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Pancreatic Neoplasms: HELP
Articles by Marina Koutsioumpa
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Marina Koutsioumpa wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Developments in miRNA gene signaling pathways in pancreatic cancer. 2016

Vorvis, Christina / Koutsioumpa, Marina / Iliopoulos, Dimitrios. ·Center for Systems Biomedicine, Division of Digestive Diseases, David Geffen School of Medicine, UCLA, Los Angeles, CA, USA. ·Future Oncol · Pubmed #26984178.

ABSTRACT: Pancreatic cancer is a devastating malignancy that ranks as the fourth leading cause of cancer-related deaths worldwide. Dismal prognosis is mainly attributable to limited knowledge of the molecular pathogenesis of the disease. miRNAs have been found to be deregulated in pancreatic cancer, affecting several steps of initiation and aggressiveness of the disease by regulating important signaling pathways, such as the KRAS and Notch pathways. Moreover, the effect of miRNAs on regulating cell cycle events and expression of transcription factors has gained a lot of attention. Recent studies have highlighted the application of miRNAs as biomarkers and therapeutic tools. The current review focuses on latest advances with respect to the roles of miRNAs in pancreatic ductal adenocarcinoma associated signaling pathways and miRNA-based therapeutics.

2 Article Lysine methyltransferase 2D regulates pancreatic carcinogenesis through metabolic reprogramming. 2019

Koutsioumpa, Marina / Hatziapostolou, Maria / Polytarchou, Christos / Tolosa, Ezequiel J / Almada, Luciana L / Mahurkar-Joshi, Swapna / Williams, Jennifer / Tirado-Rodriguez, Ana Belen / Huerta-Yepez, Sara / Karavias, Dimitrios / Kourea, Helen / Poultsides, George A / Struhl, Kevin / Dawson, David W / Donahue, Timothy R / Fernández-Zapico, Martín E / Iliopoulos, Dimitrios. ·Center for Systems Biomedicine, Vatche and Tamar Manoukian Division of Digestive Diseases, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, USA. · Biological Sciences, University of Southampton, Southampton, UK. · Biosciences, School of Science and Technology, Nottingham Trent University, Nottingham, UK. · Interdisciplinary Biomedical Research Centre, School of Science and Technology, Nottingham Trent University, Nottingham, UK. · Schulze Center for Novel Therapeutics, Division of Oncology Research, Mayo Clinic, Rochester, Minnesota, USA. · Department of Surgery, Division of General Surgery, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, USA. · Unidad de Investigacion en Enfermedades Oncologicas, Hospital Infantil de Mexico, Mexico City, Mexico. · Department of Pathology, School of Medicine, University of Patras, Patras, Greece. · Department of Surgery, Stanford University School of Medicine, Stanford, California, USA. · Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts, USA. · Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, USA. ·Gut · Pubmed #30337373.

ABSTRACT: OBJECTIVE: Despite advances in the identification of epigenetic alterations in pancreatic cancer, their biological roles in the pathobiology of this dismal neoplasm remain elusive. Here, we aimed to characterise the functional significance of histone lysine methyltransferases (KMTs) and demethylases (KDMs) in pancreatic tumourigenesis. DESIGN: DNA methylation sequencing and gene expression microarrays were employed to investigate CpG methylation and expression patterns of KMTs and KDMs in pancreatic cancer tissues versus normal tissues. Gene expression was assessed in five cohorts of patients by reverse transcription quantitative-PCR. Molecular analysis and functional assays were conducted in genetically modified cell lines. Cellular metabolic rates were measured using an XF24-3 Analyzer, while quantitative evaluation of lipids was performed by liquid chromatography-mass spectrometry (LC-MS) analysis. Subcutaneous xenograft mouse models were used to evaluate pancreatic tumour growth in vivo. RESULTS: We define a new antitumorous function of the histone lysine (K)-specific methyltransferase 2D (KMT2D) in pancreatic cancer. CONCLUSION: Together our findings define a new tumour suppressor function of KMT2D through the regulation of glucose/fatty acid metabolism in pancreatic cancer.

3 Article Transcriptomic and CRISPR/Cas9 technologies reveal FOXA2 as a tumor suppressor gene in pancreatic cancer. 2016

Vorvis, Christina / Hatziapostolou, Maria / Mahurkar-Joshi, Swapna / Koutsioumpa, Marina / Williams, Jennifer / Donahue, Timothy R / Poultsides, George A / Eibl, Guido / Iliopoulos, Dimitrios. ·Center for Systems Biomedicine, Division of Digestive Diseases, David Geffen School of Medicine, University of California, Los Angeles, California; · Centre for Biological Sciences, University of Southampton, Southampton, United Kingdom; · Department of Surgery, David Geffen School of Medicine, University of California, Los Angeles, California; and. · Department of Surgery, Stanford University School of Medicine, Stanford, California. · Center for Systems Biomedicine, Division of Digestive Diseases, David Geffen School of Medicine, University of California, Los Angeles, California; diliopoulos@mednet.ucla.edu. ·Am J Physiol Gastrointest Liver Physiol · Pubmed #27151939.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with low survival rates and limited therapeutic options. Thus elucidation of signaling pathways involved in PDAC pathogenesis is essential for identifying novel potential therapeutic gene targets. Here, we used a systems approach to elucidate those pathways by integrating gene and microRNA profiling analyses together with CRISPR/Cas9 technology to identify novel transcription factors involved in PDAC pathogenesis. FOXA2 transcription factor was found to be significantly downregulated in PDAC relative to control pancreatic tissues. Functional experiments revealed that FOXA2 has a tumor suppressor function through inhibition of pancreatic cancer cell growth, migration, invasion, and colony formation. In situ hybridization analysis revealed miR-199a to be significantly upregulated in pancreatic cancer. Bioinformatics and luciferase analyses showed that miR-199a negatively but directly regulates FOXA2 expression through binding in its 3'-untranslated region (UTR). Evaluation of the functional importance of miR-199a on pancreatic cancer revealed that miR-199a acts as an inhibitor of FOXA2 expression, inducing an increase in pancreatic cancer cell proliferation, migration, and invasion. Additionally, gene ontology and network analyses in PANC-1 cells treated with a small interfering RNA (siRNA) against FOXA2 revealed an enrichment for cell invasion mechanisms through PLAUR and ERK activation. FOXA2 deletion (FOXA2Δ) by using two CRISPR/Cas9 vectors in PANC-1 cells induced tumor growth in vivo resulting in upregulation of PLAUR and ERK pathways in FOXA2Δ xenograft tumors. We have identified FOXA2 as a novel tumor suppressor in pancreatic cancer and it is regulated directly by miR-199a, thereby enhancing our understanding of how microRNAs interplay with the transcription factors to affect pancreatic oncogenesis.