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1. Full Text GLI1 is regulated through Smoothened-independent mechanisms in neoplastic pancreatic ducts and mediates PDAC cell survival and transformation
by Nolan-Stevaux, Olivier and Lau, Janet and Truitt, Morgan L and Chu, Gerald C and Hebrok, Matthias and Fernández-Zapico, Martin E and Hanahan, Douglas
Genes and Development, ISSN 0890-9369, 01/2009, Volume 23, Issue 1, pp. 24 - 36
Pancreatic ductal adenocarcinoma (PDAC) is characterized by the deregulation of the hedgehog signaling pathway. The Sonic Hedgehog ligand (Shh), absent in the... 
Hedgehog | Smoothened | PDAC | Gli | Pancreatic cancer | Pancreatic ductal adenocarcinoma | SIGNALING PATHWAYS | HEDGEHOG PATHWAY | ADENOCARCINOMA | MOUSE | PROLIFERATION | DEVELOPMENTAL BIOLOGY | CANCER | CELL BIOLOGY | pancreatic cancer | hedgehog | BIOLOGY | GROWTH | GENETICS & HEREDITY | TUMORIGENESIS | REQUIREMENT | Pancreatic Neoplasms - metabolism | Receptors, G-Protein-Coupled - metabolism | Humans | Carcinoma, Pancreatic Ductal - metabolism | Gene Expression Regulation, Neoplastic | Hedgehog Proteins - metabolism | Pancreatic Ducts - pathology | Pancreatic Ducts - metabolism | Carcinoma, Pancreatic Ductal - genetics | Hedgehog Proteins - genetics | Kruppel-Like Transcription Factors - metabolism | Smoothened Receptor | Proto-Oncogene Proteins p21(ras) - metabolism | Cell Line | Signal Transduction | Cell Survival | Pancreatic Neoplasms - pathology | Cells, Cultured | Pancreatic Neoplasms - genetics | Carcinoma, Pancreatic Ductal - pathology | Cell Transformation, Neoplastic - metabolism | Animals | Mice | Receptors, G-Protein-Coupled - genetics | Zinc Finger Protein GLI1 | Kruppel-Like Transcription Factors - genetics | Transforming Growth Factor beta - metabolism | Index Medicus | Research Paper
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2. Full Text Adult Duct-Lining Cells Can Reprogram into β-like Cells Able to Counter Repeated Cycles of Toxin-Induced Diabetes
by Al-Hasani, Keith and Pfeifer, Anja and Courtney, Monica and Ben-Othman, Nouha and Gjernes, Elisabet and Vieira, Andhira and Druelle, Noémie and Avolio, Fabio and Ravassard, Philippe and Leuckx, Gunter and Lacas-Gervais, Sandra and Ambrosetti, Damien and Benizri, Emmanuel and Hecksher-Sorensen, Jacob and Gounon, Pierre and Ferrer, Jorge and Gradwohl, Gerard and Heimberg, Harry and Mansouri, Ahmed and Collombat, Patrick
Developmental Cell, ISSN 1534-5807, 07/2013, Volume 26, Issue 1, pp. 86 - 100
It was recently demonstrated that embryonic glucagon-producing cells in the pancreas can regenerate and convert into insulin-producing β-like cells through the... 
PROGENITOR CELLS | ENDOCRINE PANCREAS | GENE | MOUSE PANCREAS | ARX | ECTOPIC EXPRESSION | PAX4 | MICE | DEVELOPMENTAL BIOLOGY | ALPHA-CELL | LINEAGES | CELL BIOLOGY | Paired Box Transcription Factors - genetics | Streptozocin | Homeodomain Proteins - metabolism | Pancreatic Ducts - drug effects | Diabetes Mellitus, Experimental - genetics | Pancreatic Ducts - pathology | Hypertrophy - pathology | Hypertrophy - metabolism | Pancreatic Ducts - metabolism | Cellular Reprogramming | Insulin-Secreting Cells - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Glucagon-Secreting Cells - metabolism | Epithelial-Mesenchymal Transition | Cell Differentiation | Diabetes Mellitus, Experimental - metabolism | Basic Helix-Loop-Helix Transcription Factors - genetics | Blood Glucose - analysis | Glucagon-Secreting Cells - pathology | Gene Expression Regulation | Nerve Tissue Proteins - genetics | Homeodomain Proteins - genetics | Nerve Tissue Proteins - metabolism | Cell Lineage | Animals | Mice | Insulin-Secreting Cells - pathology | Paired Box Transcription Factors - metabolism | Cell Movement | Life Sciences | Development Biology
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3. Full Text Oncogenic Kras-Induced GM-CSF Production Promotes the Development of Pancreatic Neoplasia
by Pylayeva-Gupta, Yuliya and Lee, Kyoung Eun and Hajdu, Cristina H and Miller, George and Bar-Sagi, Dafna
Cancer Cell, ISSN 1535-6108, 06/2012, Volume 21, Issue 6, pp. 836 - 847
Stromal responses elicited by early stage neoplastic lesions can promote tumor growth. However, the molecular mechanisms that underlie the early recruitment of... 
COLONY-STIMULATING FACTORS | T-CELL RESPONSES | TUMOR PROGRESSION | P21 RAS | ONCOLOGY | DUCTAL ADENOCARCINOMA | INFLAMMATION | MOUSE | MICE | SUPPRESSOR-CELLS | CANCER | CELL BIOLOGY | Immunohistochemistry | Adenocarcinoma - pathology | Epithelial Cells - metabolism | Pancreatic Neoplasms - metabolism | Granulocyte-Macrophage Colony-Stimulating Factor - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Carcinoma, Pancreatic Ductal - metabolism | Immunoblotting | Green Fluorescent Proteins - genetics | Pancreatic Ducts - metabolism | Carcinoma, Pancreatic Ductal - genetics | Adenocarcinoma - metabolism | RNA Interference | HEK293 Cells | CD8-Positive T-Lymphocytes - metabolism | Adenocarcinoma - genetics | Proto-Oncogene Proteins p21(ras) - metabolism | Green Fluorescent Proteins - metabolism | Pancreatic Ducts - cytology | Mice, Inbred C57BL | Pancreatic Neoplasms - pathology | Receptors, Chemokine - metabolism | Cells, Cultured | Mice, Transgenic | Pancreatic Neoplasms - genetics | Carcinoma, Pancreatic Ductal - pathology | Granulocyte-Macrophage Colony-Stimulating Factor - genetics | Animals | Cell Transformation, Neoplastic | Myeloid Cells - metabolism | Mice | CD11b Antigen - metabolism | Microscopy, Fluorescence | T cells | Tumors | granulocyte-macrophage colony stimulating factor | immunosuppression | Kras | cancer | inflammation | pancreas
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4. Full Text Lineage Tracing Evidence for Transdifferentiation of Acinar to Duct Cells and Plasticity of Human Pancreas
by Houbracken, Isabelle and de Waele, Evelien and Lardon, Jessy and Ling, Zhidong and Heimberg, Harry and Rooman, Ilse and Bouwens, Luc
Gastroenterology, ISSN 0016-5085, 2011, Volume 141, Issue 2, pp. 731 - 741.e4
Background & Aims Animal studies have indicated that pancreatic exocrine acinar cells have phenotypic plasticity. In rodents, acinar cells can differentiate... 
Gastroenterology and Hepatology | Metaplasia | Reprogramming | Exocrine Pancreas | Tissue Engineering | BETA-CELLS | INTRAEPITHELIAL NEOPLASIA | HUMAN EXOCRINE PANCREAS | ADULT HUMAN PANCREAS | IN-VITRO | NOTCH SIGNALING PATHWAY | GENERATION | MICE | GROWTH-FACTOR | DIFFERENTIATION | GASTROENTEROLOGY & HEPATOLOGY | Cell Proliferation | Chymotrypsin - metabolism | Humans | Glycoproteins - metabolism | Carbonic Anhydrase II - metabolism | Ki-67 Antigen - metabolism | Cell Transdifferentiation - genetics | RNA, Messenger - metabolism | Pancreatic Ducts - metabolism | Antigens, CD - metabolism | Cell Transdifferentiation - physiology | Peptides - metabolism | Pancreas, Exocrine - cytology | Cell Lineage - genetics | Genes, Reporter | Hepatocyte Nuclear Factor 1-beta - metabolism | Plant Lectins - pharmacokinetics | Biomarkers - metabolism | SOX9 Transcription Factor - metabolism | Green Fluorescent Proteins - metabolism | Promoter Regions, Genetic | Pancreatic Ducts - cytology | Transduction, Genetic | Cell Survival | Cells, Cultured | Cystic Fibrosis Transmembrane Conductance Regulator - metabolism | Signal Transduction - genetics | AC133 Antigen | Cell Lineage - physiology | Phenotype | Signal Transduction - physiology | Pancreas, Exocrine - metabolism | Keratin-19 - metabolism | Mitogen-Activated Protein Kinases - metabolism | Keratin | Epidermal growth factor | Analysis | Fluorescein | Fluorescence | Cystic fibrosis | Diabetes | Universities and colleges | Research | Protein kinases
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5. Full Text Sox9+ ductal cells are multipotent progenitors throughout development but do not produce new endocrine cells in the normal or injured adult pancreas
by Kopp, Janel L and Dubois, Claire L and Schaffer, Ashleigh E and Hao, Ergeng and Shih, Hung Ping and Seymour, Philip A and Ma, Jenny and Sander, Maike
Development, ISSN 0950-1991, 02/2011, Volume 138, Issue 4, pp. 653 - 665
One major unresolved question in the field of pancreas biology is whether ductal cells have the ability to generate insulin-producing beta-cells. Conclusive... 
Regeneration | Mouse | Sox9 | Multipotent progenitor | Neogenesis | Pancreas | Partial duct ligation | MOUSE PANCREAS | BETA-CELLS | RATS | DEVELOPMENTAL BIOLOGY | GROWTH | DIFFERENTIATION | PRECURSORS | EXPRESSION | GLUCOSE-TOLERANCE | SOX9 Transcription Factor - metabolism | Pancreatic Ducts - cytology | Multipotent Stem Cells - metabolism | Pancreatic Ducts - embryology | Mice, Transgenic | Pancreas - metabolism | Pancreas - injuries | Pancreas - embryology | Pancreatic Ducts - metabolism | Endocrine Cells - metabolism | Animals | Endocrine Cells - cytology | Gene Expression Regulation, Developmental | Multipotent Stem Cells - cytology | Aging | Cell Differentiation | Mice | Pancreas - growth & development | SOX9 Transcription Factor - genetics | Development and Stem Cells
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6. Full Text Pancreatic duct cells as a source of VEGF in mice
by Xiao, Xiangwei and Prasadan, Krishna and Guo, Ping and El-Gohary, Yousef and Fischbach, Shane and Wiersch, John and Gaffar, Iljana and Shiota, Chiyo and Gittes, George K
Diabetologia, ISSN 0012-186X, 5/2014, Volume 57, Issue 5, pp. 991 - 1000
Vascular endothelial growth factor (VEGF) is essential for proper pancreatic development, islet vascularisation and insulin secretion. In the adult pancreas,... 
Duct cell | Medicine & Public Health | Human Physiology | shRNA | Laser-capture microdissection | Metabolic Diseases | Beta cell | Islet transplantation | Internal Medicine | Intrapancreatic ductal infusion | FACS | Vascular endothelial growth factor | FACTOR-A | ISLETS | ANGIOGENESIS | INDUCTION | ductal infusion | VASCULARIZATION | ENDOCRINOLOGY & METABOLISM | ADULT PANCREAS | BLOOD-VESSELS | BETA-CELL | Intrapancreatic | DIFFERENTIATION | ENDOTHELIAL GROWTH-FACTOR | Human Umbilical Vein Endothelial Cells | Humans | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor A - genetics | Pancreatic Ducts - metabolism | Gene Knockdown Techniques | Insulin-Secreting Cells - metabolism | Animals | Islets of Langerhans - cytology | Islets of Langerhans Transplantation | Mice | Epithelial Cells - cytology | SOX9 Transcription Factor - genetics | Neovascularization, Physiologic | RNA, Small Interfering - metabolism | Physiological aspects | RNA | Endothelial growth factors | Analysis
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7. Full Text IRBIT coordinates epithelial fluid and HCO3- secretion by stimulating the transporters pNBC1 and CFTR in the murine pancreatic duct
by Yang, Dongki and Shcheynikov, Nikolay and Zeng, Weizhong and Ohana, Ehud and So, Insuk and Ando, Hideaki and Mizutani, Akihiro and Mikoshiba, Katsuhiko and Muallem, Shmuel
Journal of Clinical Investigation, ISSN 0021-9738, 01/2009, Volume 119, Issue 1, pp. 193 - 202
Fluid and HCO3- secretion are vital functions of secretory epithelia. In most epithelia, this entails HCO3- entry at the basolateral membrane, mediated by the... 
Cell Line | RNA, Small Interfering - genetics | Pancreatic Ducts - cytology | Epithelium - metabolism | Humans | Sodium-Bicarbonate Symporters - genetics | Adenosylhomocysteinase - metabolism | Antiporters - metabolism | Cystic Fibrosis Transmembrane Conductance Regulator - metabolism | Pancreatic Ducts - metabolism | Sodium-Bicarbonate Symporters - metabolism | Mice, Knockout | Extracellular Fluid - metabolism | Patch-Clamp Techniques | Animals | Adenosylhomocysteinase - genetics | Antiporters - genetics | Bicarbonates - metabolism | Cystic Fibrosis Transmembrane Conductance Regulator - genetics | Female | Mice | RNA, Small Interfering - metabolism
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8. Full Text Activation of pancreatic-duct-derived progenitor cells during pancreas regeneration in adult rats
by Li, Wan-Chun and Rukstalis, J. Michael and Nishimura, Wataru and Tchipashvili, Vaja and Habener, Joel F and Sharma, Arun and Bonner-Weir, Susan
Journal of Cell Science, ISSN 0021-9533, 08/2010, Volume 123, Issue 16, pp. 2792 - 2802
The adult pancreas has considerable capacity to regenerate in response to injury. We hypothesized that after partial pancreatectomy (Px) in adult rats,... 
Regeneration | Pancreatic progenitors | Dedifferentiation | BETA-CELLS | ISLET NEOGENESIS | TUBULAR COMPLEXES | CELL BIOLOGY | EXPRESSION PATTERNS | EPITHELIAL-CELLS | DIFFERENTIATION | NKX 6.1 | TRANSCRIPTION FACTOR | GLUCOSE-TOLERANCE | ENDOCRINE-CELLS | Embryonic Stem Cells - metabolism | Embryonic Stem Cells - cytology | Pancreas - cytology | Transcription Factors - deficiency | Cell Growth Processes - physiology | Male | Pancreatic Ducts - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Islets of Langerhans - metabolism | Islets of Langerhans - cytology | Cell Differentiation - physiology | Pancreatic Ducts - cytology | Islets of Langerhans - physiology | Hepatocyte Nuclear Factor 6 - metabolism | Pancreatectomy | Rats | Pancreas - metabolism | Regeneration - physiology | Rats, Sprague-Dawley | Embryonic Stem Cells - physiology | Nerve Tissue Proteins - metabolism | Transcription Factors - metabolism | Animals | Pancreatic Ducts - physiology | Pancreas - physiology | Hepatocyte Nuclear Factor 6 - deficiency
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9. Full Text Notch and Kras Reprogram Pancreatic Acinar Cells to Ductal Intraepithelial Neoplasia
by Jean-Paul De La O and Lyska L. Emerson and Jessica L. Goodman and Scott C. Froebe and Benjamin E. Illum and Andrew B. Curtis and L. Charles Murtaugh
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2008, Volume 105, Issue 48, pp. 18907 - 18912
Efforts to model pancreatic cancer in mice have focused on mimicking genetic changes found in the human disease, particularly the activating KRAS mutations... 
Acinar cells | Metaplasia | Alleles | Pancreatic cells | Mice | Lesions | Pancreas | Progenitor cells | Pancreatic neoplasms | Tumors | Ras | PanIN | Cancer | metaplasia | REGENERATION | MULTIDISCIPLINARY SCIENCES | MOUSE | PHENOTYPE | INDUCTION | K-RAS ONCOGENE | pancreas | cancer | DIFFERENTIATION | EXPRESSION | LINEAGE | TRANSGENIC MICE | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Pancreatic Neoplasms - metabolism | Receptors, Notch - metabolism | Humans | Carcinoma, Pancreatic Ductal - metabolism | ras Proteins - metabolism | Precancerous Conditions - metabolism | Receptors, Notch - genetics | Pancreatic Ducts - pathology | Pancreatic Ducts - metabolism | Female | Precancerous Conditions - pathology | Transgenes | Proto-Oncogene Proteins - metabolism | Tamoxifen - metabolism | Pancreatic Ducts - cytology | Pancreatic Neoplasms - pathology | Proto-Oncogene Proteins - genetics | Carcinoma, Pancreatic Ductal - pathology | Pregnancy | Estrogen Antagonists - metabolism | Animals | Signal Transduction - physiology | Models | Genetic aspects | Research | Pancreatic cancer | Genotype & phenotype | Rodents | Genetics | Mutation | Cells | Biological Sciences | PanlN
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10. Full Text Plasticity of adult human pancreatic duct cells by neurogenin3-mediated reprogramming
by Swales, Nathalie and Martens, Geert A and Bonné, Stefan and Heremans, Yves and Borup, Rehannah and van de Casteele, Mark and Ling, Zhidong and Pipeleers, Daniel and Ravassard, Philippe and Nielsen, Finn and Ferrer, Jorge and Heimberg, Harry
PLoS ONE, ISSN 1932-6203, 05/2012, Volume 7, Issue 5, p. e37055
Aims/Hypothesis: Duct cells isolated from adult human pancreas can be reprogrammed to express islet beta cell genes by adenoviral transduction of the... 
ISLET DIFFERENTIATION PROGRAM | IN-VITRO | ENDOCRINE PROGENITOR CELLS | BETA-CELLS | GENES | DISTINCT | MOUSE | BIOLOGY | BIRTH | EXPRESSION | REVEALS | Receptors, Notch - metabolism | Homeodomain Proteins - metabolism | Humans | Cell Transdifferentiation - genetics | Gene Expression Profiling | Intracellular Signaling Peptides and Proteins - metabolism | RNA, Messenger - metabolism | Pancreatic Ducts - metabolism | DNA-Binding Proteins - metabolism | Maf Transcription Factors, Large - metabolism | Insulin-Secreting Cells - metabolism | Cell Transdifferentiation - physiology | Basic Helix-Loop-Helix Transcription Factors - metabolism | Maf Transcription Factors, Large - genetics | Trans-Activators - genetics | Adult | Insulin-Secreting Cells - cytology | Membrane Proteins - metabolism | Binding Sites | Recombinant Proteins - metabolism | Promoter Regions, Genetic | Pancreatic Ducts - cytology | Basic Helix-Loop-Helix Transcription Factors - genetics | Transduction, Genetic | Signal Transduction | RNA, Messenger - genetics | Cells, Cultured | Recombinant Proteins - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Nerve Tissue Proteins - genetics | Homeodomain Proteins - genetics | Nerve Tissue Proteins - metabolism | Transcription Factors - metabolism | Animals | Trans-Activators - metabolism | Mice | Pancreatic beta cells | RNA | Genes | Genomics | Genomes | Genetic transcription | DNA binding proteins | Transcription factors | Phosphorylation | Spinal cord | Diabetes mellitus | Nervous system | Tissues | Insulin | Proteins | Beta cells | Signal transduction | Signaling | Rodents | Adenoviruses | Plasticity | Plastic properties | Notch protein | Diabetes | Islets of Langerhans | Pancreas | Localization
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11. Full Text Identification and Manipulation of Biliary Metaplasia in Pancreatic Tumors
by DelGiorno, Kathleen E and Hall, Jason C and Takeuchi, Kenneth K and Pan, Fong Cheng and Halbrook, Christopher J and Washington, M. Kay and Olive, Kenneth P and R. Spence, Jason and Sipos, Bence and Wright, Christopher V.E and Wells, James M and Crawford, Howard C
Gastroenterology, ISSN 0016-5085, 2014, Volume 146, Issue 1, pp. 233 - 244.e5
Background & Aims Metaplasias often have characteristics of developmentally related tissues. Pancreatic metaplastic ducts are usually associated with... 
Gastroenterology and Hepatology | Pancreatic Cancer | Signal Transduction | Pathogenesis | Mouse Model | ADENOCARCINOMA | BRUSH CELLS | EXOCRINE PANCREAS | CANCER | INTESTINAL EPITHELIUM | TO-DUCTAL METAPLASIA | K-RAS | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | EGF RECEPTOR | TRANSGENIC MICE | Pancreatic Neoplasms - metabolism | Metaplasia - metabolism | Bile Ducts - metabolism | Humans | Carcinoma, Pancreatic Ductal - metabolism | Precancerous Conditions - metabolism | Pancreatic Ducts - pathology | SOXF Transcription Factors - metabolism | Pancreatic Ducts - metabolism | Bile Ducts - cytology | Metaplasia - complications | HMGB Proteins - metabolism | Precancerous Conditions - pathology | Proto-Oncogene Proteins p21(ras) - metabolism | Pancreatic Ducts - cytology | Pancreatic Neoplasms - pathology | Mice, Transgenic | Carcinoma, Pancreatic Ductal - complications | Carcinoma, Pancreatic Ductal - pathology | Cell Transformation, Neoplastic - metabolism | Metaplasia - pathology | Animals | Mice | Pancreatitis - metabolism | Cell Transformation, Neoplastic - pathology | Pancreatic Neoplasms - complications | Molecular genetics | Pancreatic cancer | Pancreatitis | pathogenesis | pancreatic cancer | mouse model | signal transduction
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12. Full Text Localization of dipeptidyl peptidase-4 (CD26) to human pancreatic ducts and islet alpha cells
by Augstein, Petra and Naselli, Gaetano and Loudovaris, Thomas and Hawthorne, Wayne J and Campbell, Peter and Bandala-Sanchez, Esther and Rogers, Kelly and Heinke, Peter and Thomas, Helen E and Kay, Thomas W and Harrison, Leonard C
Diabetes Research and Clinical Practice, ISSN 0168-8227, 2015, Volume 110, Issue 3, pp. 291 - 300
Highlights • In the human pancreas, DPP-4 expression is localized to duct and alpha cells. • In donors with type 1 diabetes, the majority of islet cells are... 
Endocrinology & Metabolism | Human pancreas | CD26 | Alpha cell | Islet | Beta cell | Dipeptidyl peptidase-4 | DEAMINASE COMPLEXING PROTEIN | ADENOSINE-DEAMINASE | BETA | FAMILY | GLANDS | ENDOCRINOLOGY & METABOLISM | SECRETION | INHIBITORS | EXPRESSION | SUBUNIT | Immunohistochemistry | Dipeptidyl Peptidase 4 - metabolism | Glucagon-Like Peptide 1 - metabolism | Proinsulin - metabolism | Humans | Middle Aged | Incretins - metabolism | Male | Diabetes Mellitus, Type 2 - metabolism | Pancreatic Ducts - metabolism | Young Adult | Insulin-Secreting Cells - metabolism | Glucagon-Secreting Cells - metabolism | Adult | Female | Glucagon - metabolism | Aged | Type 1 diabetes
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13. Full Text Corticosteroids Correct Aberrant CFTR Localization in the Duct and Regenerate Acinar Cells in Autoimmune Pancreatitis
by Ko, Shigeru B.H and Mizuno, Nobumasa and Yatabe, Yasushi and Yoshikawa, Toshiyuki and Ishiguro, Hiroshi and Yamamoto, Akiko and Azuma, Sakiko and Naruse, Satoru and Yamao, Kenji and Muallem, Shmuel and Goto, Hidemi
Gastroenterology, ISSN 0016-5085, 2010, Volume 138, Issue 5, pp. 1988 - 1996.e3
Background & Aims Corticosteroids are now widely accepted as a treatment for autoimmune pancreatitis (AIP). However, the molecular mechanism by which steroid... 
Gastroenterology and Hepatology | Aquaporin Water Channel | Exocrine Function Test | CFTR | CD133 | ADENOCARCINOMAS | EXOCRINE FUNCTION | TRANSMEMBRANE CONDUCTANCE REGULATOR | DEPENDENT HCO3-TRANSPORT | STEROID-THERAPY | MUTATIONS | DIAGNOSTIC-CRITERIA | GASTROENTEROLOGY & HEPATOLOGY | IDIOPATHIC CHRONIC-PANCREATITIS | EXPRESSION | CYSTIC-FIBROSIS GENE | Humans | Middle Aged | Pancreatic Ducts - drug effects | Glycoproteins - metabolism | Male | Pancreatic Ducts - immunology | Pancreatitis - drug therapy | Adrenal Cortex Hormones - therapeutic use | Pancreas, Exocrine - drug effects | Aquaporin 1 - metabolism | Pancreatic Ducts - metabolism | Antigens, CD - metabolism | Plasma Cells - drug effects | Peptides - metabolism | Time Factors | Pancreatitis - immunology | Adult | Female | Autoimmune Diseases - metabolism | Autoimmune Diseases - drug therapy | Pancreas, Exocrine - immunology | Pancreatic Juice - enzymology | Autoimmune Diseases - immunology | Treatment Outcome | Cystic Fibrosis Transmembrane Conductance Regulator - metabolism | AC133 Antigen | Protein Transport | Regeneration - drug effects | Fibrosis | Bicarbonates - metabolism | Aged | Pancreas, Exocrine - metabolism | Pancreatitis - metabolism | Immunoglobulin G - metabolism | Plasma Cells - immunology | Cell research | Corticosteroids | Aquaporins | Pancreatitis | Cystic fibrosis | Universities and colleges | Histochemistry
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