIC TARGETING OF MUTANT KRASINDUCES CHRONIC PANCREATITIS, PREINVASIVE,INDUCES CHRONIC PANCREATITIS, PREINVASIVE,INDUCES CHRONIC PANCREATITIS, PREINVASIVE,INDUCES CHRONIC PANCREATITIS, PREINVASIVE,INDUCES CHRONIC PANCREATITIS, PREINVASIVE,INVASIVE, AND METASTATIC PANCREATIC DUCTALINVASIVE, AND METASTATIC PANCREATIC DUCTALINVASIVE, AND METASTATIC PANCREATIC DUCTALINVASIVE, AND METASTATIC PANCREATIC DUCTALINVASIVE, AND METASTATIC PANCREATIC DUCTALADENOCARCINOMA. ADENOCARCINOMA. ADENOCARCINOMA. ADENOCARCINOMA. ADENOCARCINOMA. B Ji, L Tsou, H Wang, J Song, CD Logsdon.Departments of Cancer Biology, GI Medical Oncology andPathology, University of Texas M.D. Anderson Cancer Center,Houston, TX.

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Oral Session 4: Oral Session 4: Oral Session 4: Oral Session 4: Oral Session 4: PANCREATIC CANCER IIPANCREATIC CANCER IIPANCREATIC CANCER IIPANCREATIC CANCER IIPANCREATIC CANCER II(Continued from Page 21)(Continued from Page 21)(Continued from Page 21)(Continued from Page 21)(Continued from Page 21)

TRADITIONAL DIABETES RISK FACTORS IN PANCREATICTRADITIONAL DIABETES RISK FACTORS IN PANCREATICTRADITIONAL DIABETES RISK FACTORS IN PANCREATICTRADITIONAL DIABETES RISK FACTORS IN PANCREATICTRADITIONAL DIABETES RISK FACTORS IN PANCREATICCANCER ASSOCIATED DIABETES (PACDM): ACANCER ASSOCIATED DIABETES (PACDM): ACANCER ASSOCIATED DIABETES (PACDM): ACANCER ASSOCIATED DIABETES (PACDM): ACANCER ASSOCIATED DIABETES (PACDM): APROSPECTIVE STUDY OF 512 PATIENTSPROSPECTIVE STUDY OF 512 PATIENTSPROSPECTIVE STUDY OF 512 PATIENTSPROSPECTIVE STUDY OF 512 PATIENTSPROSPECTIVE STUDY OF 512 PATIENTS. R Pannala, JLeirness, W Bamlet, A Basu, G Petersen, S Chari. Mayo Clinic,Rochester, MN.

IN VIVO MOLECULAR EVIDENCE OFIN VIVO MOLECULAR EVIDENCE OFIN VIVO MOLECULAR EVIDENCE OFIN VIVO MOLECULAR EVIDENCE OFIN VIVO MOLECULAR EVIDENCE OFCHEMOSENSITIZATION BY 3,3' - DIINDOLYLMETHANECHEMOSENSITIZATION BY 3,3' - DIINDOLYLMETHANECHEMOSENSITIZATION BY 3,3' - DIINDOLYLMETHANECHEMOSENSITIZATION BY 3,3' - DIINDOLYLMETHANECHEMOSENSITIZATION BY 3,3' - DIINDOLYLMETHANEAGAINST PANCREATIC TUMOR.AGAINST PANCREATIC TUMOR.AGAINST PANCREATIC TUMOR.AGAINST PANCREATIC TUMOR.AGAINST PANCREATIC TUMOR. S Banerjee, Z Wang, D Kong,FH Sarkar. Department of Pathology, Karmanos Cancer Institute,Detroit, MI.

RefreshmentsRefreshmentsRefreshmentsRefreshmentsRefreshmentsKrumlovsky Atrium

Business MeetingBusiness MeetingBusiness MeetingBusiness MeetingBusiness MeetingMecklenberg Conference RoomPRESIDENT’S ADDRESSPRESIDENT’S ADDRESSPRESIDENT’S ADDRESSPRESIDENT’S ADDRESSPRESIDENT’S ADDRESSRaul Urrutia, MD

REPORT FROM THE APA SECRETARY-TREASURERREPORT FROM THE APA SECRETARY-TREASURERREPORT FROM THE APA SECRETARY-TREASURERREPORT FROM THE APA SECRETARY-TREASURERREPORT FROM THE APA SECRETARY-TREASURERAshok Saluja, PhD

PRESENTATION OF AWARDS:PRESENTATION OF AWARDS:PRESENTATION OF AWARDS:PRESENTATION OF AWARDS:PRESENTATION OF AWARDS:HIRSHBERG AWARD FOR BEST ABSTRACTS IN PANCREATIC CANCER

NATIONAL PANCREAS FOUNDATION AWARD FOR BEST ABSTRACTSIN PANCREATITIS

CHIRHOCLIN AWARDS FOR BEST ABSTRACT IN PANCREATOLOGY

GENE DIMAGNO PRESIDENTIAL AWARD FOR JUNIOR FACULTY

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PRESENTATION OF “GO AWARD” FOR LIFETIME ACHIEVEMENTPRESENTATION OF “GO AWARD” FOR LIFETIME ACHIEVEMENTPRESENTATION OF “GO AWARD” FOR LIFETIME ACHIEVEMENTPRESENTATION OF “GO AWARD” FOR LIFETIME ACHIEVEMENTPRESENTATION OF “GO AWARD” FOR LIFETIME ACHIEVEMENTIN PANCREATOLOGYIN PANCREATOLOGYIN PANCREATOLOGYIN PANCREATOLOGYIN PANCREATOLOGYRecipient:Howard A. Reber, M.D.Howard A. Reber, M.D.Howard A. Reber, M.D.Howard A. Reber, M.D.Howard A. Reber, M.D.Professor and ChiefGastrointestinal SurgeryDirector - Ronald S. Hirshberg Pancreatic Cancer Research LaboratoryDirector - Center for Pancreatic Diseases

REPORT FROM REPORT FROM REPORT FROM REPORT FROM REPORT FROM PANCREASPANCREASPANCREASPANCREASPANCREAS, OFFICIAL JOURNAL OF APA & JPS, OFFICIAL JOURNAL OF APA & JPS, OFFICIAL JOURNAL OF APA & JPS, OFFICIAL JOURNAL OF APA & JPS, OFFICIAL JOURNAL OF APA & JPSVay Liang W. Go, MD, Editor-in-Chief

RESEARCH FUNDING UPDATESRESEARCH FUNDING UPDATESRESEARCH FUNDING UPDATESRESEARCH FUNDING UPDATESRESEARCH FUNDING UPDATESAshok K. Saluja, PhD

Research State-of-the-Art LectureResearch State-of-the-Art LectureResearch State-of-the-Art LectureResearch State-of-the-Art LectureResearch State-of-the-Art LectureIntroduction: David Whitcomb, MD, PhDChung Owyang, MDChung Owyang, MDChung Owyang, MDChung Owyang, MDChung Owyang, MDProfessor, Department of Internal MedicineH. Marvin Pollard Collegiate ProfessorDivision Chief, GastroenterologyDirector, Digestive Health CareUniversity of MichiganAnn Arbor, Michigan

“Biology of CCK Receptors in Health & Disease”“Biology of CCK Receptors in Health & Disease”“Biology of CCK Receptors in Health & Disease”“Biology of CCK Receptors in Health & Disease”“Biology of CCK Receptors in Health & Disease”


11:45 AM - 12:30 PM11:45 AM - 12:30 PM11:45 AM - 12:30 PM11:45 AM - 12:30 PM11:45 AM - 12:30 PMControversies in Basic PancreatologyControversies in Basic PancreatologyControversies in Basic PancreatologyControversies in Basic PancreatologyControversies in Basic Pancreatology“Co-Localization of Lysosomal Enzymes and Zymogens in“Co-Localization of Lysosomal Enzymes and Zymogens in“Co-Localization of Lysosomal Enzymes and Zymogens in“Co-Localization of Lysosomal Enzymes and Zymogens in“Co-Localization of Lysosomal Enzymes and Zymogens inPancreatitis: Fact or Fiction”Pancreatitis: Fact or Fiction”Pancreatitis: Fact or Fiction”Pancreatitis: Fact or Fiction”Pancreatitis: Fact or Fiction”

Miklos Sahin-Toth, MDMiklos Sahin-Toth, MDMiklos Sahin-Toth, MDMiklos Sahin-Toth, MDMiklos Sahin-Toth, MDBoston Medical CenterBoston, MDModerator




Ashok K. Saluja, PhDAshok K. Saluja, PhDAshok K. Saluja, PhDAshok K. Saluja, PhDAshok K. Saluja, PhDDepartment of Surgery; University of MinnesotaMinneapolis, MN

Markus M. Lerch, MDMarkus M. Lerch, MDMarkus M. Lerch, MDMarkus M. Lerch, MDMarkus M. Lerch, MDDepartment of Gastroenterology, Endocrinology, and Nutrition; ErnstMoritz Arndt University of GreifswaldGriefswald, Germany

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Questions and AnswersQuestions and AnswersQuestions and AnswersQuestions and AnswersQuestions and Answers

Controversies in Basic PancreatologyControversies in Basic PancreatologyControversies in Basic PancreatologyControversies in Basic PancreatologyControversies in Basic Pancreatology(Continued from Page 23)(Continued from Page 23)(Continued from Page 23)(Continued from Page 23)(Continued from Page 23)

Complementary Luncheon &Complementary Luncheon &Complementary Luncheon &Complementary Luncheon &Complementary Luncheon &Poster ReviewPoster ReviewPoster ReviewPoster ReviewPoster ReviewKrumlovsky Atrium

Oral Session 5: Oral Session 5: Oral Session 5: Oral Session 5: Oral Session 5: PANCREATITIS IIPANCREATITIS IIPANCREATITIS IIPANCREATITIS IIPANCREATITIS IIMecklenberg Conference Room


Moderators: Gino Saccone, PhD & Isaac Samuel, MD

FLUSH OR NEW THERAPEUTIC OPTIONS: THE ROLE OFFLUSH OR NEW THERAPEUTIC OPTIONS: THE ROLE OFFLUSH OR NEW THERAPEUTIC OPTIONS: THE ROLE OFFLUSH OR NEW THERAPEUTIC OPTIONS: THE ROLE OFFLUSH OR NEW THERAPEUTIC OPTIONS: THE ROLE OFCB1-RECEPTORS IN ACUTE EXPERIMENTALCB1-RECEPTORS IN ACUTE EXPERIMENTALCB1-RECEPTORS IN ACUTE EXPERIMENTALCB1-RECEPTORS IN ACUTE EXPERIMENTALCB1-RECEPTORS IN ACUTE EXPERIMENTALPANCREATITISPANCREATITISPANCREATITISPANCREATITISPANCREATITIS. C Schäfer, J Kramer, A Malo, T Michler, B Göke,M Storr. Medical Clinic II - Campus Grosshadern, University ofMunich, Germany and Department of Medicine, University ofCalgary, Canada.

RGS6 AUGMENTS CCK-STIMULATED NFÊB ACTIVATIONRGS6 AUGMENTS CCK-STIMULATED NFÊB ACTIVATIONRGS6 AUGMENTS CCK-STIMULATED NFÊB ACTIVATIONRGS6 AUGMENTS CCK-STIMULATED NFÊB ACTIVATIONRGS6 AUGMENTS CCK-STIMULATED NFÊB ACTIVATIONVIA P38 AND ERK.VIA P38 AND ERK.VIA P38 AND ERK.VIA P38 AND ERK.VIA P38 AND ERK. I Samuel, EC Twait, RA Fisher. CCOM, UIowa, Iowa City, IA.

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3:00 PM3:00 PM3:00 PM3:00 PM3:00 PM DEFINING EARLY ORGAN FAILURE IN ACUTE PANCRE-DEFINING EARLY ORGAN FAILURE IN ACUTE PANCRE-DEFINING EARLY ORGAN FAILURE IN ACUTE PANCRE-DEFINING EARLY ORGAN FAILURE IN ACUTE PANCRE-DEFINING EARLY ORGAN FAILURE IN ACUTE PANCRE-ATITIS: A PROSPECTIVE INTERNATIONAL MULTICENTERATITIS: A PROSPECTIVE INTERNATIONAL MULTICENTERATITIS: A PROSPECTIVE INTERNATIONAL MULTICENTERATITIS: A PROSPECTIVE INTERNATIONAL MULTICENTERATITIS: A PROSPECTIVE INTERNATIONAL MULTICENTEREVALUATION OF THE SOFA-VERSUS THE MARSHALL-SYS-EVALUATION OF THE SOFA-VERSUS THE MARSHALL-SYS-EVALUATION OF THE SOFA-VERSUS THE MARSHALL-SYS-EVALUATION OF THE SOFA-VERSUS THE MARSHALL-SYS-EVALUATION OF THE SOFA-VERSUS THE MARSHALL-SYS-TEM.TEM.TEM.TEM.TEM. B.M. Rau, S. Matt, E. Kemppainen, C. Bassi, M.W. Büchler,H.G. Beger, P. Puolakkainen. Dep. of General, Visceral, and Vascu-lar Surgery, UKS, Homburg/Saar & Dep. of General Surgery, Uni-versity of Ulm, Germany, Dep. of Surgery, Helsinki UniversityCentral Hospital, Finland, Dep. of Surgery, Pancreatic Unit, Uni-versity of Verona, Italy, Dep. of Visceral and Transplantation Sur-gery, University of Bern, Switzerland.

HYPERLIPIDEMIA CAUSES PANCREATIC INFLAMMATIONHYPERLIPIDEMIA CAUSES PANCREATIC INFLAMMATIONHYPERLIPIDEMIA CAUSES PANCREATIC INFLAMMATIONHYPERLIPIDEMIA CAUSES PANCREATIC INFLAMMATIONHYPERLIPIDEMIA CAUSES PANCREATIC INFLAMMATIONAND DUCTAL PROLIFERATION IN APOLIPOPROTEIN EAND DUCTAL PROLIFERATION IN APOLIPOPROTEIN EAND DUCTAL PROLIFERATION IN APOLIPOPROTEIN EAND DUCTAL PROLIFERATION IN APOLIPOPROTEIN EAND DUCTAL PROLIFERATION IN APOLIPOPROTEIN EDEFICIENT MICE.DEFICIENT MICE.DEFICIENT MICE.DEFICIENT MICE.DEFICIENT MICE. J Mallen-St. Clair, VA Joaquin, EA Fisher, DBar-Sagi. Department of Biochemistry and Department ofMedicine, Leon Charney Division of Cardiology, New YorkUniversity School of Medicine, New York, NY.

COMPARISON OF SIMPLE SYSTEMIC INFLAMMATORY RE-COMPARISON OF SIMPLE SYSTEMIC INFLAMMATORY RE-COMPARISON OF SIMPLE SYSTEMIC INFLAMMATORY RE-COMPARISON OF SIMPLE SYSTEMIC INFLAMMATORY RE-COMPARISON OF SIMPLE SYSTEMIC INFLAMMATORY RE-SPONSE SYNDROME SCORE WITH EXPANDED CLINICALSPONSE SYNDROME SCORE WITH EXPANDED CLINICALSPONSE SYNDROME SCORE WITH EXPANDED CLINICALSPONSE SYNDROME SCORE WITH EXPANDED CLINICALSPONSE SYNDROME SCORE WITH EXPANDED CLINICALSCORE IN PREDICTING OUTCOMES OF MORBIDITY IN PA-SCORE IN PREDICTING OUTCOMES OF MORBIDITY IN PA-SCORE IN PREDICTING OUTCOMES OF MORBIDITY IN PA-SCORE IN PREDICTING OUTCOMES OF MORBIDITY IN PA-SCORE IN PREDICTING OUTCOMES OF MORBIDITY IN PA-TIENTS WITH ACUTE PANCREATITIS ON INITIAL PRESEN-TIENTS WITH ACUTE PANCREATITIS ON INITIAL PRESEN-TIENTS WITH ACUTE PANCREATITIS ON INITIAL PRESEN-TIENTS WITH ACUTE PANCREATITIS ON INITIAL PRESEN-TIENTS WITH ACUTE PANCREATITIS ON INITIAL PRESEN-TATIONTATIONTATIONTATIONTATION. SS Vege, M Pelaez-Luna, FC Gleeson, RK Pearson, MDTopazian, BT Petersen, JE Clain, MJ Levy, MB Farnell, MK Kendrick,M Sarr, ST Chari. Divisions of Gastroenterology and Hepatology& Gastrointestinal Surgery, Mayo Clinic College of Medicine, Roch-ester, MN.

GENETIC DELETIONS OF NF-ÊB PROTEINS AMELIORATEGENETIC DELETIONS OF NF-ÊB PROTEINS AMELIORATEGENETIC DELETIONS OF NF-ÊB PROTEINS AMELIORATEGENETIC DELETIONS OF NF-ÊB PROTEINS AMELIORATEGENETIC DELETIONS OF NF-ÊB PROTEINS AMELIORATECERULEIN-INDUCED PANCREATITIS. CERULEIN-INDUCED PANCREATITIS. CERULEIN-INDUCED PANCREATITIS. CERULEIN-INDUCED PANCREATITIS. CERULEIN-INDUCED PANCREATITIS. G Zhao, CN Reyes, KHermann, KF Sung, AS Gukovskaya, A Hoffmann, SJ Pandol, IGukovsky. VA Greater Los Angeles Healthcare System &University of California at Los Angeles, CA; Beijing Hospital,Beijing, China; Chang Gung Memorial Hospital, Taipei, Taiwan;University of California at San Diego, La Jolla, CA.

ADMINISTRATION OF IL-12 AND IL-18 WHICH INDUCESADMINISTRATION OF IL-12 AND IL-18 WHICH INDUCESADMINISTRATION OF IL-12 AND IL-18 WHICH INDUCESADMINISTRATION OF IL-12 AND IL-18 WHICH INDUCESADMINISTRATION OF IL-12 AND IL-18 WHICH INDUCESSEVERE PANCREATIC DAMAGE IN OBESE, LEPTIN-SEVERE PANCREATIC DAMAGE IN OBESE, LEPTIN-SEVERE PANCREATIC DAMAGE IN OBESE, LEPTIN-SEVERE PANCREATIC DAMAGE IN OBESE, LEPTIN-SEVERE PANCREATIC DAMAGE IN OBESE, LEPTIN-DEFICIENT OB/OB MICE CAN BE USED AS ADEFICIENT OB/OB MICE CAN BE USED AS ADEFICIENT OB/OB MICE CAN BE USED AS ADEFICIENT OB/OB MICE CAN BE USED AS ADEFICIENT OB/OB MICE CAN BE USED AS APATHOLOGICALLY RELEVANT MODEL OF ACUTEPATHOLOGICALLY RELEVANT MODEL OF ACUTEPATHOLOGICALLY RELEVANT MODEL OF ACUTEPATHOLOGICALLY RELEVANT MODEL OF ACUTEPATHOLOGICALLY RELEVANT MODEL OF ACUTEPANCREATITIS.PANCREATITIS.PANCREATITIS.PANCREATITIS.PANCREATITIS. J Sennello, M Pini, R Fayad, M Gove, G Fantuzzi.University of Illinois, Chicago, IL.

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Oral Session 5: Pancreatitis IIOral Session 5: Pancreatitis IIOral Session 5: Pancreatitis IIOral Session 5: Pancreatitis IIOral Session 5: Pancreatitis II(Continued from Page 25)(Continued from Page 25)(Continued from Page 25)(Continued from Page 25)(Continued from Page 25)4:15 PM4:15 PM4:15 PM4:15 PM4:15 PM

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ENDOSCOPIC ULTRASOUND IN MINIMAL CHANGEENDOSCOPIC ULTRASOUND IN MINIMAL CHANGEENDOSCOPIC ULTRASOUND IN MINIMAL CHANGEENDOSCOPIC ULTRASOUND IN MINIMAL CHANGEENDOSCOPIC ULTRASOUND IN MINIMAL CHANGECHRONIC PANCREATITIS; IS IT AN IDEAL DIAGNOSTICCHRONIC PANCREATITIS; IS IT AN IDEAL DIAGNOSTICCHRONIC PANCREATITIS; IS IT AN IDEAL DIAGNOSTICCHRONIC PANCREATITIS; IS IT AN IDEAL DIAGNOSTICCHRONIC PANCREATITIS; IS IT AN IDEAL DIAGNOSTICTOOL? CORRELATION OF EUS CRITERIA WITHTOOL? CORRELATION OF EUS CRITERIA WITHTOOL? CORRELATION OF EUS CRITERIA WITHTOOL? CORRELATION OF EUS CRITERIA WITHTOOL? CORRELATION OF EUS CRITERIA WITHHISTOPATHOLOGY IN PATIENTS UNDERGOING TOTALHISTOPATHOLOGY IN PATIENTS UNDERGOING TOTALHISTOPATHOLOGY IN PATIENTS UNDERGOING TOTALHISTOPATHOLOGY IN PATIENTS UNDERGOING TOTALHISTOPATHOLOGY IN PATIENTS UNDERGOING TOTALPANCREATECTOMY WITH AUTOLOGUS ISLET CELLPANCREATECTOMY WITH AUTOLOGUS ISLET CELLPANCREATECTOMY WITH AUTOLOGUS ISLET CELLPANCREATECTOMY WITH AUTOLOGUS ISLET CELLPANCREATECTOMY WITH AUTOLOGUS ISLET CELLTRANSPLANTATION. TRANSPLANTATION. TRANSPLANTATION. TRANSPLANTATION. TRANSPLANTATION. K Gupta, A Carlson, T Kobayashi, CManivel, R Lai, S Mallery, DE Sutherland, ML Freeman. Universityof Minnesota and Hennepin County Medical Center, Minneapolis,MN.

VAMP-8 IS THE V-SNARE MEDIATING BASOLATERALVAMP-8 IS THE V-SNARE MEDIATING BASOLATERALVAMP-8 IS THE V-SNARE MEDIATING BASOLATERALVAMP-8 IS THE V-SNARE MEDIATING BASOLATERALVAMP-8 IS THE V-SNARE MEDIATING BASOLATERALEXOCYTOSIS IN ALCHOLIC PANCREATITIS.EXOCYTOSIS IN ALCHOLIC PANCREATITIS.EXOCYTOSIS IN ALCHOLIC PANCREATITIS.EXOCYTOSIS IN ALCHOLIC PANCREATITIS.EXOCYTOSIS IN ALCHOLIC PANCREATITIS. L Cosen-Binker, M Binker, C Wang, W Hong, H Gaisano. Departments ofMedicine and Physiology, University Health Network, Universityof Toronto, Toronto, Ontario, Canada; Institute of Molecularand Cell Biology, Proteos, Singapore.

CYCLIC-AMP INCREASES THE SPEED OF CARBACHOL-CYCLIC-AMP INCREASES THE SPEED OF CARBACHOL-CYCLIC-AMP INCREASES THE SPEED OF CARBACHOL-CYCLIC-AMP INCREASES THE SPEED OF CARBACHOL-CYCLIC-AMP INCREASES THE SPEED OF CARBACHOL-INDUCED APICAL TO BASAL CALCIUM WAVES IN PAN-INDUCED APICAL TO BASAL CALCIUM WAVES IN PAN-INDUCED APICAL TO BASAL CALCIUM WAVES IN PAN-INDUCED APICAL TO BASAL CALCIUM WAVES IN PAN-INDUCED APICAL TO BASAL CALCIUM WAVES IN PAN-CREATIC ACINAR CELLS.CREATIC ACINAR CELLS.CREATIC ACINAR CELLS.CREATIC ACINAR CELLS.CREATIC ACINAR CELLS. WM Grant, AU Shah, SU Latif, SZHusain. Dept. of Pediatrics, Yale University, New Haven, CT, Dept.of Internal Medicine, Michigan State University, Lansing, MI.

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CRHSP-28 IS A PHOSPOINOSITIDE BINDING PROTEINCRHSP-28 IS A PHOSPOINOSITIDE BINDING PROTEINCRHSP-28 IS A PHOSPOINOSITIDE BINDING PROTEINCRHSP-28 IS A PHOSPOINOSITIDE BINDING PROTEINCRHSP-28 IS A PHOSPOINOSITIDE BINDING PROTEINTHAT COLOCALIZES WITH ADP-RIBOSYLATION FAC-THAT COLOCALIZES WITH ADP-RIBOSYLATION FAC-THAT COLOCALIZES WITH ADP-RIBOSYLATION FAC-THAT COLOCALIZES WITH ADP-RIBOSYLATION FAC-THAT COLOCALIZES WITH ADP-RIBOSYLATION FAC-TOR-6, A MODULATOR OF CATOR-6, A MODULATOR OF CATOR-6, A MODULATOR OF CATOR-6, A MODULATOR OF CATOR-6, A MODULATOR OF CA2+2+2+2+2+-DEPENDENT PHOSPHO--DEPENDENT PHOSPHO--DEPENDENT PHOSPHO--DEPENDENT PHOSPHO--DEPENDENT PHOSPHO-LIPID METABOLISM IN THE SECRETORY PATHWAY.LIPID METABOLISM IN THE SECRETORY PATHWAY.LIPID METABOLISM IN THE SECRETORY PATHWAY.LIPID METABOLISM IN THE SECRETORY PATHWAY.LIPID METABOLISM IN THE SECRETORY PATHWAY. MAFalkowski, DDH Thomas, CL Martin, MD Baumler, GE Groblewski.Department of Nutritional Sciences, University of Wisconsin-Madison, Madison, WI.TOPOLOGY ANALYSIS OF PANCREATIC ZYMOGEN GRAN-TOPOLOGY ANALYSIS OF PANCREATIC ZYMOGEN GRAN-TOPOLOGY ANALYSIS OF PANCREATIC ZYMOGEN GRAN-TOPOLOGY ANALYSIS OF PANCREATIC ZYMOGEN GRAN-TOPOLOGY ANALYSIS OF PANCREATIC ZYMOGEN GRAN-ULE MEMBRANE PROTEINS.ULE MEMBRANE PROTEINS.ULE MEMBRANE PROTEINS.ULE MEMBRANE PROTEINS.ULE MEMBRANE PROTEINS. X Chen, ES Simon, PC Andrews,JA Williams. The University of Michigan, Ann Arbor, MI.

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BOARD#BOARD#BOARD#BOARD#BOARD# TITLETITLETITLETITLETITLEINTERACTION BETWEEN PANCREATIC CANCER CELLSINTERACTION BETWEEN PANCREATIC CANCER CELLSINTERACTION BETWEEN PANCREATIC CANCER CELLSINTERACTION BETWEEN PANCREATIC CANCER CELLSINTERACTION BETWEEN PANCREATIC CANCER CELLSAND TUMOUR STROMAL MONOCYTES. AND TUMOUR STROMAL MONOCYTES. AND TUMOUR STROMAL MONOCYTES. AND TUMOUR STROMAL MONOCYTES. AND TUMOUR STROMAL MONOCYTES. AA Sheikh, DVimalachandran, R Jenkins, F Campbell, AR Dodson, JPNeoptolemos, E Costello. Division of Surgery and Oncology,University of Liverpool, UK, Biomedical Sciences ProteomicsFacility, Department of Pharmacology and Therapeutics, Uni-versity of Liverpool, UK, Department of Pathology, University ofLiverpool, UK.ZYMOGEN GRANULE EXOCYTOSIS IN RESPONSE TO DI-ZYMOGEN GRANULE EXOCYTOSIS IN RESPONSE TO DI-ZYMOGEN GRANULE EXOCYTOSIS IN RESPONSE TO DI-ZYMOGEN GRANULE EXOCYTOSIS IN RESPONSE TO DI-ZYMOGEN GRANULE EXOCYTOSIS IN RESPONSE TO DI-RECT ACTIVATION OF CHOLECYSTOKININ RECEPTORSRECT ACTIVATION OF CHOLECYSTOKININ RECEPTORSRECT ACTIVATION OF CHOLECYSTOKININ RECEPTORSRECT ACTIVATION OF CHOLECYSTOKININ RECEPTORSRECT ACTIVATION OF CHOLECYSTOKININ RECEPTORSON ISOLATED HUMAN PANCREATIC ACINAR CELLS. ON ISOLATED HUMAN PANCREATIC ACINAR CELLS. ON ISOLATED HUMAN PANCREATIC ACINAR CELLS. ON ISOLATED HUMAN PANCREATIC ACINAR CELLS. ON ISOLATED HUMAN PANCREATIC ACINAR CELLS. JAMurphy, DN Criddle, M Sherwood, M Chvanov, E Mclaughlin, JVGerasimenko, MGT Raraty, P Ghaneh, JP Neoptolemos, OVGerasmenko, AV Tepikin, GM Green, JR Reeve, OH Petersen, RSutton. Physiological Laboratory and Division of Surgery andOncology, University of Liverpool, UK; Department of Physiol-ogy, University of Texas Health Sciences Center, San Antonio,TX; CURE: Digestive Diseases Research Centre, VA GLAHS, Di-gestive Diseases Division, University of California, LA, CA.NOVEL INSIGHTS INTO HEREDITARY PANCREATITIS: HIS-NOVEL INSIGHTS INTO HEREDITARY PANCREATITIS: HIS-NOVEL INSIGHTS INTO HEREDITARY PANCREATITIS: HIS-NOVEL INSIGHTS INTO HEREDITARY PANCREATITIS: HIS-NOVEL INSIGHTS INTO HEREDITARY PANCREATITIS: HIS-TOPATHOLOGICAL FEATURES OF PATIENTS WITH PRSS1TOPATHOLOGICAL FEATURES OF PATIENTS WITH PRSS1TOPATHOLOGICAL FEATURES OF PATIENTS WITH PRSS1TOPATHOLOGICAL FEATURES OF PATIENTS WITH PRSS1TOPATHOLOGICAL FEATURES OF PATIENTS WITH PRSS1R122H AND A121T MUTATIONS – EVALUATION OF BRAFR122H AND A121T MUTATIONS – EVALUATION OF BRAFR122H AND A121T MUTATIONS – EVALUATION OF BRAFR122H AND A121T MUTATIONS – EVALUATION OF BRAFR122H AND A121T MUTATIONS – EVALUATION OF BRAFAND KRAS2 MUTATIONS AS A POSSIBLE ONCOGENETICAND KRAS2 MUTATIONS AS A POSSIBLE ONCOGENETICAND KRAS2 MUTATIONS AS A POSSIBLE ONCOGENETICAND KRAS2 MUTATIONS AS A POSSIBLE ONCOGENETICAND KRAS2 MUTATIONS AS A POSSIBLE ONCOGENETICPATHWAY.PATHWAY.PATHWAY.PATHWAY.PATHWAY. P Felderbauer, I Stricker, K Bulut, W Uhl, A Tannapfel,WE Schmidt. Department of Medicine I, Department of Surgery,St. Josef Hospital, Ruhr-University School of Medicine, Bochum,Institute of Pathology, Ruhr-University School of Medicine,Bochum, Germany.EFFECT OF PERITONEAL LAVAGE ON SYSTEMIC INFLAM-EFFECT OF PERITONEAL LAVAGE ON SYSTEMIC INFLAM-EFFECT OF PERITONEAL LAVAGE ON SYSTEMIC INFLAM-EFFECT OF PERITONEAL LAVAGE ON SYSTEMIC INFLAM-EFFECT OF PERITONEAL LAVAGE ON SYSTEMIC INFLAM-MATORY RESPONSES IN RATS WITH ACUTE PANCREATI-MATORY RESPONSES IN RATS WITH ACUTE PANCREATI-MATORY RESPONSES IN RATS WITH ACUTE PANCREATI-MATORY RESPONSES IN RATS WITH ACUTE PANCREATI-MATORY RESPONSES IN RATS WITH ACUTE PANCREATI-TIS.TIS.TIS.TIS.TIS. LJ Souza, AMM Coelho, NA Molan, SN Sampietre, JE MonteiroCunha, MCC Machado. Gastrointestinal Surgery, University ofSao Paulo, Sao Paulo, Brazil.HSP70 AND XIAP ARE POTENTIAL KEY MOLECULARHSP70 AND XIAP ARE POTENTIAL KEY MOLECULARHSP70 AND XIAP ARE POTENTIAL KEY MOLECULARHSP70 AND XIAP ARE POTENTIAL KEY MOLECULARHSP70 AND XIAP ARE POTENTIAL KEY MOLECULARMECHANISMS CAUSING IMPAIRED APOPTOSIS AND SE-MECHANISMS CAUSING IMPAIRED APOPTOSIS AND SE-MECHANISMS CAUSING IMPAIRED APOPTOSIS AND SE-MECHANISMS CAUSING IMPAIRED APOPTOSIS AND SE-MECHANISMS CAUSING IMPAIRED APOPTOSIS AND SE-VERE ACUTE PANCREATITIS (AP) IN CF MICE.VERE ACUTE PANCREATITIS (AP) IN CF MICE.VERE ACUTE PANCREATITIS (AP) IN CF MICE.VERE ACUTE PANCREATITIS (AP) IN CF MICE.VERE ACUTE PANCREATITIS (AP) IN CF MICE. K Moon, SYZhou, SH Lee, C Owyang, MJ DiMagno. University of MichiganSchool of Medecine, Ann Arbor, MI.GEMCITABINE RESISTANCE IN PANCREATIC CANCERGEMCITABINE RESISTANCE IN PANCREATIC CANCERGEMCITABINE RESISTANCE IN PANCREATIC CANCERGEMCITABINE RESISTANCE IN PANCREATIC CANCERGEMCITABINE RESISTANCE IN PANCREATIC CANCERCELLS IS ASSOCIATED WITH INCREASED EXPRESSION OFCELLS IS ASSOCIATED WITH INCREASED EXPRESSION OFCELLS IS ASSOCIATED WITH INCREASED EXPRESSION OFCELLS IS ASSOCIATED WITH INCREASED EXPRESSION OFCELLS IS ASSOCIATED WITH INCREASED EXPRESSION OFSTEM CELL-LIKE MARKERS AND A CONCOMITANTSTEM CELL-LIKE MARKERS AND A CONCOMITANTSTEM CELL-LIKE MARKERS AND A CONCOMITANTSTEM CELL-LIKE MARKERS AND A CONCOMITANTSTEM CELL-LIKE MARKERS AND A CONCOMITANTDOWN-REGULATION OF PTEN AND ACTIVATION OF AKT.DOWN-REGULATION OF PTEN AND ACTIVATION OF AKT.DOWN-REGULATION OF PTEN AND ACTIVATION OF AKT.DOWN-REGULATION OF PTEN AND ACTIVATION OF AKT.DOWN-REGULATION OF PTEN AND ACTIVATION OF AKT.MP Kim, AN Shah, NU Parikh, GE Gallick. Department of CancerBiology, University of Texas MD Anderson Cancer Center, Hous-ton, TX.









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ABROGATION OF TGFÂ SIGNALING IN THE PANCREASABROGATION OF TGFÂ SIGNALING IN THE PANCREASABROGATION OF TGFÂ SIGNALING IN THE PANCREASABROGATION OF TGFÂ SIGNALING IN THE PANCREASABROGATION OF TGFÂ SIGNALING IN THE PANCREASOF MICE OVEREXPRESSING DOMINANT NEGATIVE TGFÂOF MICE OVEREXPRESSING DOMINANT NEGATIVE TGFÂOF MICE OVEREXPRESSING DOMINANT NEGATIVE TGFÂOF MICE OVEREXPRESSING DOMINANT NEGATIVE TGFÂOF MICE OVEREXPRESSING DOMINANT NEGATIVE TGFÂRECEPTOR II SHOWS ALTERATION OF ONCOGENICRECEPTOR II SHOWS ALTERATION OF ONCOGENICRECEPTOR II SHOWS ALTERATION OF ONCOGENICRECEPTOR II SHOWS ALTERATION OF ONCOGENICRECEPTOR II SHOWS ALTERATION OF ONCOGENICCOMPONENTS OF THE P53 PATHWAYCOMPONENTS OF THE P53 PATHWAYCOMPONENTS OF THE P53 PATHWAYCOMPONENTS OF THE P53 PATHWAYCOMPONENTS OF THE P53 PATHWAY..... W Evans, C Lokko,ME Fernandez-Zapico, A Randriamahefa, G Lomberk, R Urrutia.Oakwood College, Huntsville, AL, Department of Biochemistryand Molecular Biology, Biophysics, Medicine and GI ResearchUnit, Mayo Clinic, Rochester, MN.CONTROL OF SOMATOSTATIN SECRETION BY CCK-1CONTROL OF SOMATOSTATIN SECRETION BY CCK-1CONTROL OF SOMATOSTATIN SECRETION BY CCK-1CONTROL OF SOMATOSTATIN SECRETION BY CCK-1CONTROL OF SOMATOSTATIN SECRETION BY CCK-1AND CCK-2 RECEPTORS IN RIN-14B CELLS, A RAT PAN-AND CCK-2 RECEPTORS IN RIN-14B CELLS, A RAT PAN-AND CCK-2 RECEPTORS IN RIN-14B CELLS, A RAT PAN-AND CCK-2 RECEPTORS IN RIN-14B CELLS, A RAT PAN-AND CCK-2 RECEPTORS IN RIN-14B CELLS, A RAT PAN-CREATIC ISLET CELL LINE.CREATIC ISLET CELL LINE.CREATIC ISLET CELL LINE.CREATIC ISLET CELL LINE.CREATIC ISLET CELL LINE. K El-Kouhen, J Morisset.Département de Médecine, Service de Gastroentérologie,Faculté de Médecine, Université de Sherbrooke, Sherbrooke,QC, Canada.THE SECRETED LEUKOCYTE PROTEIN HETERODIMERTHE SECRETED LEUKOCYTE PROTEIN HETERODIMERTHE SECRETED LEUKOCYTE PROTEIN HETERODIMERTHE SECRETED LEUKOCYTE PROTEIN HETERODIMERTHE SECRETED LEUKOCYTE PROTEIN HETERODIMERS100A8/A9 DISSOCIATES PANCREATIC CELL-CELLS100A8/A9 DISSOCIATES PANCREATIC CELL-CELLS100A8/A9 DISSOCIATES PANCREATIC CELL-CELLS100A8/A9 DISSOCIATES PANCREATIC CELL-CELLS100A8/A9 DISSOCIATES PANCREATIC CELL-CELLCONTACTS IN VIVO.CONTACTS IN VIVO.CONTACTS IN VIVO.CONTACTS IN VIVO.CONTACTS IN VIVO. J Schnekenburger, V Hlouschek, BNeumann, W Domschke, C Kerckhoff. Dept. of Medicine B, De-partment of Experimental Dermatology, University of Münster,Germany.ROLE OF D-DIMER IN PREDICTION OF ORGAN FAILUREROLE OF D-DIMER IN PREDICTION OF ORGAN FAILUREROLE OF D-DIMER IN PREDICTION OF ORGAN FAILUREROLE OF D-DIMER IN PREDICTION OF ORGAN FAILUREROLE OF D-DIMER IN PREDICTION OF ORGAN FAILUREIN ACUTE PANCREATITIS.IN ACUTE PANCREATITIS.IN ACUTE PANCREATITIS.IN ACUTE PANCREATITIS.IN ACUTE PANCREATITIS. D. Radenkovic, Dj. Bajec, N.Ivancevic, V. Jeremic, P. Gregoric, V. Djukic, B. Stefanovic. ClinicalCenter of Serbia and School of Medicine, University of Belgrade,Serbia.HEAT SHOCK FACTOR 1: A POTENTIAL THERAPEUTICHEAT SHOCK FACTOR 1: A POTENTIAL THERAPEUTICHEAT SHOCK FACTOR 1: A POTENTIAL THERAPEUTICHEAT SHOCK FACTOR 1: A POTENTIAL THERAPEUTICHEAT SHOCK FACTOR 1: A POTENTIAL THERAPEUTICCANDIDATE FOR THE TREATMENT OF PANCREATICCANDIDATE FOR THE TREATMENT OF PANCREATICCANDIDATE FOR THE TREATMENT OF PANCREATICCANDIDATE FOR THE TREATMENT OF PANCREATICCANDIDATE FOR THE TREATMENT OF PANCREATICCANCER.CANCER.CANCER.CANCER.CANCER. V Dudeja, R Chugh, Y Yokoyama, R Talukdar, D Borja-Cacho, P Zwolak, R Dawra, S Vickers, A Saluja. Department ofSurgery, University of Minnesota, Minneapolis, MNPANCREATIC CYST FLUID CEA AND AMYLASE IN THEPANCREATIC CYST FLUID CEA AND AMYLASE IN THEPANCREATIC CYST FLUID CEA AND AMYLASE IN THEPANCREATIC CYST FLUID CEA AND AMYLASE IN THEPANCREATIC CYST FLUID CEA AND AMYLASE IN THEDIFFERENTIAL DIAGNOSIS OF PANCREATIC CYSTS: ADIFFERENTIAL DIAGNOSIS OF PANCREATIC CYSTS: ADIFFERENTIAL DIAGNOSIS OF PANCREATIC CYSTS: ADIFFERENTIAL DIAGNOSIS OF PANCREATIC CYSTS: ADIFFERENTIAL DIAGNOSIS OF PANCREATIC CYSTS: ASTUDY OF 163 CASES. STUDY OF 163 CASES. STUDY OF 163 CASES. STUDY OF 163 CASES. STUDY OF 163 CASES. M Pelaez-Luna, R Mascarenhas, JEClain, MJ Levy, E Rajan, MD Topazian, ST Chari. Division of Gas-troenterology and Hepatology. Mayo Clinic, Rochester MN.RELATIONSHIP OF THE SYSTEMIC INFLAMMATORY RE-RELATIONSHIP OF THE SYSTEMIC INFLAMMATORY RE-RELATIONSHIP OF THE SYSTEMIC INFLAMMATORY RE-RELATIONSHIP OF THE SYSTEMIC INFLAMMATORY RE-RELATIONSHIP OF THE SYSTEMIC INFLAMMATORY RE-SPONSE SYNDROME (SIRS) AT ADMISSION TO MORTAL-SPONSE SYNDROME (SIRS) AT ADMISSION TO MORTAL-SPONSE SYNDROME (SIRS) AT ADMISSION TO MORTAL-SPONSE SYNDROME (SIRS) AT ADMISSION TO MORTAL-SPONSE SYNDROME (SIRS) AT ADMISSION TO MORTAL-ITY IN ACUTE PANCREATITISITY IN ACUTE PANCREATITISITY IN ACUTE PANCREATITISITY IN ACUTE PANCREATITISITY IN ACUTE PANCREATITIS. BU Wu, RS Johannes, X Sun,PA Banks. Division of Gastroenterology, Center for PancreaticDisease, Brigham and Women’s Hospital, Boston, MA; CardinalHealth-MediQual, Marlborough, MA.










BOARD#BOARD#BOARD#BOARD#BOARD# TITLETITLETITLETITLETITLEINHIBITION OF PANCREATIC ADENOCARCINOMA CELLINHIBITION OF PANCREATIC ADENOCARCINOMA CELLINHIBITION OF PANCREATIC ADENOCARCINOMA CELLINHIBITION OF PANCREATIC ADENOCARCINOMA CELLINHIBITION OF PANCREATIC ADENOCARCINOMA CELLPROLIFERATION AND INVASION BY RNAI-MEDIATEDPROLIFERATION AND INVASION BY RNAI-MEDIATEDPROLIFERATION AND INVASION BY RNAI-MEDIATEDPROLIFERATION AND INVASION BY RNAI-MEDIATEDPROLIFERATION AND INVASION BY RNAI-MEDIATEDKNOCKDOWN OF THE PRL-2 TYROSINE PHOSPHATASEKNOCKDOWN OF THE PRL-2 TYROSINE PHOSPHATASEKNOCKDOWN OF THE PRL-2 TYROSINE PHOSPHATASEKNOCKDOWN OF THE PRL-2 TYROSINE PHOSPHATASEKNOCKDOWN OF THE PRL-2 TYROSINE PHOSPHATASE.P.L. Crowell, A.M. Wilson, S.R. Werner, and R.M. Thomas. Depart-ment of Biology and the Indiana University Simon Cancer Cen-ter, Indiana University-Purdue University, Indianapolis, IN.KYNURENINE CATABOLITES OF TRYPTOPHAN CARRIEDKYNURENINE CATABOLITES OF TRYPTOPHAN CARRIEDKYNURENINE CATABOLITES OF TRYPTOPHAN CARRIEDKYNURENINE CATABOLITES OF TRYPTOPHAN CARRIEDKYNURENINE CATABOLITES OF TRYPTOPHAN CARRIEDIN MESENTERIC LYMPH CONTRIBUTE TO PANCREATI-IN MESENTERIC LYMPH CONTRIBUTE TO PANCREATI-IN MESENTERIC LYMPH CONTRIBUTE TO PANCREATI-IN MESENTERIC LYMPH CONTRIBUTE TO PANCREATI-IN MESENTERIC LYMPH CONTRIBUTE TO PANCREATI-TIS-ASSOCIATED ORGAN FAILURE IN RATS AND HU-TIS-ASSOCIATED ORGAN FAILURE IN RATS AND HU-TIS-ASSOCIATED ORGAN FAILURE IN RATS AND HU-TIS-ASSOCIATED ORGAN FAILURE IN RATS AND HU-TIS-ASSOCIATED ORGAN FAILURE IN RATS AND HU-MANS.MANS.MANS.MANS.MANS. DJ Mole, NV McFerran, G Collett, C O’Neill, T Diamond, OJGarden, L Kylanpaa, H Repo, EA Deitch. Clinical & Surgical Sci-ences, University of Edinburgh, UK; Queen’s University of Belfast,UK; niversity of Oxford, UK; University of Helsinki, Finland; De-partment of Surgery, UMDNJ-New Jersey Medical School, NJ.IMPROVED OUTCOME OF PANCREATIC ADENOCARCI-IMPROVED OUTCOME OF PANCREATIC ADENOCARCI-IMPROVED OUTCOME OF PANCREATIC ADENOCARCI-IMPROVED OUTCOME OF PANCREATIC ADENOCARCI-IMPROVED OUTCOME OF PANCREATIC ADENOCARCI-NOMA ARISING IN INTRADUCTAL PAPILLARY MUCINOUSNOMA ARISING IN INTRADUCTAL PAPILLARY MUCINOUSNOMA ARISING IN INTRADUCTAL PAPILLARY MUCINOUSNOMA ARISING IN INTRADUCTAL PAPILLARY MUCINOUSNOMA ARISING IN INTRADUCTAL PAPILLARY MUCINOUSTUMORS IS DUE TO EARLIER STAGE AT PRESENTATION.TUMORS IS DUE TO EARLIER STAGE AT PRESENTATION.TUMORS IS DUE TO EARLIER STAGE AT PRESENTATION.TUMORS IS DUE TO EARLIER STAGE AT PRESENTATION.TUMORS IS DUE TO EARLIER STAGE AT PRESENTATION.BM Alexander, AF Hezel, C Fernandez Del-Castillo, LA Kachnic,A Niemierko, KR Kozak, LS Blaszkowsky, AL Warshaw, CG Willett,DP Ryan, JW Clark, TS Hong. Massachusetts General Hospital,Harvard Medical School, Boston, MA; Duke University MedicalCenter, Durham, NC.IN-VIVO IMAGING OF RADIATED ORTHOTOPIC PANCRE-IN-VIVO IMAGING OF RADIATED ORTHOTOPIC PANCRE-IN-VIVO IMAGING OF RADIATED ORTHOTOPIC PANCRE-IN-VIVO IMAGING OF RADIATED ORTHOTOPIC PANCRE-IN-VIVO IMAGING OF RADIATED ORTHOTOPIC PANCRE-ATIC XENOGRAFTS IN NOD-SCID MICE: A NOVELATIC XENOGRAFTS IN NOD-SCID MICE: A NOVELATIC XENOGRAFTS IN NOD-SCID MICE: A NOVELATIC XENOGRAFTS IN NOD-SCID MICE: A NOVELATIC XENOGRAFTS IN NOD-SCID MICE: A NOVELMETHOD FOR ASSAYING CLINICAL EFFICACY OF ION-METHOD FOR ASSAYING CLINICAL EFFICACY OF ION-METHOD FOR ASSAYING CLINICAL EFFICACY OF ION-METHOD FOR ASSAYING CLINICAL EFFICACY OF ION-METHOD FOR ASSAYING CLINICAL EFFICACY OF ION-IZING RADIATION.IZING RADIATION.IZING RADIATION.IZING RADIATION.IZING RADIATION. CJ Lee, L Wang, DM Simeone. Departmentsof Surgery and Molecular and Integrative Physiology, Universityof Michigan, Ann Arbor, MI.PROSPECTIVE ENDOSCOPIC ULTRASOUND-BASEDPROSPECTIVE ENDOSCOPIC ULTRASOUND-BASEDPROSPECTIVE ENDOSCOPIC ULTRASOUND-BASEDPROSPECTIVE ENDOSCOPIC ULTRASOUND-BASEDPROSPECTIVE ENDOSCOPIC ULTRASOUND-BASEDSTRATEGY FOR THE EVALUATION OF A SINGLE ATTACKSTRATEGY FOR THE EVALUATION OF A SINGLE ATTACKSTRATEGY FOR THE EVALUATION OF A SINGLE ATTACKSTRATEGY FOR THE EVALUATION OF A SINGLE ATTACKSTRATEGY FOR THE EVALUATION OF A SINGLE ATTACKOF UNEXPLAINED PANCREATITIS.OF UNEXPLAINED PANCREATITIS.OF UNEXPLAINED PANCREATITIS.OF UNEXPLAINED PANCREATITIS.OF UNEXPLAINED PANCREATITIS. CM Wilcox, T Seay, MPhadnis, S Varadarajulu, M Eloubeidi. Division of Gastroenterol-ogy and Hepatology, University of Alabama at Birmingham, Bir-mingham, ALTOXIC GLOBALISATION OF SECRETAGOGUE-ELICITEDTOXIC GLOBALISATION OF SECRETAGOGUE-ELICITEDTOXIC GLOBALISATION OF SECRETAGOGUE-ELICITEDTOXIC GLOBALISATION OF SECRETAGOGUE-ELICITEDTOXIC GLOBALISATION OF SECRETAGOGUE-ELICITEDACINAR CELL CAACINAR CELL CAACINAR CELL CAACINAR CELL CAACINAR CELL CA2+2+2+2+2+ SIGNALING AND PREVENTION BY ATP SIGNALING AND PREVENTION BY ATP SIGNALING AND PREVENTION BY ATP SIGNALING AND PREVENTION BY ATP SIGNALING AND PREVENTION BY ATPOR REMOVAL OF CAOR REMOVAL OF CAOR REMOVAL OF CAOR REMOVAL OF CAOR REMOVAL OF CA2+2+2+2+2+ FROM THE CELL EXTERIOR. FROM THE CELL EXTERIOR. FROM THE CELL EXTERIOR. FROM THE CELL EXTERIOR. FROM THE CELL EXTERIOR. JAMurphy, DN Criddle, JP Neoptolemos, OV Gerasimenko, AVTepikin, OH Petersen, R Sutton, MRC Group. Physiological Labo-ratory and Division of Surgery and Oncology, University ofLiverpool, UK.RAP1 PLAYS A REGULATORY ROLE IN PANCREATIC AMY-RAP1 PLAYS A REGULATORY ROLE IN PANCREATIC AMY-RAP1 PLAYS A REGULATORY ROLE IN PANCREATIC AMY-RAP1 PLAYS A REGULATORY ROLE IN PANCREATIC AMY-RAP1 PLAYS A REGULATORY ROLE IN PANCREATIC AMY-LASE RELEASE. LASE RELEASE. LASE RELEASE. LASE RELEASE. LASE RELEASE. ME Sabbatini, X Chen, JA Williams. Departmentof Molecular & Integrative Physiology, University of Michigan,Ann Arbor, MI.











METABOLOMICS OF THE FATTY PANCREAS: IMPLICAT-METABOLOMICS OF THE FATTY PANCREAS: IMPLICAT-METABOLOMICS OF THE FATTY PANCREAS: IMPLICAT-METABOLOMICS OF THE FATTY PANCREAS: IMPLICAT-METABOLOMICS OF THE FATTY PANCREAS: IMPLICAT-ING FAT IN PANCREATIC PATHOLOGY.ING FAT IN PANCREATIC PATHOLOGY.ING FAT IN PANCREATIC PATHOLOGY.ING FAT IN PANCREATIC PATHOLOGY.ING FAT IN PANCREATIC PATHOLOGY. NJ Zyromski, GANGowda, A Mathur, DA Swartz-Basile, HA Pitt, D Raftery. Depart-ment of Surgery, Indiana University, Indianapolis, IN; Depart-ment of Chemistry, Purdue University, West Layfayette, IN.MONOCYTES-MACROPHAGES MEDIATE RECOVERYMONOCYTES-MACROPHAGES MEDIATE RECOVERYMONOCYTES-MACROPHAGES MEDIATE RECOVERYMONOCYTES-MACROPHAGES MEDIATE RECOVERYMONOCYTES-MACROPHAGES MEDIATE RECOVERYFROM ACUTE PANCREATITISFROM ACUTE PANCREATITISFROM ACUTE PANCREATITISFROM ACUTE PANCREATITISFROM ACUTE PANCREATITIS. G Perides, J Laukkarinen, ERWeiss, J Duffield, ML Steer. Depts. of Surgery, Tufts-New En-gland Medical Center, Boston, MA, Tampere University Hospi-tal, Tampere, Finland, Dept of Medicine, Brigham and Women’sHospital, Boston, MA.CHEMICAL STRESS-INDUCED HSP70 PROTECTSCHEMICAL STRESS-INDUCED HSP70 PROTECTSCHEMICAL STRESS-INDUCED HSP70 PROTECTSCHEMICAL STRESS-INDUCED HSP70 PROTECTSCHEMICAL STRESS-INDUCED HSP70 PROTECTSAGAINST L-ARGININE-INDUCED PANCREATITIS INAGAINST L-ARGININE-INDUCED PANCREATITIS INAGAINST L-ARGININE-INDUCED PANCREATITIS INAGAINST L-ARGININE-INDUCED PANCREATITIS INAGAINST L-ARGININE-INDUCED PANCREATITIS INRATS.RATS.RATS.RATS.RATS. R Dawra, R Talukdar, S Vickers, D Borja, L Bhagat, ASaluja. Department of Surgery, University of Minnesota, Min-neapolis, MN.BOTH THE P38 AND ERK MAP KINASES REGULATE NF-BOTH THE P38 AND ERK MAP KINASES REGULATE NF-BOTH THE P38 AND ERK MAP KINASES REGULATE NF-BOTH THE P38 AND ERK MAP KINASES REGULATE NF-BOTH THE P38 AND ERK MAP KINASES REGULATE NF-ÊB-DEPENDENT GENE TRANSCRIPTION.ÊB-DEPENDENT GENE TRANSCRIPTION.ÊB-DEPENDENT GENE TRANSCRIPTION.ÊB-DEPENDENT GENE TRANSCRIPTION.ÊB-DEPENDENT GENE TRANSCRIPTION. I Samuel, LTephly, AB Carter. Carver COM, Univ. of Iowa, Iowa City, IA.INVERSE RELATIONSHIP BETWEEN PIGMENT EPITHELIUMINVERSE RELATIONSHIP BETWEEN PIGMENT EPITHELIUMINVERSE RELATIONSHIP BETWEEN PIGMENT EPITHELIUMINVERSE RELATIONSHIP BETWEEN PIGMENT EPITHELIUMINVERSE RELATIONSHIP BETWEEN PIGMENT EPITHELIUMDERIVED FACTOR (PEDF) AND VASCULAR ENDOTHE-DERIVED FACTOR (PEDF) AND VASCULAR ENDOTHE-DERIVED FACTOR (PEDF) AND VASCULAR ENDOTHE-DERIVED FACTOR (PEDF) AND VASCULAR ENDOTHE-DERIVED FACTOR (PEDF) AND VASCULAR ENDOTHE-LIAL GROWTH FACTOR (VEGF) IN HUMAN PANCREATICLIAL GROWTH FACTOR (VEGF) IN HUMAN PANCREATICLIAL GROWTH FACTOR (VEGF) IN HUMAN PANCREATICLIAL GROWTH FACTOR (VEGF) IN HUMAN PANCREATICLIAL GROWTH FACTOR (VEGF) IN HUMAN PANCREATICCANCER.CANCER.CANCER.CANCER.CANCER. DM Heiferman, MR Salabat, V Papavero, MJ Heiferman,M Strouch, DB Van Beek, S Pappas, S Ahrendt, Yang GY, PJ Grippo,DJ Bentrem. Northwestern Memorial Hospital, Lurie Compre-hensive Cancer Center, Chicago, IL.A NOVEL TRANSCRIPTIONAL MECHANISM TO EXPLAINA NOVEL TRANSCRIPTIONAL MECHANISM TO EXPLAINA NOVEL TRANSCRIPTIONAL MECHANISM TO EXPLAINA NOVEL TRANSCRIPTIONAL MECHANISM TO EXPLAINA NOVEL TRANSCRIPTIONAL MECHANISM TO EXPLAINLONG TERM REPONSES FOR G-PROTEIN COUPLEDLONG TERM REPONSES FOR G-PROTEIN COUPLEDLONG TERM REPONSES FOR G-PROTEIN COUPLEDLONG TERM REPONSES FOR G-PROTEIN COUPLEDLONG TERM REPONSES FOR G-PROTEIN COUPLEDRECEPTORS WHICH IS DISRUPTED IN PANCREATIC CELLRECEPTORS WHICH IS DISRUPTED IN PANCREATIC CELLRECEPTORS WHICH IS DISRUPTED IN PANCREATIC CELLRECEPTORS WHICH IS DISRUPTED IN PANCREATIC CELLRECEPTORS WHICH IS DISRUPTED IN PANCREATIC CELLPATHOBIOLOGY.PATHOBIOLOGY.PATHOBIOLOGY.PATHOBIOLOGY.PATHOBIOLOGY. JS Zhang, G Lomberk, R Urrutia. Departmentof Biochemistry and Molecular Biology, Biophysics, Medicineand GI Research Unit Mayo Clinic, Rochester, MN.CROSS-PLATFORM MOLECULAR PROFILING OF CELLU-CROSS-PLATFORM MOLECULAR PROFILING OF CELLU-CROSS-PLATFORM MOLECULAR PROFILING OF CELLU-CROSS-PLATFORM MOLECULAR PROFILING OF CELLU-CROSS-PLATFORM MOLECULAR PROFILING OF CELLU-LAR PATHWAYS INVOLVED IN PANCREATIC CANCER. LAR PATHWAYS INVOLVED IN PANCREATIC CANCER. LAR PATHWAYS INVOLVED IN PANCREATIC CANCER. LAR PATHWAYS INVOLVED IN PANCREATIC CANCER. LAR PATHWAYS INVOLVED IN PANCREATIC CANCER. JCarter, C Logsdon, M Fazier, A Killary, S Sen. The University ofTexas M. D. Anderson Cancer Center, Houston, TX.ASSESSMENT OF RESECTABILITY AFTER AN INITIAL DI-ASSESSMENT OF RESECTABILITY AFTER AN INITIAL DI-ASSESSMENT OF RESECTABILITY AFTER AN INITIAL DI-ASSESSMENT OF RESECTABILITY AFTER AN INITIAL DI-ASSESSMENT OF RESECTABILITY AFTER AN INITIAL DI-AGNOSIS OF UNRESECTABLE PANCREATIC CANCER:AGNOSIS OF UNRESECTABLE PANCREATIC CANCER:AGNOSIS OF UNRESECTABLE PANCREATIC CANCER:AGNOSIS OF UNRESECTABLE PANCREATIC CANCER:AGNOSIS OF UNRESECTABLE PANCREATIC CANCER:IMPACT OF PATIENT CENTRALIZATIONIMPACT OF PATIENT CENTRALIZATIONIMPACT OF PATIENT CENTRALIZATIONIMPACT OF PATIENT CENTRALIZATIONIMPACT OF PATIENT CENTRALIZATION..... M. Erkan, CW.Michalski, J. Bachmann, J. AlKhatib, I. Esposito, H. Friess, J. Kleeff,MW. Buechler. Department of Surgery, University of Heidel-berg; Department of Surgery, Technical University of Munich;Institute of Pathology, University of Heidelberg.











BOARD#BOARD#BOARD#BOARD#BOARD# TITLETITLETITLETITLETITLEDIFFERENT EZH2 ISOFORMS ARE EXPRESSED IN PAN-DIFFERENT EZH2 ISOFORMS ARE EXPRESSED IN PAN-DIFFERENT EZH2 ISOFORMS ARE EXPRESSED IN PAN-DIFFERENT EZH2 ISOFORMS ARE EXPRESSED IN PAN-DIFFERENT EZH2 ISOFORMS ARE EXPRESSED IN PAN-CREATIC CELLS: EVIDENCE FOR A POLYCOMB-MEDIATEDCREATIC CELLS: EVIDENCE FOR A POLYCOMB-MEDIATEDCREATIC CELLS: EVIDENCE FOR A POLYCOMB-MEDIATEDCREATIC CELLS: EVIDENCE FOR A POLYCOMB-MEDIATEDCREATIC CELLS: EVIDENCE FOR A POLYCOMB-MEDIATEDSUBCODE WITHIN THE CONTEXT OF THE HISTONE CODE.SUBCODE WITHIN THE CONTEXT OF THE HISTONE CODE.SUBCODE WITHIN THE CONTEXT OF THE HISTONE CODE.SUBCODE WITHIN THE CONTEXT OF THE HISTONE CODE.SUBCODE WITHIN THE CONTEXT OF THE HISTONE CODE.AL Grzenda, G Lomberk, R Urrutia. Department of Biochemistryand Molecular Biology, Biophysics, Medicine and GI ResearchUnit, Mayo Clinic, Rochester, MN.HISTONE-DEACETYLATION REGULATES EXPRESSION OFHISTONE-DEACETYLATION REGULATES EXPRESSION OFHISTONE-DEACETYLATION REGULATES EXPRESSION OFHISTONE-DEACETYLATION REGULATES EXPRESSION OFHISTONE-DEACETYLATION REGULATES EXPRESSION OFHUMAN E-CADHERIN IN PANCREATIC CANCER.HUMAN E-CADHERIN IN PANCREATIC CANCER.HUMAN E-CADHERIN IN PANCREATIC CANCER.HUMAN E-CADHERIN IN PANCREATIC CANCER.HUMAN E-CADHERIN IN PANCREATIC CANCER. AAghdassi, M Sendler, J Mayerle, FU Weiss, CD Heidecke, H Friess,MW Büchler, MM Lerch. Department of Medicine A, Departmentof Surgery, Ernst-Moritz-Arndt-University Greifswald, Germany;Department of Surgery, University of Heidelberg, Germany.QUALITY OF LIFE IN SUBJECTS WHO UNDERWENT PAN-QUALITY OF LIFE IN SUBJECTS WHO UNDERWENT PAN-QUALITY OF LIFE IN SUBJECTS WHO UNDERWENT PAN-QUALITY OF LIFE IN SUBJECTS WHO UNDERWENT PAN-QUALITY OF LIFE IN SUBJECTS WHO UNDERWENT PAN-CREATIC HEAD RESECTION. THE INTERIM REPORT OF ACREATIC HEAD RESECTION. THE INTERIM REPORT OF ACREATIC HEAD RESECTION. THE INTERIM REPORT OF ACREATIC HEAD RESECTION. THE INTERIM REPORT OF ACREATIC HEAD RESECTION. THE INTERIM REPORT OF AMULTICENTER STUDY.MULTICENTER STUDY.MULTICENTER STUDY.MULTICENTER STUDY.MULTICENTER STUDY. R. Pezzilli, M. Falconi, A. Zerbi, R.Casadei, L. Fantini, L. Valli, R. Varale, N. Zanini, G. Armatura,A.M. Morselli-Labate. Departments of Internal Medicine and Gas-troenterology, Department of Surgery, S. Orsola-Malpighi Hos-pital, Bologna, Department of Surgery, GB Rossi Hospital, Verona,Department of Surgery, S. Raffaele Hospital, Milan, Italy.DOES IMMUNOSUPPRESSION (IS) CHANGE THE NATU-DOES IMMUNOSUPPRESSION (IS) CHANGE THE NATU-DOES IMMUNOSUPPRESSION (IS) CHANGE THE NATU-DOES IMMUNOSUPPRESSION (IS) CHANGE THE NATU-DOES IMMUNOSUPPRESSION (IS) CHANGE THE NATU-RAL HISTORY OF IPMNS?RAL HISTORY OF IPMNS?RAL HISTORY OF IPMNS?RAL HISTORY OF IPMNS?RAL HISTORY OF IPMNS? KRS Gill, SA Gross, M Al-Haddad,DM Harnois, AP Keaveny, TA Woodward, MB Wallace, M Raimondo.Division of Gastroenterology & Hepatology, Mayo Clinic, Jack-sonville, FL.A NOTE OF CAUTION FOR THE DOCTOR ON DUTY: TAKEA NOTE OF CAUTION FOR THE DOCTOR ON DUTY: TAKEA NOTE OF CAUTION FOR THE DOCTOR ON DUTY: TAKEA NOTE OF CAUTION FOR THE DOCTOR ON DUTY: TAKEA NOTE OF CAUTION FOR THE DOCTOR ON DUTY: TAKETHE ACUTE ATTACK IN CHRONIC PANCREATITIS SERI-THE ACUTE ATTACK IN CHRONIC PANCREATITIS SERI-THE ACUTE ATTACK IN CHRONIC PANCREATITIS SERI-THE ACUTE ATTACK IN CHRONIC PANCREATITIS SERI-THE ACUTE ATTACK IN CHRONIC PANCREATITIS SERI-OUSLY! OUSLY! OUSLY! OUSLY! OUSLY! PG Lankisch, G Brinkmann, P Maisonneuve, AB Lowenfels.Department of Internal Medicine, Institute of Diagnostic Radiol-ogy, Municipal Clinic of Lueneburg, Germany; European Insti-tute of Oncology, Milan, Italy; New York Medical College, Valhalla,NY.TIMING OF THE VIDEOLAPAROCHOLECYSTECTOMY FORTIMING OF THE VIDEOLAPAROCHOLECYSTECTOMY FORTIMING OF THE VIDEOLAPAROCHOLECYSTECTOMY FORTIMING OF THE VIDEOLAPAROCHOLECYSTECTOMY FORTIMING OF THE VIDEOLAPAROCHOLECYSTECTOMY FORMILD ACUTE BILIARY PANCREATITIS.MILD ACUTE BILIARY PANCREATITIS.MILD ACUTE BILIARY PANCREATITIS.MILD ACUTE BILIARY PANCREATITIS.MILD ACUTE BILIARY PANCREATITIS. TP Valentino, CSantacroce, A Fersini, N Tartaglia, V Neri. University of Foggia,Department of Surgical Sciences, Division of General Surgery,Polyclinic of Foggia, Foggia, Italy.CHANGING OF THE ETIOLOGIES OF ACUTE PANCREATI-CHANGING OF THE ETIOLOGIES OF ACUTE PANCREATI-CHANGING OF THE ETIOLOGIES OF ACUTE PANCREATI-CHANGING OF THE ETIOLOGIES OF ACUTE PANCREATI-CHANGING OF THE ETIOLOGIES OF ACUTE PANCREATI-TIS AFTER A SYSTEMATIC SEARCH WITH A GUIDELINE.TIS AFTER A SYSTEMATIC SEARCH WITH A GUIDELINE.TIS AFTER A SYSTEMATIC SEARCH WITH A GUIDELINE.TIS AFTER A SYSTEMATIC SEARCH WITH A GUIDELINE.TIS AFTER A SYSTEMATIC SEARCH WITH A GUIDELINE. SPongprasobchai, R Thammacharoen. Division of Gastroenter-ology, Department of Medicine, Siriraj Hospital, Bangkok, Thai-land.THE PROTEOME OF NORMAL PANCREATIC JUICE.THE PROTEOME OF NORMAL PANCREATIC JUICE.THE PROTEOME OF NORMAL PANCREATIC JUICE.THE PROTEOME OF NORMAL PANCREATIC JUICE.THE PROTEOME OF NORMAL PANCREATIC JUICE. KYancey, HA Pitt, M Wang, M Yip-Schneider, S Sherman, KDLillemoe, MD Goggins, CM Schmidt. Indiana University, IndianaCenters for Applied Protein Sciences, Indianapolis, IN; JohnsHopkins University, Baltimore, MD.












DISSEMINATION OF HUMAN PANCREATIC TUMORDISSEMINATION OF HUMAN PANCREATIC TUMORDISSEMINATION OF HUMAN PANCREATIC TUMORDISSEMINATION OF HUMAN PANCREATIC TUMORDISSEMINATION OF HUMAN PANCREATIC TUMORCELLS IS MEDIATED BY SRC-INDUCED PHOSPHORY-CELLS IS MEDIATED BY SRC-INDUCED PHOSPHORY-CELLS IS MEDIATED BY SRC-INDUCED PHOSPHORY-CELLS IS MEDIATED BY SRC-INDUCED PHOSPHORY-CELLS IS MEDIATED BY SRC-INDUCED PHOSPHORY-LATION OF CAVEOLIN.LATION OF CAVEOLIN.LATION OF CAVEOLIN.LATION OF CAVEOLIN.LATION OF CAVEOLIN. L Orlichenko, SG Weller, MAwoniyi, MA McNiven. Mayo Clinic College of Medicine, Roch-ester, MN.SUPPRESSION OF MAFS EXPRESSION BY THE SIRNASUPPRESSION OF MAFS EXPRESSION BY THE SIRNASUPPRESSION OF MAFS EXPRESSION BY THE SIRNASUPPRESSION OF MAFS EXPRESSION BY THE SIRNASUPPRESSION OF MAFS EXPRESSION BY THE SIRNATECHNIQUE ALTERS THE GENE PROFILE RELATED TOTECHNIQUE ALTERS THE GENE PROFILE RELATED TOTECHNIQUE ALTERS THE GENE PROFILE RELATED TOTECHNIQUE ALTERS THE GENE PROFILE RELATED TOTECHNIQUE ALTERS THE GENE PROFILE RELATED TOPANCREATIC ENDOCRINE HORMONE ANDPANCREATIC ENDOCRINE HORMONE ANDPANCREATIC ENDOCRINE HORMONE ANDPANCREATIC ENDOCRINE HORMONE ANDPANCREATIC ENDOCRINE HORMONE ANDADIPOCYTOKINE IN VIVO AND IN VITRO.ADIPOCYTOKINE IN VIVO AND IN VITRO.ADIPOCYTOKINE IN VIVO AND IN VITRO.ADIPOCYTOKINE IN VIVO AND IN VITRO.ADIPOCYTOKINE IN VIVO AND IN VITRO. M Tsuchiya,A Hayashi, J Tanaka, A Maeda, K Tsuchiya. Institute of Geri-atrics, Department of Medicine IV, Tokyo Women’s MedicalUniversity, Tokyo, Japan.MISSENSE MUTATIONS IN PANCREATIC SECRETORYMISSENSE MUTATIONS IN PANCREATIC SECRETORYMISSENSE MUTATIONS IN PANCREATIC SECRETORYMISSENSE MUTATIONS IN PANCREATIC SECRETORYMISSENSE MUTATIONS IN PANCREATIC SECRETORYTRYPSIN INHIBITOR (SPINK1) CAUSE INTRACELLU-TRYPSIN INHIBITOR (SPINK1) CAUSE INTRACELLU-TRYPSIN INHIBITOR (SPINK1) CAUSE INTRACELLU-TRYPSIN INHIBITOR (SPINK1) CAUSE INTRACELLU-TRYPSIN INHIBITOR (SPINK1) CAUSE INTRACELLU-LAR RETENTION AND DEGRADATIONLAR RETENTION AND DEGRADATIONLAR RETENTION AND DEGRADATIONLAR RETENTION AND DEGRADATIONLAR RETENTION AND DEGRADATION..... O Király, TWartmann, M Sahin-Tóth. Department of Molecular and CellBiology, Boston University, Goldman School of Dental Medi-cine, Boston, MA; Division of Experimental Surgery, De-partment of Surgery, Otto-von-Guericke-Universität,Magdeburg Germany.THE EFFECT OF HYPOXIA ON RAT PANCREATIC STEL-THE EFFECT OF HYPOXIA ON RAT PANCREATIC STEL-THE EFFECT OF HYPOXIA ON RAT PANCREATIC STEL-THE EFFECT OF HYPOXIA ON RAT PANCREATIC STEL-THE EFFECT OF HYPOXIA ON RAT PANCREATIC STEL-LATE CELLS. LATE CELLS. LATE CELLS. LATE CELLS. LATE CELLS. S Watanabe, Y Nagashio, H Asaumi, YNomiyama, M Taguchi, Y Kihara, H Nakamura, M Otsuki.Third Department of Internal Medicine, University of Occu-pational and Environmental Health, Kitakyushu, Japan.LEPTIN RESISTANCE LEADS TO INCREASED ACCU-LEPTIN RESISTANCE LEADS TO INCREASED ACCU-LEPTIN RESISTANCE LEADS TO INCREASED ACCU-LEPTIN RESISTANCE LEADS TO INCREASED ACCU-LEPTIN RESISTANCE LEADS TO INCREASED ACCU-MULATION OF TOXIC PANCREATIC FAT.MULATION OF TOXIC PANCREATIC FAT.MULATION OF TOXIC PANCREATIC FAT.MULATION OF TOXIC PANCREATIC FAT.MULATION OF TOXIC PANCREATIC FAT. A Mathur,KW Yancey, D Lu, DA Swartz-Basile, KD Lillemoe, HA Pitt, NJZyromski. Indiana University School of Medicine, Indianapo-lis, IN.HYPERTONIC SALINE SOLUTION INHIBITS SYSTEMICHYPERTONIC SALINE SOLUTION INHIBITS SYSTEMICHYPERTONIC SALINE SOLUTION INHIBITS SYSTEMICHYPERTONIC SALINE SOLUTION INHIBITS SYSTEMICHYPERTONIC SALINE SOLUTION INHIBITS SYSTEMICINFLAMMATORY RESPONSE BUT NOT LOCAL LE-INFLAMMATORY RESPONSE BUT NOT LOCAL LE-INFLAMMATORY RESPONSE BUT NOT LOCAL LE-INFLAMMATORY RESPONSE BUT NOT LOCAL LE-INFLAMMATORY RESPONSE BUT NOT LOCAL LE-SIONS IN EXPERIMENTAL ACUTE PANCREATITIS.SIONS IN EXPERIMENTAL ACUTE PANCREATITIS.SIONS IN EXPERIMENTAL ACUTE PANCREATITIS.SIONS IN EXPERIMENTAL ACUTE PANCREATITIS.SIONS IN EXPERIMENTAL ACUTE PANCREATITIS. AMMCoelho, J Jukemura, B Lindkvist, SN Sampietre, NAT Molan, RPatzina, JEM Cunha, MCC Machado. Department of Gastro-enterology-University of Sao Paulo, Brazil; Department ofSurgery, Lund University, Malmö, Sweden.RESISTANT ORGANISMS PREDICT POOR OUTCOMERESISTANT ORGANISMS PREDICT POOR OUTCOMERESISTANT ORGANISMS PREDICT POOR OUTCOMERESISTANT ORGANISMS PREDICT POOR OUTCOMERESISTANT ORGANISMS PREDICT POOR OUTCOMEIN NECROTIZING PANCREATITIS: A PLEA TO DO NOIN NECROTIZING PANCREATITIS: A PLEA TO DO NOIN NECROTIZING PANCREATITIS: A PLEA TO DO NOIN NECROTIZING PANCREATITIS: A PLEA TO DO NOIN NECROTIZING PANCREATITIS: A PLEA TO DO NOHARM. HARM. HARM. HARM. HARM. Y Zhukov, TJ Howard, L McHenry, EL Fogel, A Nakeeb,HA Pitt, KD Lillemoe, CM Schmidt, NJ Zyromski. Depart-ments of Surgery and 2Gastroenterology, Indiana Univer-sity, Indianapolis, IN.










BOARD#BOARD#BOARD#BOARD#BOARD# TITLETITLETITLETITLETITLEDELIVERY OF DELIVERY OF DELIVERY OF DELIVERY OF DELIVERY OF sisisisisiRNA TO PANCREATIC CANCER CELLSRNA TO PANCREATIC CANCER CELLSRNA TO PANCREATIC CANCER CELLSRNA TO PANCREATIC CANCER CELLSRNA TO PANCREATIC CANCER CELLSUSING NOVEL NON-VIRAL BIODEGRADABLEUSING NOVEL NON-VIRAL BIODEGRADABLEUSING NOVEL NON-VIRAL BIODEGRADABLEUSING NOVEL NON-VIRAL BIODEGRADABLEUSING NOVEL NON-VIRAL BIODEGRADABLENANOPARTICLES.NANOPARTICLES.NANOPARTICLES.NANOPARTICLES.NANOPARTICLES. J McCarroll, V Dudeja, P Phillips, R Dawra,D Borja-Cacho, S Vickers, C Wang, A Saluja. Department ofSurgery and Department of Biomedical Engineering,University of Minnesota, Minneapolis, MN.VORINOSTAT RADIOSENSITIZES PANCREATIC CANCERSVORINOSTAT RADIOSENSITIZES PANCREATIC CANCERSVORINOSTAT RADIOSENSITIZES PANCREATIC CANCERSVORINOSTAT RADIOSENSITIZES PANCREATIC CANCERSVORINOSTAT RADIOSENSITIZES PANCREATIC CANCERSBY INHIBITING DNA REPAIR AND RADIATION-INDUCEDBY INHIBITING DNA REPAIR AND RADIATION-INDUCEDBY INHIBITING DNA REPAIR AND RADIATION-INDUCEDBY INHIBITING DNA REPAIR AND RADIATION-INDUCEDBY INHIBITING DNA REPAIR AND RADIATION-INDUCEDEGFR AND NF-KB SIGNALING. EGFR AND NF-KB SIGNALING. EGFR AND NF-KB SIGNALING. EGFR AND NF-KB SIGNALING. EGFR AND NF-KB SIGNALING. A Deorukhkar, H Park, SShentu, P Diagaradjane, S Krishnan. MD Anderson CancerCenter, Houston, TX.EXPRESSION OF NESTIN IN PANCREATIC CANCER COR-EXPRESSION OF NESTIN IN PANCREATIC CANCER COR-EXPRESSION OF NESTIN IN PANCREATIC CANCER COR-EXPRESSION OF NESTIN IN PANCREATIC CANCER COR-EXPRESSION OF NESTIN IN PANCREATIC CANCER COR-RELATES WITH OF INVASIVE ABILITY.RELATES WITH OF INVASIVE ABILITY.RELATES WITH OF INVASIVE ABILITY.RELATES WITH OF INVASIVE ABILITY.RELATES WITH OF INVASIVE ABILITY. M Kawamoto, T Tajiri,T Ishiwata, E Uchida, T Aimoto, Y Nakamura, A Matsushita, AKatsuno, K Cho, Y Ono, T Yamamoto, Y Matsuda, Z Naito. Sur-gery for Organ and Biological Regulation (Department of Sur-gery), Graduate School of Medicine, Nippon Medical School,Tokyo, Japan, Department of Pathology, Integrative Oncologi-cal Pathology, Nippon Medical School, Tokyo, Japan.SERUM FRUCTOSESERUM FRUCTOSESERUM FRUCTOSESERUM FRUCTOSESERUM FRUCTOSE IN PANCREATIC CANCER PATIENTS.IN PANCREATIC CANCER PATIENTS.IN PANCREATIC CANCER PATIENTS.IN PANCREATIC CANCER PATIENTS.IN PANCREATIC CANCER PATIENTS.H Hui, McArthur, N Nissen, VLW Go, A. Heaney. Division of Endo-crinology, Division of Neurosurgery, Division of Digestive Dis-eases, David Geffen School of Medicine at UCLA, Los Angeles,CA; Department of Surgery, Cedars-Sinai Medical Center, LosAngeles, CA.DOWN-REGULATION OF PDGF-D INHIBITS CELL GROWTHDOWN-REGULATION OF PDGF-D INHIBITS CELL GROWTHDOWN-REGULATION OF PDGF-D INHIBITS CELL GROWTHDOWN-REGULATION OF PDGF-D INHIBITS CELL GROWTHDOWN-REGULATION OF PDGF-D INHIBITS CELL GROWTHAND ANGIOGENESIS THROUGH INACTIVATION OFAND ANGIOGENESIS THROUGH INACTIVATION OFAND ANGIOGENESIS THROUGH INACTIVATION OFAND ANGIOGENESIS THROUGH INACTIVATION OFAND ANGIOGENESIS THROUGH INACTIVATION OFNOTCH-1 AND NOTCH-1 AND NOTCH-1 AND NOTCH-1 AND NOTCH-1 AND NF-NF-NF-NF-NF-κκκκκBBBBB SIGNALING. SIGNALING. SIGNALING. SIGNALING. SIGNALING. Z Wang, D Kong, SBanerjee, Y Li, FH Sarkar. Department of Pathology, KarmanosCancer Institute, Wayne State University, Detroit, MI.A NOVEL MECHANISM FOR OVEREXPRESSION OF TRKB-A NOVEL MECHANISM FOR OVEREXPRESSION OF TRKB-A NOVEL MECHANISM FOR OVEREXPRESSION OF TRKB-A NOVEL MECHANISM FOR OVEREXPRESSION OF TRKB-A NOVEL MECHANISM FOR OVEREXPRESSION OF TRKB-T1-INDUCED PANCREATIC CANCER METASTASIS. T1-INDUCED PANCREATIC CANCER METASTASIS. T1-INDUCED PANCREATIC CANCER METASTASIS. T1-INDUCED PANCREATIC CANCER METASTASIS. T1-INDUCED PANCREATIC CANCER METASTASIS. Z Li, BPeng, DB Evans, J Chiao, Department of Surgical Oncology,Department of Molecular and Cellular Oncology, the Universityof Texas M.D. Anderson Cancer Center, Houston, TX, TheProgram in Cancer Biology, the University of Texas GraduateSchool of Biomedical Sciences at Houston, Houston, TX.MYRICETIN INDUCES APOPTOSIS VIA CASPASE ACTIVA-MYRICETIN INDUCES APOPTOSIS VIA CASPASE ACTIVA-MYRICETIN INDUCES APOPTOSIS VIA CASPASE ACTIVA-MYRICETIN INDUCES APOPTOSIS VIA CASPASE ACTIVA-MYRICETIN INDUCES APOPTOSIS VIA CASPASE ACTIVA-TION AND INHIBITION OF PI-3 KINASE/AKT AND ERKTION AND INHIBITION OF PI-3 KINASE/AKT AND ERKTION AND INHIBITION OF PI-3 KINASE/AKT AND ERKTION AND INHIBITION OF PI-3 KINASE/AKT AND ERKTION AND INHIBITION OF PI-3 KINASE/AKT AND ERKPATHWAYS IN HUMAN PANCREATIC CELLS. PATHWAYS IN HUMAN PANCREATIC CELLS. PATHWAYS IN HUMAN PANCREATIC CELLS. PATHWAYS IN HUMAN PANCREATIC CELLS. PATHWAYS IN HUMAN PANCREATIC CELLS. P Zwolak, DBorja-Cacho, PA Phillips, V Dudeja, R Dawra, JS Ankeny, R Talukdar,R Chugh, S Vickers, A Saluja. Department of Surgery, Universityof Minnesota, Minneapolis, MN.











CANCER VACCINES TARGETING SURVIVIN IN PANCRE-CANCER VACCINES TARGETING SURVIVIN IN PANCRE-CANCER VACCINES TARGETING SURVIVIN IN PANCRE-CANCER VACCINES TARGETING SURVIVIN IN PANCRE-CANCER VACCINES TARGETING SURVIVIN IN PANCRE-ATIC CANCER. ATIC CANCER. ATIC CANCER. ATIC CANCER. ATIC CANCER. DZ Chang, K Zhu, H Qin, JL Abbrussze, LKawk, P Hwu, L Radvanyi. The U.T. M D Anderson Cancer Cen-ter, Houston, TX.MEDIAN PANCREATECTOMY FOR BENIGN OR LOW-MEDIAN PANCREATECTOMY FOR BENIGN OR LOW-MEDIAN PANCREATECTOMY FOR BENIGN OR LOW-MEDIAN PANCREATECTOMY FOR BENIGN OR LOW-MEDIAN PANCREATECTOMY FOR BENIGN OR LOW-GRADE MALIGNANT TUMORSGRADE MALIGNANT TUMORSGRADE MALIGNANT TUMORSGRADE MALIGNANT TUMORSGRADE MALIGNANT TUMORS. Z Xu , Z Qian, C Dai, K Jiang,J Wu, Y Miao. Department of General Surgery, the First Affili-ated Hospital of Nanjing Medical University, Nanjing, ChinaDIFFERENT GLYCOSYLATION PATTERNS OF LUMICANDIFFERENT GLYCOSYLATION PATTERNS OF LUMICANDIFFERENT GLYCOSYLATION PATTERNS OF LUMICANDIFFERENT GLYCOSYLATION PATTERNS OF LUMICANDIFFERENT GLYCOSYLATION PATTERNS OF LUMICANCORRELATE WITH INVASION AND PROGNOSIS IN PAN-CORRELATE WITH INVASION AND PROGNOSIS IN PAN-CORRELATE WITH INVASION AND PROGNOSIS IN PAN-CORRELATE WITH INVASION AND PROGNOSIS IN PAN-CORRELATE WITH INVASION AND PROGNOSIS IN PAN-CREATIC CANCER.CREATIC CANCER.CREATIC CANCER.CREATIC CANCER.CREATIC CANCER. T Yamamoto, T Ishiwata, K Cho, KKawahara, T Fujii, Y Ono, Y Matsuda, E Uchida, T Tajiri, Z Naito.Department of Pathology, Integrative Oncological Pathology,Nippon Medical School, Surgery for Organ and Biological Regu-lation (First Department of Surgery), Graduate School of Medi-cine, Nippon Medical School.THE N-3 POLYUNSATURATED FATTY ACID EPA INHIB-THE N-3 POLYUNSATURATED FATTY ACID EPA INHIB-THE N-3 POLYUNSATURATED FATTY ACID EPA INHIB-THE N-3 POLYUNSATURATED FATTY ACID EPA INHIB-THE N-3 POLYUNSATURATED FATTY ACID EPA INHIB-ITS PANCREATIC CANCER CELL GROWTH BY COX-2ITS PANCREATIC CANCER CELL GROWTH BY COX-2ITS PANCREATIC CANCER CELL GROWTH BY COX-2ITS PANCREATIC CANCER CELL GROWTH BY COX-2ITS PANCREATIC CANCER CELL GROWTH BY COX-2DEPENDENT AND INDEPENDENT MECHANISMS.DEPENDENT AND INDEPENDENT MECHANISMS.DEPENDENT AND INDEPENDENT MECHANISMS.DEPENDENT AND INDEPENDENT MECHANISMS.DEPENDENT AND INDEPENDENT MECHANISMS. H.Funahashi, M. Satake, S. Hasan, E. Angst, H. A. Reber, O. J. Hines,G. Eibl. Department of Surgery, David Geffen School of Medi-cine at UCLA, Los Angeles, CA.CHEMOPREVENTIVE EFFECTS OF OMEGA-3 FATTY AC-CHEMOPREVENTIVE EFFECTS OF OMEGA-3 FATTY AC-CHEMOPREVENTIVE EFFECTS OF OMEGA-3 FATTY AC-CHEMOPREVENTIVE EFFECTS OF OMEGA-3 FATTY AC-CHEMOPREVENTIVE EFFECTS OF OMEGA-3 FATTY AC-IDS IN PANCREATIC CANCER MAY FUNCTION THROUGHIDS IN PANCREATIC CANCER MAY FUNCTION THROUGHIDS IN PANCREATIC CANCER MAY FUNCTION THROUGHIDS IN PANCREATIC CANCER MAY FUNCTION THROUGHIDS IN PANCREATIC CANCER MAY FUNCTION THROUGHCOX-2 AND 5-LOX-INDEPENDENT MECHANISMS.COX-2 AND 5-LOX-INDEPENDENT MECHANISMS.COX-2 AND 5-LOX-INDEPENDENT MECHANISMS.COX-2 AND 5-LOX-INDEPENDENT MECHANISMS.COX-2 AND 5-LOX-INDEPENDENT MECHANISMS. MJStrouch, LG Melstrom, K Adrian, BM Milam, MR Salabat, DJBentrem, PJ Grippo. Department of Surgery, Northwestern Uni-versity, Chicago, IL.HEMOCONCENTRATION ALONE IS AN UNRELIABLE PRE-HEMOCONCENTRATION ALONE IS AN UNRELIABLE PRE-HEMOCONCENTRATION ALONE IS AN UNRELIABLE PRE-HEMOCONCENTRATION ALONE IS AN UNRELIABLE PRE-HEMOCONCENTRATION ALONE IS AN UNRELIABLE PRE-DICTOR OF MORTALITY IN ACUTE PANCREATITIS.DICTOR OF MORTALITY IN ACUTE PANCREATITIS.DICTOR OF MORTALITY IN ACUTE PANCREATITIS.DICTOR OF MORTALITY IN ACUTE PANCREATITIS.DICTOR OF MORTALITY IN ACUTE PANCREATITIS. BUWu, RS Johannes, X Sun, PA Banks. Division of Gastroenterol-ogy, Center for Pancreatic Disease, Brigham and Women’sHospital, Boston, MA, Cardinal Health-MediQual, Marlborough,MA.HEDGEHOG PATHWAY REGULATES G1 TO S TRANSI-HEDGEHOG PATHWAY REGULATES G1 TO S TRANSI-HEDGEHOG PATHWAY REGULATES G1 TO S TRANSI-HEDGEHOG PATHWAY REGULATES G1 TO S TRANSI-HEDGEHOG PATHWAY REGULATES G1 TO S TRANSI-TION BY MODULATING A DEFINED CELL CYCLE TRAN-TION BY MODULATING A DEFINED CELL CYCLE TRAN-TION BY MODULATING A DEFINED CELL CYCLE TRAN-TION BY MODULATING A DEFINED CELL CYCLE TRAN-TION BY MODULATING A DEFINED CELL CYCLE TRAN-SCRIPTIONALSCRIPTIONALSCRIPTIONALSCRIPTIONALSCRIPTIONAL PROGRAM IN PANCREATIC CANCER CELLS. SBangarulingam, JJ Han, J Zhu, C Lokko, ME Fernandez-Zapico.Gastroenterology Research Unit, Mayo Clinic College of Medi-cine, Rochester, MN.










BOARD#BOARD#BOARD#BOARD#BOARD# TITLETITLETITLETITLETITLECORRELATION OF MALIGNANCY AND CEA LEVEL INCORRELATION OF MALIGNANCY AND CEA LEVEL INCORRELATION OF MALIGNANCY AND CEA LEVEL INCORRELATION OF MALIGNANCY AND CEA LEVEL INCORRELATION OF MALIGNANCY AND CEA LEVEL INIPMNIPMNIPMNIPMNIPMN. AN Schore, SA Gross, M Al-Haddad, S Pungpapong, TAWoodward, MB Wallace, M Raimondo. Division of Gastroenterol-ogy & Hepatology, Mayo Clinic College of Medicine, Jackson-ville, FL.CONTROLLED RELEASE OF BASIC FIBROBLAST GROWTHCONTROLLED RELEASE OF BASIC FIBROBLAST GROWTHCONTROLLED RELEASE OF BASIC FIBROBLAST GROWTHCONTROLLED RELEASE OF BASIC FIBROBLAST GROWTHCONTROLLED RELEASE OF BASIC FIBROBLAST GROWTHFACTOR PROMOTES HEALING OF THEFACTOR PROMOTES HEALING OF THEFACTOR PROMOTES HEALING OF THEFACTOR PROMOTES HEALING OF THEFACTOR PROMOTES HEALING OF THEPANCREATICOJEJUNAL ANASTOMOSIS: A NOVEL AP-PANCREATICOJEJUNAL ANASTOMOSIS: A NOVEL AP-PANCREATICOJEJUNAL ANASTOMOSIS: A NOVEL AP-PANCREATICOJEJUNAL ANASTOMOSIS: A NOVEL AP-PANCREATICOJEJUNAL ANASTOMOSIS: A NOVEL AP-PROACH TOWARD ZERO PANCREATIC FISTULA.PROACH TOWARD ZERO PANCREATIC FISTULA.PROACH TOWARD ZERO PANCREATIC FISTULA.PROACH TOWARD ZERO PANCREATIC FISTULA.PROACH TOWARD ZERO PANCREATIC FISTULA. T Aimoto,E Uchida, A Matsushita, Y Tabata, T Takano, M Miyamoto, TTajiri. Department of Surgery, Nippon Medical School, Tokyo,Department of Biomaterials, Institute for Frontier Medical Sci-ences, Kyoto University, Kyoto, Department of Internal Medi-cine, Nippon Medical School, Tokyo.PROBIOTICS REDUCE OXIDATIVE STRESS AND PRO-IN-PROBIOTICS REDUCE OXIDATIVE STRESS AND PRO-IN-PROBIOTICS REDUCE OXIDATIVE STRESS AND PRO-IN-PROBIOTICS REDUCE OXIDATIVE STRESS AND PRO-IN-PROBIOTICS REDUCE OXIDATIVE STRESS AND PRO-IN-FLAMMATORY MARKERS IN LIVER IN THE EARLY PHASEFLAMMATORY MARKERS IN LIVER IN THE EARLY PHASEFLAMMATORY MARKERS IN LIVER IN THE EARLY PHASEFLAMMATORY MARKERS IN LIVER IN THE EARLY PHASEFLAMMATORY MARKERS IN LIVER IN THE EARLY PHASEOF ACUTE PANCREATITIS. OF ACUTE PANCREATITIS. OF ACUTE PANCREATITIS. OF ACUTE PANCREATITIS. OF ACUTE PANCREATITIS. F Lutgendorff, LM Trulsson, LPvan Minnen, GT Rijkers, HM Timmerman, HG Gooszen, JDSöderholm, LMA Akkermans, PA Sandström. Department ofSurgery, University Hospital, Linköping, Sweden, Departmentof Surgery, University Medical Center, Utrecht, The Netherlands.ISLET AMYLOID POLYPEPTIDE PLAYS AISLET AMYLOID POLYPEPTIDE PLAYS AISLET AMYLOID POLYPEPTIDE PLAYS AISLET AMYLOID POLYPEPTIDE PLAYS AISLET AMYLOID POLYPEPTIDE PLAYS APROINFLAMMATORY ROLE IN ACUTE PANCREATITIS BYPROINFLAMMATORY ROLE IN ACUTE PANCREATITIS BYPROINFLAMMATORY ROLE IN ACUTE PANCREATITIS BYPROINFLAMMATORY ROLE IN ACUTE PANCREATITIS BYPROINFLAMMATORY ROLE IN ACUTE PANCREATITIS BYUPREGULATION OF CHEMOKINE GENE EXPRESSION.UPREGULATION OF CHEMOKINE GENE EXPRESSION.UPREGULATION OF CHEMOKINE GENE EXPRESSION.UPREGULATION OF CHEMOKINE GENE EXPRESSION.UPREGULATION OF CHEMOKINE GENE EXPRESSION. R.Segersvärd, J. Tsai, A Capitano, U Arnelo, Division of Surgery,CLINTEC, Dept of Pathology, LabMed, Karolinska Institutet,Karolinska University Hospital Huddinge, Stockholm, Sweden.INVOLVEMENT OF S100A6 (CALCYCLIN) IN PANCREATICINVOLVEMENT OF S100A6 (CALCYCLIN) IN PANCREATICINVOLVEMENT OF S100A6 (CALCYCLIN) IN PANCREATICINVOLVEMENT OF S100A6 (CALCYCLIN) IN PANCREATICINVOLVEMENT OF S100A6 (CALCYCLIN) IN PANCREATICCANCER PROGRESSION. CANCER PROGRESSION. CANCER PROGRESSION. CANCER PROGRESSION. CANCER PROGRESSION. T Nedjadi, R Smith, RE Jenkins, ECostello. Division of Surgery and Oncology, Royal LiverpoolUniversity Hospital, Biomedical Sciences Proteomics Facility,Department of Pharmacology and Therapeutics, University ofLiverpool. Liverpool, United Kingdom.TUMOR SUPPRESSOR PROTEIN, KL11, MODULATES PGE2TUMOR SUPPRESSOR PROTEIN, KL11, MODULATES PGE2TUMOR SUPPRESSOR PROTEIN, KL11, MODULATES PGE2TUMOR SUPPRESSOR PROTEIN, KL11, MODULATES PGE2TUMOR SUPPRESSOR PROTEIN, KL11, MODULATES PGE2SYNTHESIS VIA THE REGULATION OF THE CPLSYNTHESIS VIA THE REGULATION OF THE CPLSYNTHESIS VIA THE REGULATION OF THE CPLSYNTHESIS VIA THE REGULATION OF THE CPLSYNTHESIS VIA THE REGULATION OF THE CPLAÁ..... N Buttar,C DeMars, M Madhavan, V Mokkala, ME Fernandez-Zapico, KWang, L Lutzke, R Urrutia. GI Research Unit, Mayo Clinic Collegeof Medicine, Rochester, MN.

IMMEDIATELY FOLLOWINGIMMEDIATELY FOLLOWINGIMMEDIATELY FOLLOWINGIMMEDIATELY FOLLOWINGIMMEDIATELY FOLLOWINGAPA/LUSTGARTEN SYMPOSIUM, PANCREATIC CANCER 2007:APA/LUSTGARTEN SYMPOSIUM, PANCREATIC CANCER 2007:APA/LUSTGARTEN SYMPOSIUM, PANCREATIC CANCER 2007:APA/LUSTGARTEN SYMPOSIUM, PANCREATIC CANCER 2007:APA/LUSTGARTEN SYMPOSIUM, PANCREATIC CANCER 2007:STEM CELLS IN THE PANCREAS AND PANCREATIC CANCERSTEM CELLS IN THE PANCREAS AND PANCREATIC CANCERSTEM CELLS IN THE PANCREAS AND PANCREATIC CANCERSTEM CELLS IN THE PANCREAS AND PANCREATIC CANCERSTEM CELLS IN THE PANCREAS AND PANCREATIC CANCER










The American Pancreatic Association / Lustgarten Foundation“Pancreatic Cancer 2007: Stem Cells in the Pancreas“Pancreatic Cancer 2007: Stem Cells in the Pancreas“Pancreatic Cancer 2007: Stem Cells in the Pancreas“Pancreatic Cancer 2007: Stem Cells in the Pancreas“Pancreatic Cancer 2007: Stem Cells in the Pancreas

and Pancreatic Cancer”and Pancreatic Cancer”and Pancreatic Cancer”and Pancreatic Cancer”and Pancreatic Cancer”

Friday, November 2, 2007Friday, November 2, 2007Friday, November 2, 2007Friday, November 2, 2007Friday, November 2, 20076:00 PM6:00 PM6:00 PM6:00 PM6:00 PM Max Wicha, MD6:45 PM6:45 PM6:45 PM6:45 PM6:45 PM Diane Simeone, MD7:30 PM 7:30 PM 7:30 PM 7:30 PM 7:30 PM Scott Kern, MD

8:15 PM Reception8:15 PM Reception8:15 PM Reception8:15 PM Reception8:15 PM Reception

Saturday, November 3, 2007Saturday, November 3, 2007Saturday, November 3, 2007Saturday, November 3, 2007Saturday, November 3, 2007Morning Session: Model OrganismsModerators: Sarah Thayer, MD, PhD and Steven Leach, MD8:30 AM8:30 AM8:30 AM8:30 AM8:30 AM James Abbruzzese, MD9:00 AM 9:00 AM 9:00 AM 9:00 AM 9:00 AM Benjamin Ohlstein, MD, PhD9:30 AM9:30 AM9:30 AM9:30 AM9:30 AM Steven Leach, MD10:00 AM Break10:00 AM Break10:00 AM Break10:00 AM Break10:00 AM Break10:15 AM10:15 AM10:15 AM10:15 AM10:15 AM Sarah Thayer, MD, PhD10:45 AM10:45 AM10:45 AM10:45 AM10:45 AM Anirban Maitra, MD11:1511:1511:1511:1511:15 AMAMAMAMAM Point/CounterPoint: Stem Cell Theory

12:00 PM Lunch12:00 PM Lunch12:00 PM Lunch12:00 PM Lunch12:00 PM Lunch

Afternoon Session: Stem Cell Lineage MappingModerators: Suriender Batra, PhD and Martin Fernandez-Zapico, MD1:00 PM1:00 PM1:00 PM1:00 PM1:00 PM Brian Lewis, PhD1:25 PM 1:25 PM 1:25 PM 1:25 PM 1:25 PM Stephen Konieczny, PhD1:50 PM1:50 PM1:50 PM1:50 PM1:50 PM Craig Logsdon, PhD2:15 PM2:15 PM2:15 PM2:15 PM2:15 PM Murray Korc, MD2:40 PM Break2:40 PM Break2:40 PM Break2:40 PM Break2:40 PM Break2:55 PM2:55 PM2:55 PM2:55 PM2:55 PM Raul Urrutia, MD3:20 PM 3:20 PM 3:20 PM 3:20 PM 3:20 PM Young Investigator Talks

Jennifer LaFemina, MDJodi PeatOliver Strobel, MD

4:00 PM4:00 PM4:00 PM4:00 PM4:00 PM Closing Statements/Evaluation

Please see separate program for specific details

at northwestern memorial hospital convention center 251 ......pancreatitis i mecklenburg conference...

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