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Journal Article
by Bailey, Peter and Chang, David K and Nones, Katia and Johns, Amber L and Patch, Ann-Marie and Gingras, Marie-Claude and Miller, David K and Christ, Angelika N and Bruxner, Tim J. C and Quinn, Michael C and Nourse, Craig and Murtaugh, L. Charles and Harliwong, Ivon and Idrisoglu, Senel and Manning, Suzanne and Nourbakhsh, Ehsan and Wani, Shivangi and Fink, Lynn and Holmes, Oliver and Chin, Venessa and Anderson, Matthew J and Kazakoff, Stephen and Leonard, Conrad and Newell, Felicity and Waddell, Nick and Wood, Scott and Xu, Qinying and Wilson, Peter J and Cloonan, Nicole and Kassahn, Karin S and Taylor, Darrin and Quek, Kelly and Robertson, Alan and Pantano, Lorena and Mincarelli, Laura and Sanchez, Luis N and Evers, Lisa and Wu, Jianmin and Pinese, Mark and Cowley, Mark J and Jones, Marc D and Colvin, Emily K and Nagrial, Adnan M and Humphrey, Emily S and Chantrill, Lorraine A and Mawson, Amanda and Humphris, Jeremy and Chou, Angela and Pajic, Marina and Scarlett, Christopher J and Pinho, Andreia V and Giry-Laterriere, Marc and Rooman, Ilse and Samra, Jaswinder S and Kench, James G and Lovell, Jessica A and Merrett, Neil D and Toon, Christopher W and Epari, Krishna and Nguyen, Nam Q and Barbour, Andrew and Zeps, Nikolajs and Moran-Jones, Kim and Jamieson, Nigel B and Graham, Janet S and Duthie, Fraser and Oien, Karin and Hair, Jane and Grützmann, Robert and Maitra, Anirban and Iacobuzio-Donahue, Christine A and Wolfgang, Christopher L and Morgan, Richard A and Lawlor, Rita T and Corbo, Vincenzo and Bassi, Claudio and Rusev, Borislav and Capelli, Paola and Salvia, Roberto and Tortora, Giampaolo and Mukhopadhyay, Debabrata and Petersen, Gloria M and Munzy, Donna M and Fisher, William E and Karim, Saadia A and Eshleman, James R and Hruban, Ralph H and Pilarsky, Christian and Morton, Jennifer P and Sansom, Owen J and Scarpa, Aldo and Musgrove, Elizabeth A and Bailey, Ulla-Maja Hagbo and Hofmann, Oliver and Sutherland, Robert L and Wheeler, David A and Gill, Anthony J and Gibbs, Richard A and Pearson, John V and Waddell, Nicola and ... and Australian Pancreatic Canc Genome and Australian Pancreatic Cancer Genome Initiative
Nature, ISSN 0028-0836, 03/2016, Volume 531, Issue 7592, pp. 47 - 52
Integrated genomic analysis of 456 pancreatic ductal adenocarcinomas identified 32 recurrently mutated genes that aggregate into 10 pathways: KRAS, TGF-beta,... 
PATHWAYS | METASTASIS | DUCTAL ADENOCARCINOMA | PACKAGE | MULTIDISCIPLINARY SCIENCES | TUMOR | MUTATIONS | DIFFERENTIATION | Pancreatic Neoplasms - metabolism | Prognosis | Hepatocyte Nuclear Factor 3-beta - genetics | Genomics | Humans | Carcinoma, Pancreatic Ductal - metabolism | Gene Expression Regulation, Neoplastic | Transcriptome | Hepatocyte Nuclear Factor 3-gamma - genetics | Gene Regulatory Networks | Histone Demethylases - genetics | Tumor Suppressor Protein p53 - genetics | Carcinoma, Pancreatic Ductal - genetics | DNA Methylation | Tumor Suppressor Proteins - genetics | Carcinoma, Pancreatic Ductal - classification | Trans-Activators - genetics | Pancreatic Neoplasms - classification | Transcription, Genetic | Nuclear Proteins - genetics | Carcinoma, Pancreatic Ductal - immunology | Genes, Neoplasm - genetics | Basic Helix-Loop-Helix Transcription Factors - genetics | Pancreatic Neoplasms - pathology | Pancreatic Neoplasms - genetics | Receptors, Cytoplasmic and Nuclear - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Mutation - genetics | Carcinoma, Pancreatic Ductal - pathology | Genome, Human - genetics | Homeodomain Proteins - genetics | Animals | Pancreatic Neoplasms - immunology | Survival Analysis | Cell Line, Tumor | Mice | Physiological aspects | Pancreatic cancer | Methods | Genes | Genomes | Mutation | Gene expression | Tumors
Journal Article
Gut, ISSN 0017-5749, 06/2018, Volume 67, Issue 6, pp. 1112 - 1123
Journal Article
Cancer Cell, ISSN 1535-6108, 06/2012, Volume 21, Issue 6, pp. 822 - 835
Cancer-associated inflammation is thought to be a barrier to immune surveillance, particularly in pancreatic ductal adenocarcinoma (PDA). Gr-1 CD11b cells are... 
OVEREXPRESSION | MICROENVIRONMENT | ONCOLOGY | DUCTAL ADENOCARCINOMA | INTERLEUKIN-1-BETA | MICE | SUPPRESSOR-CELLS | INDUCTION | DIFFERENTIATION | MAMMARY CARCINOMAS | MOUSE MODELS | CELL BIOLOGY | Immunohistochemistry | Adenocarcinoma - pathology | CD8-Positive T-Lymphocytes - pathology | Pancreatic Neoplasms - metabolism | Granulocyte-Macrophage Colony-Stimulating Factor - metabolism | Humans | Carcinoma, Pancreatic Ductal - metabolism | Inflammation - metabolism | Adenocarcinoma - metabolism | RNA Interference | T-Lymphocytes - metabolism | Myeloid Cells - immunology | CD8-Positive T-Lymphocytes - metabolism | T-Lymphocytes - pathology | Carcinoma, Pancreatic Ductal - immunology | CD11b Antigen - immunology | Adenocarcinoma - immunology | Pancreatic Neoplasms - pathology | Receptors, Chemokine - metabolism | Mice, Transgenic | Inflammation - immunology | Receptors, Chemokine - immunology | Carcinoma, Pancreatic Ductal - pathology | Granulocyte-Macrophage Colony-Stimulating Factor - genetics | Mice, Knockout | Tumor Microenvironment - immunology | Models, Immunological | Animals | Granulocyte-Macrophage Colony-Stimulating Factor - immunology | Pancreatic Neoplasms - immunology | Cell Line, Tumor | Myeloid Cells - metabolism | T-Lymphocytes - immunology | Mice | CD11b Antigen - metabolism | Myeloid Cells - pathology | CD8-Positive T-Lymphocytes - immunology | Medical colleges | Analysis | Pancreatic cancer | Oncology, Experimental | Genetically modified organisms | Inflammation | Macrophage colony stimulating factor | Research | T cells | Tumors | Cancer | granulocyte-macrophage colony stimulating factor | myeloid cells | T lymphocyte | carcinoma | pancreas
Journal Article
Immunity, ISSN 1074-7613, 08/2017, Volume 47, Issue 2, pp. 323 - 338.e6
Journal Article
Cancer Discovery, ISSN 2159-8274, 08/2016, Volume 6, Issue 8, pp. 870 - 885
Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease with a low 5-year survival rate, yet new immunotherapeutic modalities may offer hope for this... 
CELLS | ACTIVATION | PI3K | ONCOLOGY | MICE | INHIBITOR | CANCER | TUMOR INFLAMMATION | GEMCITABINE | DISCOVERY | CHECKPOINT BLOCKADE | Macrophage Activation - genetics | Pancreatic Neoplasms - metabolism | Class Ib Phosphatidylinositol 3-Kinase - genetics | Humans | Carcinoma, Pancreatic Ductal - metabolism | Male | Platelet-Derived Growth Factor - genetics | Cell Movement - genetics | Carcinoma, Pancreatic Ductal - genetics | Neoplasm Metastasis | Heterografts | Class Ib Phosphatidylinositol 3-Kinase - metabolism | Antineoplastic Agents - pharmacology | Carcinoma, Pancreatic Ductal - immunology | Macrophages - immunology | Disease Models, Animal | Phenols - pharmacology | Gene Expression | Pteridines - pharmacology | Immunomodulation | Macrophage Activation - immunology | Mortality | Pancreatic Neoplasms - pathology | Mice, Transgenic | Pancreatic Neoplasms - genetics | Gene Knockout Techniques | Carcinoma, Pancreatic Ductal - pathology | Disease Progression | Mice, Knockout | Xenograft Model Antitumor Assays | Macrophages - metabolism | Platelet-Derived Growth Factor - metabolism | Animals | Pancreatic Neoplasms - immunology | Biomarkers | Cell Line, Tumor | Mice | Class Ib Phosphatidylinositol 3-Kinase - antagonists & inhibitors | macrophages | transcription | desmoplasia | metastasis | PDGF | Arginase | gemcitabine | PI3Kγ | immune suppression | chemotherapy | pancreatic ductal adenocarcinoma
Journal Article
Cancer Research, ISSN 0008-5472, 07/2014, Volume 74, Issue 18, pp. 5057 - 5069
Cancer immunotherapy generally offers limited clinical benefit without coordinated strategies to mitigate the immunosuppressive nature of the tumor... 
ACTIVATION | INHIBITION | MICROENVIRONMENT | ONCOLOGY | ADENOCARCINOMA | INFLAMMATION | KINASE | CSF | POLARIZATION | IPILIMUMAB | PROGRESSION | Receptor, Macrophage Colony-Stimulating Factor - antagonists & inhibitors | Immunotherapy - methods | Receptor, Macrophage Colony-Stimulating Factor - immunology | Adenocarcinoma - pathology | Macrophage Colony-Stimulating Factor - biosynthesis | Mannose-Binding Lectins - biosynthesis | Tissue Array Analysis | Humans | Lectins, C-Type - immunology | Tumor Microenvironment | Deoxycytidine - pharmacology | Lectins, C-Type - biosynthesis | Female | Receptors, Cell Surface - biosynthesis | Carcinoma, Pancreatic Ductal - immunology | Macrophages - immunology | Signal Transduction | Macrophage Colony-Stimulating Factor - antagonists & inhibitors | Adenocarcinoma - immunology | Mice, Inbred C57BL | Pancreatic Neoplasms - pathology | Carcinoma, Pancreatic Ductal - therapy | Random Allocation | Carcinoma, Pancreatic Ductal - pathology | Receptors, Cell Surface - immunology | Macrophage Colony-Stimulating Factor - immunology | Animals | Mannose-Binding Lectins - immunology | Pancreatic Neoplasms - immunology | T-Lymphocytes - immunology | Mice | Deoxycytidine - analogs & derivatives | Cohort Studies | Pancreatic Neoplasms - therapy | macrophage | chemoresistance | pancreatic cancer | cytokines | innate immunity | immune checkpoint
Journal Article
Journal Article