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1. Full Text Pancreatic cancer–associated stroma production
by Korc, Murray, M.D
American Journal of Surgery, The, ISSN 0002-9610, 2007, Volume 194, Issue 4, pp. S84 - S86
Abstract One of the defining features of pancreatic ductal adenocarcinoma (PDAC) is the presence of extensive desmoplasia. The desmoplastic stroma consists of... 
Surgery | Stroma | Heparan sulfate proteoglycans | Tumor microenvironment | Targeted therapy | Growth factors | Pancreatic cancer | SURGERY | targeted therapy | KAPPA-B ACTIVATION | METASTASIS | growth factors | CARCINOMA CELLS | DUCTAL ADENOCARCINOMA | stroma | PROLIFERATION | TUMORIGENICITY | COOPERATE | pancreatic cancer | TISSUE GROWTH-FACTOR | GENE-EXPRESSION | tumor microenvironment | heparan sulfate proteoglycans | TUMOR-GROWTH | Gene Expression | Adenocarcinoma - pathology | Cell Proliferation | Immediate-Early Proteins - physiology | Neoplasm Invasiveness | Stromal Cells - pathology | Humans | Pancreatic Neoplasms - pathology | Pancreatic Neoplasms - genetics | Disease Progression | Intercellular Signaling Peptides and Proteins - physiology | Animals | Adenocarcinoma - physiopathology | Adenocarcinoma - genetics | Pancreatic Neoplasms - physiopathology | Vascular Endothelial Growth Factor A - physiology | Connective Tissue Growth Factor | Genes, ras - genetics | Heparan sulfate | Angiogenesis | Cell growth | Rodents | Cyclin-dependent kinases | Mortality | Insulin-like growth factors | Mutation | Pancreas | Kinases | Gene expression
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2. Full Text Pancreatic Cancer–Associated Diabetes Is an “Exosomopathy”
by Korc, Murray
Clinical cancer research : an official journal of the American Association for Cancer Research, ISSN 1078-0432, 4/2015, Volume 21, Issue 7, pp. 1508 - 1510
Diabetes may be a consequence of pancreatic cancer, preceding cancer diagnosis. The underlying mechanism is the release exosomes delivering adrenomedullin to... 
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3. Full Text Pancreatic cancer-associated diabetes is an "exosomopathy"
by Korc, Murray
Clinical Cancer Research, ISSN 1078-0432, 04/2015, Volume 21, Issue 7, pp. 1508 - 1510
Diabetes may be a consequence of pancreatic cancer, preceding cancer diagnosis. The underlying mechanism is the release of exosomes delivering adrenomedullin... 
PLASMA | MELLITUS | ONCOLOGY | BURDEN | ADRENOMEDULLIN | Exosomes - metabolism | Diabetes Mellitus - etiology | Insulin-Secreting Cells - metabolism | Adrenomedullin - metabolism | Pancreatic Neoplasms - complications | Humans
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4. Full Text Pathogenesis of Pancreatic Cancer-Related Diabetes Mellitus: Quo Vadis?
by Korc, Murray
Pancreas, ISSN 0885-3177, 05/2019, Volume 48, Issue 5, pp. 594 - 597
DIAGNOSIS | DUCTAL ADENOCARCINOMA | INFLAMMATION | LINKS | COHORT | TIME | PREVALENCE | TYPE-1 | GASTROENTEROLOGY & HEPATOLOGY
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5. Full Text RelA: A tale of a stitch in time
by Korc, Murray
Journal of Clinical Investigation, ISSN 0021-9738, 08/2016, Volume 126, Issue 8, pp. 2799 - 2801
Pancreatic ductal adenocarcinoma (PDAC) is a deadly cancer in which NF-kappa B pathways promote biological aggressiveness. In this issue of the JCI, Lesina et... 
UNITED-STATES | MEDICINE, RESEARCH & EXPERIMENTAL | PANCREATIC DUCTAL ADENOCARCINOMA | SENESCENCE | CANCER | Animals | Carcinoma in Situ - genetics | NF-kappa B - genetics | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Pancreatic Neoplasms - genetics | Mice | Genes, ras | Carcinoma, Pancreatic Ductal - genetics | Care and treatment | Transcription factors | Pancreatic cancer | Development and progression | Genetic aspects | Gene expression | Health aspects | Proteins | Cell growth | Senescence | Cytokines | Cell cycle | Mutation | Kinases | Cancer therapies | Growth factors
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6. Full Text P38 MAPK in pancreatic cancer: Finding a protective needle in the haystack
by Korc, Murray
Clinical Cancer Research, ISSN 1078-0432, 12/2014, Volume 20, Issue 23, pp. 5866 - 5868
Activated p38 MAPK alpha (pp38 alpha) is a good prognostic marker in pancreatic ductal adenocarcinoma that could be used to personalize therapy. pp38 alpha... 
PATHWAYS | ONCOLOGY | JNK | Animals | Pancreatic Neoplasms - metabolism | Humans | Pancreatic Neoplasms - pathology | JNK Mitogen-Activated Protein Kinases - metabolism | Male | p38 Mitogen-Activated Protein Kinases - metabolism
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7. Full Text Pancreatic Cancer Stroma: Friend or Foe?
by Gore, Jesse and Korc, Murray
Cancer Cell, ISSN 1535-6108, 06/2014, Volume 25, Issue 6, pp. 711 - 712
Pancreatic cancer desmoplasia is thought to confer biological aggressiveness. In this issue of , Özdemir and colleagues and Rhim and colleagues demonstrate... 
ONCOLOGY | DUCTAL ADENOCARCINOMA | CELL BIOLOGY | Animals | Stromal Cells - pathology | Carcinoma, Pancreatic Ductal - pathology | Humans | Pancreatic Neoplasms - pathology | Pancreatic cancer
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8. Full Text Pancreatic Cancer: Stroma and its Current and Emerging Targeted Therapies
by Kota, Janaiah and Hancock, Julie and Kwon, Jason and Korc, Murray
Cancer Letters, ISSN 0304-3835, 2017, Volume 391, pp. 38 - 49
Abstract Pancreatic Ductal Adenocarcinoma (PDAC) is one of the most lethal human malignancies with a 5-year survival rate of 8%. Dense, fibrotic stroma... 
Hematology, Oncology and Palliative Medicine | Targeted therapies | Stroma | Pancreatic Cancer | Tumor microenvironment | miRNAS | TUMOR-STROMA | DUCTAL ADENOCARCINOMA | NAB-PACLITAXEL | STELLATE CELLS | PHASE-III TRIAL | TISSUE GROWTH-FACTOR | ONCOLOGY | THERAPEUTIC TARGET | PACLITAXEL PLUS GEMCITABINE | HEDGEHOG PATHWAY INHIBITOR | PULMONARY-FIBROSIS | Adenocarcinoma - pathology | Adenocarcinoma - therapy | Stromal Cells - pathology | Humans | Tumor Microenvironment | MicroRNAs - metabolism | Carcinoma, Pancreatic Ductal - therapy | Carcinoma, Pancreatic Ductal - pathology | Drugs | Medical colleges | Ablation (Surgery) | Drug delivery systems | Pancreatic cancer | Development and progression | Molecular biology | Vehicles | Medical research | Cytokines | Metastasis | Grants | Cancer therapies | Proteins | Chemotherapy | Surgery | Medical prognosis | Fibroblasts | Hypoxia | Extracellular matrix | Growth factors | Tumors | Index Medicus
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9. Full Text Designer hydrogels: Shedding light on the physical chemistry of the pancreatic cancer microenvironment
by Lin, Chien-Chi and Korc, Murray
Cancer Letters, ISSN 0304-3835, 11/2018, Volume 436, pp. 22 - 27
Pancreatic ductal adenocarcinoma (PDAC) is currently the third leading cause of cancer mortality in the United States, with a 5-year survival of ∼8%. PDAC is... 
Epithelial-mesenchymal transition | 3D culture | Hydrogels | Tumor microenvironment | Pancreatic ductal adenocarcinoma | TGF-BETA | EFFICACY | NETWORKS | HYPOXIA | INHIBITION | STIFFNESS | ONCOLOGY | GROWTH | STROMA | CARCINOMA | PROGRESSION | Drugs | Fibronectins | Medical colleges | Drug delivery systems | Oncology, Experimental | Mortality | Development and progression | Research | Vehicles | Pancreatic cancer | Collagen | Stem cells | Hyaluronic acid | Cancer | Biomedical engineering | Adenocarcinoma | Cell culture | Physical chemistry | Collagens | Drug delivery | Insulin-like growth factors | Cell interactions | Kinases | Macrophages | Cancer therapies | Fibronectin | Epidermal growth factor | Cell fate | Fibroblasts | Immune system | Cytokines | Stroma | Metabolism | Organic chemistry | Chemotherapy | Acids | Hypoxia | Influence | Ligands | Mutation | hydrogels | epithelial-mesenchymal transition | tumor microenvironment
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10. Full Text Smad4: Gatekeeper gene in head and neck squamous cell carcinoma
by Korc, Murray
Journal of Clinical Investigation, ISSN 0021-9738, 11/2009, Volume 119, Issue 11, pp. 3208 - 3212
Unchecked cell growth is a hallmark of cancer. During oncogenesis, cancerous cells become resistant to the TGF-beta signaling pathway that usually keeps cell... 
INACTIVATION | MEDICINE, RESEARCH & EXPERIMENTAL | OVEREXPRESSION | GROWTH-INHIBITION | CANCER CELLS | ONCOGENIC RAS | ANGIOGENESIS | MICROSATELLITE INSTABILITY | PANCREATIC-CANCER | TGF-BETA RECEPTOR | FANCONI ANEMIA/BRCA PATHWAY | Animals | Smad4 Protein - genetics | Humans | Gene Expression Regulation, Neoplastic | Head and Neck Neoplasms - physiopathology | Mice | Carcinoma, Squamous Cell - physiopathology | Smad4 Protein - metabolism | Transforming Growth Factor beta - metabolism | Genomic Instability - genetics | Inflammation - physiopathology | Squamous cell carcinoma | Physiological aspects | Head and neck cancer | Genetic aspects | Research | Gene expression | Transforming growth factors | Risk factors
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11. Full Text A microRNA signature in circulating exosomes is superior to exosomal glypican-1 levels for diagnosing pancreatic cancer
by Lai, Xianyin and Wang, Mu and McElyea, Samantha Deitz and Sherman, Stuart and House, Michael and Korc, Murray
Cancer Letters, ISSN 0304-3835, 2017, Volume 393, pp. 86 - 93
Abstract Pancreatic ductal adenocarcinoma (PDAC) is a deadly malignancy that often presents clinically at an advanced stage and that may be confused with... 
Hematology, Oncology and Palliative Medicine | Glypican-1 | Exosomes | MicroRNAs | Pancreatic cancer | SURVIVAL | CELLS | SOLID TUMORS | ANGIOGENESIS | DUCTAL ADENOCARCINOMA | PLASMA | ONCOLOGY | REGULATORS | HEPARAN-SULFATE PROTEOGLYCANS | EXPRESSION | EGF RECEPTOR | Exosomes - metabolism | Predictive Value of Tests | Oligonucleotide Array Sequence Analysis | Area Under Curve | Pancreatic Neoplasms - diagnosis | Humans | Pancreatitis, Chronic - diagnosis | Transcriptome | Carcinoma, Pancreatic Ductal - surgery | Case-Control Studies | Glypicans - blood | Carcinoma, Pancreatic Ductal - genetics | Tandem Mass Spectrometry | Pancreatitis, Chronic - blood | Carcinoma, Pancreatic Ductal - diagnosis | Chromatography, Liquid | CA-19-9 Antigen - blood | Pancreatic Neoplasms - blood | Diagnosis, Differential | Reproducibility of Results | Pancreatic Neoplasms - surgery | Gene Expression Profiling - methods | Pancreatic Neoplasms - genetics | Pancreatitis, Chronic - genetics | Biomarkers, Tumor - blood | Carcinoma, Pancreatic Ductal - blood | ROC Curve | Biomarkers, Tumor - genetics | MicroRNAs - blood | MicroRNAs - genetics | Medical colleges | MicroRNA | Diagnosis | Molecular biology | Pancreatitis | Phosphates | Analysis | Albumin | Nitriles | Sulfates | Mass spectrometry | High performance liquid chromatography | Proteins | Angiogenesis | Acids | Peptides | Biomarkers | Chromatography
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12. Full Text 14-3-3σ Modulates Pancreatic Cancer Cell Survival and Invasiveness
by Divas Neupane and Murray Korc
Clinical Cancer Research, ISSN 1078-0432, 12/2008, Volume 14, Issue 23, pp. 7614 - 7623
Purpose: The purpose of the present study was to investigate the potential role of 14-3-3σ in pancreatic ductal adenocarcinoma (PDAC). Experimental Design:... 
apoptosis | pancreatic cancer | 14-3-3σ | invasion | EGF
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13. Full Text Driver mutations
: A roadmap for getting close and personal in pancreatic cancer
by Korc, Murray
Cancer Biology & Therapy, ISSN 1538-4047, 09/2010, Volume 10, Issue 6, pp. 588 - 591
Commentary to: Prioritization of driver mutations in pancreatic cancer using cancer-specific high-throughput annotation of somatic mutations (CHASM) Hannah... 
Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | Nek8 | Sonic hedgehog | Driver mutations | PI3K | Pancreatic cancer | Stroma | Kras | Cilia | CHOLECYSTOKININ | CELLS | RNA | DUCTAL ADENOCARCINOMA | stroma | KINASE | PHOSPHOINOSITIDE 3-KINASE | driver mutations | COOPERATE | pancreatic cancer | ONCOLOGY | BIOLOGY | cilia | AURORA | Genetic Predisposition to Disease - genetics | Humans | Pancreatic Neoplasms - genetics | Models, Genetic | Signal Transduction - genetics | Mutation | DNA Mutational Analysis - methods
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14. Full Text Cdk4/6 inhibition induces epithelial-mesenchymal transition and enhances invasiveness in pancreatic cancer cells
by Liu, Fang and Korc, Murray
Molecular Cancer Therapeutics, ISSN 1535-7163, 10/2012, Volume 11, Issue 10, pp. 2138 - 2148
Aberrant activation of Cyclin D-Cdk4/6 signaling pathway is commonly found in pancreatic ductal adenocarcinoma (PDAC). Here, we show that PD-0332991, a highly... 
SIGNAL | TGF-BETA | METASTASIS | LAMININ GAMMA-2 | ONCOLOGY | PHOSPHORYLATION | KINASE 4/6 | SUPPRESSION | TUMOR-GROWTH | PD 0332991 | EXPRESSION | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Transcription, Genetic - drug effects | Humans | Epithelial-Mesenchymal Transition - drug effects | Epithelial-Mesenchymal Transition - genetics | Gene Knockdown Techniques | Gene Expression Regulation, Neoplastic - drug effects | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Tumor Stem Cell Assay | Piperazines | Neoplasm Invasiveness | Pancreatic Neoplasms - pathology | Pancreatic Neoplasms - enzymology | Pancreatic Neoplasms - genetics | Smad Proteins - genetics | Cyclin-Dependent Kinase 6 - metabolism | Imidazoles - pharmacology | Signal Transduction - genetics | Cyclin-Dependent Kinase 4 - metabolism | Drug Synergism | Neoplasm Metastasis - genetics | Transforming Growth Factor beta - pharmacology | Signal Transduction - drug effects | Cell Line, Tumor | Cell Proliferation - drug effects | Pyridines - pharmacology | Smad Proteins - metabolism | Benzodioxoles - pharmacology | Drug Screening Assays, Antitumor | RNA, Small Interfering - metabolism | PD-0332991 | TGF-β | Cdk4 | EMT | Pancreatic cancer
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15. Full Text Overview of pre-clinical and clinical studies targeting angiogenesis in pancreatic ductal adenocarcinoma
by Craven, Kelly E and Gore, Jesse and Korc, Murray
Cancer Letters, ISSN 0304-3835, 2015, Volume 381, Issue 1, pp. 201 - 210
Highlights • Pancreatic ductal adenocarcinoma (PDAC) is hypovascular. • Vascular endothelial growth factor A (gene: VEGFA) (VEGF-A) is overexpressed in PDAC. •... 
Hematology, Oncology and Palliative Medicine | Angiogenesis | Pancreatic cancer | Vascular endothelial growth factor (VEGF) | PLUS GEMCITABINE | NUDE-MICE | ENDOTHELIAL-GROWTH-FACTOR | DOSE RATE GEMCITABINE | FACTOR RECEPTOR | CANCER | PHASE-II TRIAL | ONCOLOGY | MOUSE MODEL | 1ST-LINE THERAPY | TUMOR-GROWTH | Pancreatic Neoplasms - metabolism | Humans | Pancreatic Neoplasms - blood supply | Pancreatic Neoplasms - pathology | Carcinoma, Pancreatic Ductal - metabolism | Neovascularization, Pathologic | Tumor Microenvironment | Drug Resistance, Neoplasm | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor A - antagonists & inhibitors | Molecular Targeted Therapy | Carcinoma, Pancreatic Ductal - pathology | Pancreatic Neoplasms - drug therapy | Carcinoma, Pancreatic Ductal - drug therapy | Animals | Receptors, Vascular Endothelial Growth Factor - metabolism | Signal Transduction - drug effects | Angiogenic Proteins - antagonists & inhibitors | Angiogenesis Inhibitors - therapeutic use | Receptors, Vascular Endothelial Growth Factor - antagonists & inhibitors | Carcinoma, Pancreatic Ductal - blood supply | Angiogenesis Inhibitors - adverse effects | Angiogenic Proteins - metabolism | Adenocarcinoma | Clinical trials | Medicine, Experimental | Medical research | Vascular endothelial growth factor | Cell division | Metastasis | Kinases | Endothelium | Proteins | Confidence intervals | Chemotherapy | Rodents | Response rates | Physiology | Tumorigenesis | Pancreas | Tumors
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16. Full Text Abstract 2951: DUSP1 is a novel target for enhancing pancreatic cancer cell sensitivity to gemcitabine
by Liu, Fang and Korc, Murray
Cancer Research, ISSN 0008-5472, 04/2013, Volume 73, Issue 8 Supplement, pp. 2951 - 2951
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17. Full Text A method for conducting highly sensitive microRNA in situ hybridization and immunohistochemical analysis in pancreatic cancer
by Sempere, Lorenzo F and Korc, Murray
Methods in molecular biology (Clifton, N.J.), ISSN 1064-3745, 2013, Volume 980, pp. 43 - 59
Profiling experiments in whole tissue biopsies have linked altered expression of microRNAs (miRNAs) to different types of cancer, including pancreatic ductal... 
Immunohistochemistry | Multiplexing | Genetically engineered mouse models | MicroRNA | Pancreatic cancer | Pancreatic adenocarcinoma | In situ hybridization | Locked nucleic acid | Fluorescence microscopy | Immunohistochemistry - methods | Pancreatic Neoplasms - genetics | MicroRNAs - genetics | Pancreatic Neoplasms - metabolism | In Situ Hybridization - methods | Humans
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