ONTOLOGY SOURCE REFERENCE
Term Source Name	"EFO"	"NCBITaxon"	"CHEBI"	"PR"	"MI"	"BTO"	
Term Source File	"http://www.ebi.ac.uk/efo/efo.owl"	"http://bioportal.bioontology.org/ontologies/47845"	"http://bioportal.bioontology.org/ontologies/50716"	"http://bioportal.bioontology.org/ontologies/50525"	"http://bioportal.bioontology.org/ontologies/39508"	"http://bioportal.bioontology.org/ontologies/50688"	
Term Source Version	""	"47845"	"50716"	"50525"	"39508"	"50688"	
Term Source Description	""	"National Center for Biotechnology Information (NCBI) Organismal Classification"	"Chemical Entities of Biological Interest Ontology"	"Protein Ontology"	"Protein-Protein Interaction Ontology"	"BRENDA Tissue and Enzyme Source Ontology"	
INVESTIGATION
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INVESTIGATION PUBLICATIONS
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STUDY
Study Identifier	"E-GEOD-38988"
Study Title	"Cell Intrinsic role of Cox-2 in pancreatic cancer development"
Study Description	"Cyclooxygenase-2 (COX-2) is upregulated in pancreatic ductal adenocarcinomas (PDAC). However, how COX-2 promotes PDAC development is unclear. While previous studies have evaluated the efficacy of COX-2 inhibition via the use of non steroidal anti-inflammatory drugs (NSAIDs) or the COX-2 inhibitor celecoxib in PDAC models, none have addressed the cell intrinsic vs. microenvironment roles of COX-2 in modulating PDAC initiation and progression. We tested the cell intrinsic role of COX-2 in PDAC progression, using both loss-of-function and gain-of-function approaches. Cox-2 deletion in Pdx1+ pancreatic progenitor cells significantly delays the development of PDAC in mice with K-ras activation and Pten haploinsufficiency. Conversely, COX-2 over-expression promotes early onset and progression of PDAC in the K-ras mouse model. Loss of PTEN function is a critical factor in determining lethal PDAC onset and overall survival. Mechanistically, COX-2 over-expression increases P-AKT levels in the precursor lesions of Pdx1+;K-rasG12D/+;Ptenlox/+ mice in the absence of Pten LOH. In contrast, Cox-2 deletion in the same setting diminishes P-AKT levels and delays cancer progression. These data suggest an important cell intrinsic role for COX-2 in tumor initiation and progression through activation of the PI3K/AKT pathway. PDAC that is independent of intrinsic COX-2 expression eventually develops with decreased FKBP5 and increased GRP78 expression, two alternate pathways leading to AKT activation. Together, these results support a cell intrinsic role for COX-2 in PDAC development and suggest that, while anti-COX-2 therapy may delay the development and progression of PDAC, mechanisms known to increase chemoresistance through AKT activation must also be overcome. Murine mutants with pancreatic specific loss of Pten (Pten +/-) and K-ras activation (K-rasG12D) and either COX-2 over-expression (Cox-2 COE) or knockout (Cox-2 KO) under regulation of the Pdx-1 promoter developed pancreatic ductal adenocarcinoma. RNA was extracted from pancreatic tumors from individual mutants with pathology thought to closely mimic the human disease. Pancreatic tissue was subject to RNA extraction and hybridization on Affymetrix cDNA microarrays."
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Study Submission Date	""
Study Public Release Date	"2012-06-28"
Study File Name	"s_E-GEOD-38988_study_samples.txt"
STUDY DESIGN DESCRIPTORS
Study Design Type	"transcription profiling by array"
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STUDY PUBLICATIONS
Study PubMed ID	"22784710"
Study Publication DOI	"10.1158/1535-7163.mct-12-0342"
Study Publication Author List	"Hill R, Li Y, Tran LM, Dry S, Calvopina JH, Garcia A, Kim C, Wang Y, Donahue TR, Herschman HR, Wu H."
Study Publication Title	"Cell intrinsic role of COX-2 in pancreatic cancer development."
Study Publication Status	"Published"
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STUDY FACTORS
Study Factor Name	"variation"
Study Factor Type	"variation"
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STUDY ASSAYS
Study Assay File Name	"a_E-GEOD-38988_GeneChip_assay.txt"
Study Assay Measurement Type	"transcription profiling"
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Study Assay Technology Type	"DNA microarray"
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STUDY PROTOCOLS
Study Protocol Name	"P-GSE38988-2"	"P-GSE38988-3"	"P-GSE38988-4"	"P-GSE38988-5"	"P-GSE38988-6"	"P-GSE38988-1"
Study Protocol Type	"nucleic_acid_extraction"	"labeling"	"hybridization"	"image_acquisition"	"feature_extraction"	"bioassay_data_transformation"
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Study Protocol Description	"Roche's MagNA Pure Compact Nucleic Acid Purification System was used for automated RNA isolation."	"As recommended by manufacturer"	"As recommended by manufacturer"	"GeneChip Scanner 3000 7G was used for scanning. Affymetrix GeneChip Command Console software (AGCC 3.2) was used for image processing"	"Data was normalized by GCRMA (Bioconductor v.2.8/ R v.2.13)."	"ID_REF = <br>VALUE = log2 GC-RMA signal"
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STUDY CONTACTS
Study Person Last Name	"Tran"	"Hill"	"Li"	"Tran"	"Dry"	"Calvopina"	"Garcia"	"Kim"	"Wang"	"Donahue"	"Herschman"	"Wu"
Study Person First Name	"Linh"	"Reginald"	"Yunfeng"	"Linh"	"Sarah"	"Joseph"	"Alejandro"	"Christine"	"Ying"	"Timothy"	"Harvey"	"Hong"
Study Person Mid Initials	"My"	""	""	"M"	""	"H"	""	""	""	""	""	""
Study Person Email	"linhmtran@ucla.edu"	""	""	""	""	""	""	""	""	""	""	""
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Study Person Address	"1Department of Molecular and Medical Pharmacology, University of Los Angeles, 650 CE Young Drive South, Los Angeles, California, USA"	""	""	""	""	""	""	""	""	""	""	""
Study Person Affiliation	"University of Los Angeles"	""	""	""	""	""	""	""	""	""	""	""
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