A genome-wide investigation of microRNA expression identifies biologically-meaningful microRNAs that distinguish between high-risk and low-risk intraductal papillary mucinous neoplasms of the pancreas
Intraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursors. Differentiating between high-risk IPMNs that warrant surgical resection and low-risk IPMNs that can be monitored is a significant clinical problem, and we sought to discover a panel of mi(cro)RNA...
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| Published in: | PloS one Vol. 10; no. 1; p. e0116869 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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Public Library of Science
21-01-2015
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| Abstract | Intraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursors. Differentiating between high-risk IPMNs that warrant surgical resection and low-risk IPMNs that can be monitored is a significant clinical problem, and we sought to discover a panel of mi(cro)RNAs that accurately classify IPMN risk status.
In a discovery phase, genome-wide miRNA expression profiling was performed on 28 surgically-resected, pathologically-confirmed IPMNs (19 high-risk, 9 low-risk) using Taqman MicroRNA Arrays. A validation phase was performed in 21 independent IPMNs (13 high-risk, 8 low-risk). We also explored associations between miRNA expression level and various clinical and pathological factors and examined genes and pathways regulated by the identified miRNAs by integrating data from bioinformatic analyses and microarray analysis of miRNA gene targets. Six miRNAs (miR-100, miR-99b, miR-99a, miR-342-3p, miR-126, miR-130a) were down-regulated in high-risk versus low-risk IPMNs and distinguished between groups (P<10-3, area underneath the curve (AUC) = 87%). The same trend was observed in the validation phase (AUC = 74%). Low miR-99b expression was associated with main pancreatic duct involvement (P = 0.021), and serum albumin levels were positively correlated with miR-99a (r = 0.52, P = 0.004) and miR-100 expression (r = 0.49, P = 0.008). Literature, validated miRNA:target gene interactions, and pathway enrichment analysis supported the candidate miRNAs as tumor suppressors and regulators of PDAC development. Microarray analysis revealed that oncogenic targets of miR-130a (ATG2B, MEOX2), miR-342-3p (DNMT1), and miR-126 (IRS-1) were up-regulated in high- versus low-risk IPMNs (P<0.10).
This pilot study highlights miRNAs that may aid in preoperative risk stratification of IPMNs and provides novel insights into miRNA-mediated progression to pancreatic malignancy. The miRNAs identified here and in other recent investigations warrant evaluation in biofluids in a well-powered prospective cohort of individuals newly-diagnosed with IPMNs and other pancreatic cysts and those at increased genetic risk for these lesions. |
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| AbstractList | Background Intraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursors. Differentiating between high-risk IPMNs that warrant surgical resection and low-risk IPMNs that can be monitored is a significant clinical problem, and we sought to discover a panel of mi(cro)RNAs that accurately classify IPMN risk status. Methodology/Principal Findings In a discovery phase, genome-wide miRNA expression profiling was performed on 28 surgically-resected, pathologically-confirmed IPMNs (19 high-risk, 9 low-risk) using Taqman MicroRNA Arrays. A validation phase was performed in 21 independent IPMNs (13 high-risk, 8 low-risk). We also explored associations between miRNA expression level and various clinical and pathological factors and examined genes and pathways regulated by the identified miRNAs by integrating data from bioinformatic analyses and microarray analysis of miRNA gene targets. Six miRNAs (miR-100, miR-99b, miR-99a, miR-342-3p, miR-126, miR-130a) were down-regulated in high-risk versus low-risk IPMNs and distinguished between groups (P<10.sup.-3, area underneath the curve (AUC) = 87%). The same trend was observed in the validation phase (AUC = 74%). Low miR-99b expression was associated with main pancreatic duct involvement (P = 0.021), and serum albumin levels were positively correlated with miR-99a (r = 0.52, P = 0.004) and miR-100 expression (r = 0.49, P = 0.008). Literature, validated miRNA:target gene interactions, and pathway enrichment analysis supported the candidate miRNAs as tumor suppressors and regulators of PDAC development. Microarray analysis revealed that oncogenic targets of miR-130a (ATG2B, MEOX2), miR-342-3p (DNMT1), and miR-126 (IRS-1) were up-regulated in high- versus low-risk IPMNs (P<0.10). Conclusions This pilot study highlights miRNAs that may aid in preoperative risk stratification of IPMNs and provides novel insights into miRNA-mediated progression to pancreatic malignancy. The miRNAs identified here and in other recent investigations warrant evaluation in biofluids in a well-powered prospective cohort of individuals newly-diagnosed with IPMNs and other pancreatic cysts and those at increased genetic risk for these lesions. Background Intraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursors. Differentiating between high-risk IPMNs that warrant surgical resection and low-risk IPMNs that can be monitored is a significant clinical problem, and we sought to discover a panel of mi(cro)RNAs that accurately classify IPMN risk status. Methodology/Principal Findings In a discovery phase, genome-wide miRNA expression profiling was performed on 28 surgically-resected, pathologically-confirmed IPMNs (19 high-risk, 9 low-risk) using Taqman MicroRNA Arrays. A validation phase was performed in 21 independent IPMNs (13 high-risk, 8 low-risk). We also explored associations between miRNA expression level and various clinical and pathological factors and examined genes and pathways regulated by the identified miRNAs by integrating data from bioinformatic analyses and microarray analysis of miRNA gene targets. Six miRNAs (miR-100, miR-99b, miR-99a, miR-342-3p, miR-126, miR-130a) were down-regulated in high-risk versus low-risk IPMNs and distinguished between groups (P<10−3, area underneath the curve (AUC) = 87%). The same trend was observed in the validation phase (AUC = 74%). Low miR-99b expression was associated with main pancreatic duct involvement (P = 0.021), and serum albumin levels were positively correlated with miR-99a (r = 0.52, P = 0.004) and miR-100 expression (r = 0.49, P = 0.008). Literature, validated miRNA:target gene interactions, and pathway enrichment analysis supported the candidate miRNAs as tumor suppressors and regulators of PDAC development. Microarray analysis revealed that oncogenic targets of miR-130a (ATG2B, MEOX2), miR-342-3p (DNMT1), and miR-126 (IRS-1) were up-regulated in high- versus low-risk IPMNs (P<0.10). Conclusions This pilot study highlights miRNAs that may aid in preoperative risk stratification of IPMNs and provides novel insights into miRNA-mediated progression to pancreatic malignancy. The miRNAs identified here and in other recent investigations warrant evaluation in biofluids in a well-powered prospective cohort of individuals newly-diagnosed with IPMNs and other pancreatic cysts and those at increased genetic risk for these lesions. Background Intraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursors. Differentiating between high-risk IPMNs that warrant surgical resection and low-risk IPMNs that can be monitored is a significant clinical problem, and we sought to discover a panel of mi(cro)RNAs that accurately classify IPMN risk status. Methodology/Principal Findings In a discovery phase, genome-wide miRNA expression profiling was performed on 28 surgically-resected, pathologically-confirmed IPMNs (19 high-risk, 9 low-risk) using Taqman MicroRNA Arrays. A validation phase was performed in 21 independent IPMNs (13 high-risk, 8 low-risk). We also explored associations between miRNA expression level and various clinical and pathological factors and examined genes and pathways regulated by the identified miRNAs by integrating data from bioinformatic analyses and microarray analysis of miRNA gene targets. Six miRNAs (miR-100, miR-99b, miR-99a, miR-342-3p, miR-126, miR-130a) were down-regulated in high-risk versus low-risk IPMNs and distinguished between groups (P<10−3, area underneath the curve (AUC) = 87%). The same trend was observed in the validation phase (AUC = 74%). Low miR-99b expression was associated with main pancreatic duct involvement (P = 0.021), and serum albumin levels were positively correlated with miR-99a (r = 0.52, P = 0.004) and miR-100 expression (r = 0.49, P = 0.008). Literature, validated miRNA:target gene interactions, and pathway enrichment analysis supported the candidate miRNAs as tumor suppressors and regulators of PDAC development. Microarray analysis revealed that oncogenic targets of miR-130a (ATG2B, MEOX2), miR-342-3p (DNMT1), and miR-126 (IRS-1) were up-regulated in high- versus low-risk IPMNs (P<0.10). Conclusions This pilot study highlights miRNAs that may aid in preoperative risk stratification of IPMNs and provides novel insights into miRNA-mediated progression to pancreatic malignancy. The miRNAs identified here and in other recent investigations warrant evaluation in biofluids in a well-powered prospective cohort of individuals newly-diagnosed with IPMNs and other pancreatic cysts and those at increased genetic risk for these lesions. Intraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursors. Differentiating between high-risk IPMNs that warrant surgical resection and low-risk IPMNs that can be monitored is a significant clinical problem, and we sought to discover a panel of mi(cro)RNAs that accurately classify IPMN risk status. In a discovery phase, genome-wide miRNA expression profiling was performed on 28 surgically-resected, pathologically-confirmed IPMNs (19 high-risk, 9 low-risk) using Taqman MicroRNA Arrays. A validation phase was performed in 21 independent IPMNs (13 high-risk, 8 low-risk). We also explored associations between miRNA expression level and various clinical and pathological factors and examined genes and pathways regulated by the identified miRNAs by integrating data from bioinformatic analyses and microarray analysis of miRNA gene targets. Six miRNAs (miR-100, miR-99b, miR-99a, miR-342-3p, miR-126, miR-130a) were down-regulated in high-risk versus low-risk IPMNs and distinguished between groups (P<10.sup.-3, area underneath the curve (AUC) = 87%). The same trend was observed in the validation phase (AUC = 74%). Low miR-99b expression was associated with main pancreatic duct involvement (P = 0.021), and serum albumin levels were positively correlated with miR-99a (r = 0.52, P = 0.004) and miR-100 expression (r = 0.49, P = 0.008). Literature, validated miRNA:target gene interactions, and pathway enrichment analysis supported the candidate miRNAs as tumor suppressors and regulators of PDAC development. Microarray analysis revealed that oncogenic targets of miR-130a (ATG2B, MEOX2), miR-342-3p (DNMT1), and miR-126 (IRS-1) were up-regulated in high- versus low-risk IPMNs (P<0.10). This pilot study highlights miRNAs that may aid in preoperative risk stratification of IPMNs and provides novel insights into miRNA-mediated progression to pancreatic malignancy. The miRNAs identified here and in other recent investigations warrant evaluation in biofluids in a well-powered prospective cohort of individuals newly-diagnosed with IPMNs and other pancreatic cysts and those at increased genetic risk for these lesions. Intraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursors. Differentiating between high-risk IPMNs that warrant surgical resection and low-risk IPMNs that can be monitored is a significant clinical problem, and we sought to discover a panel of mi(cro)RNAs that accurately classify IPMN risk status. In a discovery phase, genome-wide miRNA expression profiling was performed on 28 surgically-resected, pathologically-confirmed IPMNs (19 high-risk, 9 low-risk) using Taqman MicroRNA Arrays. A validation phase was performed in 21 independent IPMNs (13 high-risk, 8 low-risk). We also explored associations between miRNA expression level and various clinical and pathological factors and examined genes and pathways regulated by the identified miRNAs by integrating data from bioinformatic analyses and microarray analysis of miRNA gene targets. Six miRNAs (miR-100, miR-99b, miR-99a, miR-342-3p, miR-126, miR-130a) were down-regulated in high-risk versus low-risk IPMNs and distinguished between groups (P<10-3, area underneath the curve (AUC) = 87%). The same trend was observed in the validation phase (AUC = 74%). Low miR-99b expression was associated with main pancreatic duct involvement (P = 0.021), and serum albumin levels were positively correlated with miR-99a (r = 0.52, P = 0.004) and miR-100 expression (r = 0.49, P = 0.008). Literature, validated miRNA:target gene interactions, and pathway enrichment analysis supported the candidate miRNAs as tumor suppressors and regulators of PDAC development. Microarray analysis revealed that oncogenic targets of miR-130a (ATG2B, MEOX2), miR-342-3p (DNMT1), and miR-126 (IRS-1) were up-regulated in high- versus low-risk IPMNs (P<0.10). This pilot study highlights miRNAs that may aid in preoperative risk stratification of IPMNs and provides novel insights into miRNA-mediated progression to pancreatic malignancy. The miRNAs identified here and in other recent investigations warrant evaluation in biofluids in a well-powered prospective cohort of individuals newly-diagnosed with IPMNs and other pancreatic cysts and those at increased genetic risk for these lesions. BACKGROUNDIntraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursors. Differentiating between high-risk IPMNs that warrant surgical resection and low-risk IPMNs that can be monitored is a significant clinical problem, and we sought to discover a panel of mi(cro)RNAs that accurately classify IPMN risk status.METHODOLOGY/PRINCIPAL FINDINGSIn a discovery phase, genome-wide miRNA expression profiling was performed on 28 surgically-resected, pathologically-confirmed IPMNs (19 high-risk, 9 low-risk) using Taqman MicroRNA Arrays. A validation phase was performed in 21 independent IPMNs (13 high-risk, 8 low-risk). We also explored associations between miRNA expression level and various clinical and pathological factors and examined genes and pathways regulated by the identified miRNAs by integrating data from bioinformatic analyses and microarray analysis of miRNA gene targets. Six miRNAs (miR-100, miR-99b, miR-99a, miR-342-3p, miR-126, miR-130a) were down-regulated in high-risk versus low-risk IPMNs and distinguished between groups (P<10-3, area underneath the curve (AUC) = 87%). The same trend was observed in the validation phase (AUC = 74%). Low miR-99b expression was associated with main pancreatic duct involvement (P = 0.021), and serum albumin levels were positively correlated with miR-99a (r = 0.52, P = 0.004) and miR-100 expression (r = 0.49, P = 0.008). Literature, validated miRNA:target gene interactions, and pathway enrichment analysis supported the candidate miRNAs as tumor suppressors and regulators of PDAC development. Microarray analysis revealed that oncogenic targets of miR-130a (ATG2B, MEOX2), miR-342-3p (DNMT1), and miR-126 (IRS-1) were up-regulated in high- versus low-risk IPMNs (P<0.10).CONCLUSIONSThis pilot study highlights miRNAs that may aid in preoperative risk stratification of IPMNs and provides novel insights into miRNA-mediated progression to pancreatic malignancy. The miRNAs identified here and in other recent investigations warrant evaluation in biofluids in a well-powered prospective cohort of individuals newly-diagnosed with IPMNs and other pancreatic cysts and those at increased genetic risk for these lesions. BACKGROUND:Intraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursors. Differentiating between high-risk IPMNs that warrant surgical resection and low-risk IPMNs that can be monitored is a significant clinical problem, and we sought to discover a panel of mi(cro)RNAs that accurately classify IPMN risk status. METHODOLOGY/PRINCIPAL FINDINGS:In a discovery phase, genome-wide miRNA expression profiling was performed on 28 surgically-resected, pathologically-confirmed IPMNs (19 high-risk, 9 low-risk) using Taqman MicroRNA Arrays. A validation phase was performed in 21 independent IPMNs (13 high-risk, 8 low-risk). We also explored associations between miRNA expression level and various clinical and pathological factors and examined genes and pathways regulated by the identified miRNAs by integrating data from bioinformatic analyses and microarray analysis of miRNA gene targets. Six miRNAs (miR-100, miR-99b, miR-99a, miR-342-3p, miR-126, miR-130a) were down-regulated in high-risk versus low-risk IPMNs and distinguished between groups (P<10-3, area underneath the curve (AUC) = 87%). The same trend was observed in the validation phase (AUC = 74%). Low miR-99b expression was associated with main pancreatic duct involvement (P = 0.021), and serum albumin levels were positively correlated with miR-99a (r = 0.52, P = 0.004) and miR-100 expression (r = 0.49, P = 0.008). Literature, validated miRNA:target gene interactions, and pathway enrichment analysis supported the candidate miRNAs as tumor suppressors and regulators of PDAC development. Microarray analysis revealed that oncogenic targets of miR-130a (ATG2B, MEOX2), miR-342-3p (DNMT1), and miR-126 (IRS-1) were up-regulated in high- versus low-risk IPMNs (P<0.10). CONCLUSIONS:This pilot study highlights miRNAs that may aid in preoperative risk stratification of IPMNs and provides novel insights into miRNA-mediated progression to pancreatic malignancy. The miRNAs identified here and in other recent investigations warrant evaluation in biofluids in a well-powered prospective cohort of individuals newly-diagnosed with IPMNs and other pancreatic cysts and those at increased genetic risk for these lesions. |
| Audience | Academic |
| Author | Lloyd, Mark C Yeatman, Timothy Fisher, Kate Centeno, Barbara Ann Springett, Gregory M Chen, Y Ann Hall, Laura McCarthy, Susan Ghia, Kavita M Coppola, Domenico Yoder, Sean J Chen, Dung-Tsa Malafa, Mokenge Olaoye, Funmilayo Permuth-Wey, Jennifer Fournier, Michelle Williams, Vonetta L Qu, Xiaotao Kasprzak, Agnieszka Klapman, Jason Husain, Kazim Georgeades, Christina |
| AuthorAffiliation | 8 Department of Gastrointestinal Oncology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America 2 Department of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America 10 Department of Gastroenterology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America 4 Department of Analytic Microscopy, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America University of Massachusetts Medical, UNITED STATES 6 Department of Information Shared Services, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America 1 Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America 3 Department of Clinical Testing Development, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America 11 Department of Gastrointestinal Surgical Oncology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America 7 Department of Molecular Genomics, H. Lee Moffitt Cancer Center, Tampa, FL, United |
| AuthorAffiliation_xml | – name: 2 Department of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – name: 6 Department of Information Shared Services, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – name: 7 Department of Molecular Genomics, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – name: 9 Department of Anatomic Pathology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – name: 1 Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – name: 3 Department of Clinical Testing Development, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – name: 12 Department of Surgery, Gibbs Cancer Center and Research Institute, Spartanburg, SC, United States of America – name: 11 Department of Gastrointestinal Surgical Oncology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – name: 5 Department of Tissue Core Administration, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – name: 10 Department of Gastroenterology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – name: 4 Department of Analytic Microscopy, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – name: 8 Department of Gastrointestinal Oncology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – name: University of Massachusetts Medical, UNITED STATES |
| Author_xml | – sequence: 1 givenname: Jennifer surname: Permuth-Wey fullname: Permuth-Wey, Jennifer organization: Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 2 givenname: Y Ann surname: Chen fullname: Chen, Y Ann organization: Department of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 3 givenname: Kate surname: Fisher fullname: Fisher, Kate organization: Department of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 4 givenname: Susan surname: McCarthy fullname: McCarthy, Susan organization: Department of Clinical Testing Development, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 5 givenname: Xiaotao surname: Qu fullname: Qu, Xiaotao organization: Department of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 6 givenname: Mark C surname: Lloyd fullname: Lloyd, Mark C organization: Department of Analytic Microscopy, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 7 givenname: Agnieszka surname: Kasprzak fullname: Kasprzak, Agnieszka organization: Department of Analytic Microscopy, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 8 givenname: Michelle surname: Fournier fullname: Fournier, Michelle organization: Department of Tissue Core Administration, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 9 givenname: Vonetta L surname: Williams fullname: Williams, Vonetta L organization: Department of Information Shared Services, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 10 givenname: Kavita M surname: Ghia fullname: Ghia, Kavita M organization: Department of Information Shared Services, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 11 givenname: Sean J surname: Yoder fullname: Yoder, Sean J organization: Department of Molecular Genomics, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 12 givenname: Laura surname: Hall fullname: Hall, Laura organization: Department of Molecular Genomics, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 13 givenname: Christina surname: Georgeades fullname: Georgeades, Christina organization: Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 14 givenname: Funmilayo surname: Olaoye fullname: Olaoye, Funmilayo organization: Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 15 givenname: Kazim surname: Husain fullname: Husain, Kazim organization: Department of Gastrointestinal Oncology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 16 givenname: Gregory M surname: Springett fullname: Springett, Gregory M organization: Department of Gastrointestinal Oncology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 17 givenname: Dung-Tsa surname: Chen fullname: Chen, Dung-Tsa organization: Department of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 18 givenname: Timothy surname: Yeatman fullname: Yeatman, Timothy organization: Department of Surgery, Gibbs Cancer Center and Research Institute, Spartanburg, SC, United States of America – sequence: 19 givenname: Barbara Ann surname: Centeno fullname: Centeno, Barbara Ann organization: Department of Anatomic Pathology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 20 givenname: Jason surname: Klapman fullname: Klapman, Jason organization: Department of Gastroenterology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 21 givenname: Domenico surname: Coppola fullname: Coppola, Domenico organization: Department of Anatomic Pathology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America – sequence: 22 givenname: Mokenge surname: Malafa fullname: Malafa, Mokenge organization: Department of Gastrointestinal Surgical Oncology, H. Lee Moffitt Cancer Center, Tampa, FL, United States of America |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25607660$$D View this record in MEDLINE/PubMed |
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| Copyright | COPYRIGHT 2015 Public Library of Science 2015 Permuth-Wey et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2015 Permuth-Wey et al 2015 Permuth-Wey et al |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Conceived and designed the experiments: JPW YAC SM MCL DC MM. Performed the experiments: SM SJY LH. Analyzed the data: YAC KF JPW MM. Contributed reagents/materials/analysis tools: JPW SM XQ MCL AK MF VLW KMG SJY LH CG FO KH GMS BAC DC. Wrote the paper: JPW YAC KF SM XQ MCL CG TY BAC JK DC MM. Competing Interests: The authors of this manuscript have the following competing interests: A patent for this work entitled ‘MicroRNA Assay to Assess Malignancy Risk of Pancreatic Lesions’ has been filed (docket number 13MB078PR). |
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| Snippet | Intraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursors. Differentiating between high-risk IPMNs that warrant... Background Intraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursors. Differentiating between high-risk IPMNs... BACKGROUNDIntraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursors. Differentiating between high-risk IPMNs that... BACKGROUND:Intraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursors. Differentiating between high-risk IPMNs... Background Intraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursors. Differentiating between high-risk IPMNs... |
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| SubjectTerms | Adenocarcinoma Adenocarcinoma, Mucinous - genetics Adenocarcinoma, Mucinous - pathology Adenocarcinoma, Papillary - genetics Adenocarcinoma, Papillary - pathology Aged Aged, 80 and over Bioinformatics Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - pathology Cellular biology Cysts Data processing Deoxyribonucleic acid Diagnosis, Differential DNA DNA microarrays DNMT1 protein Epidemiology Female Gene expression Gene Expression Profiling - methods Gene Expression Regulation, Neoplastic Gene Regulatory Networks Genomes Genomics Humans Insulin receptor substrate 1 Investigations Kinases Lesions Male Malignancy Medical diagnosis Medical imaging Medical prognosis MicroRNA MicroRNAs MicroRNAs - genetics Microscopy Middle Aged miRNA Mortality Neoplasms Oligonucleotide Array Sequence Analysis - methods Oncology Pancreas Pancreatic cancer Pancreatic Neoplasms - genetics Pancreatic Neoplasms - pathology Pathology Pilot Projects Proteins Regulators Ribonucleic acid Risk RNA Serum albumin Serum Albumin - metabolism Suppressors Surgery Tumors |
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| Title | A genome-wide investigation of microRNA expression identifies biologically-meaningful microRNAs that distinguish between high-risk and low-risk intraductal papillary mucinous neoplasms of the pancreas |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/25607660 https://www.proquest.com/docview/1658106958 https://search.proquest.com/docview/1652401057 https://pubmed.ncbi.nlm.nih.gov/PMC4301643 https://doaj.org/article/f9b5e8d0fb8b46b4957c592ee9a83ced http://dx.doi.org/10.1371/journal.pone.0116869 |
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