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Pancreatic Neoplasms: HELP
Articles by Emman Mascariñas
Based on 5 articles published since 2010
(Why 5 articles?)
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Between 2010 and 2020, Emman Mascariñas wrote the following 5 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Omega-3 Fatty Acids Prevent Early Pancreatic Carcinogenesis via Repression of the AKT Pathway. 2018

Ding, Yongzeng / Mullapudi, Bhargava / Torres, Carolina / Mascariñas, Emman / Mancinelli, Georgina / Diaz, Andrew M / McKinney, Ronald / Barron, Morgan / Schultz, Michelle / Heiferman, Michael / Wojtanek, Mireille / Adrian, Kevin / DeCant, Brian / Rao, Sambasiva / Ouellette, Michel / Tsao, Ming-Sound / Bentrem, David J / Grippo, Paul J. ·Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. ding.zheng@northwestern.edu. · Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. mullapudi.bhargav@gmail.com. · Division of Gastroenterology, Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA. ctorres@uic.edu. · Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. wemascarinas@gmail.com. · Division of Gastroenterology, Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA. wemascarinas@gmail.com. · Division of Gastroenterology, Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA. gms891@gmail.com. · Division of Gastroenterology, Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA. amdiaz@atsu.edu. · Division of Gastroenterology, Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA. mckinney@uic.edu. · Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. mrbarron01@gmail.com. · Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. buffalosoldierms@gmail.com. · Division of Gastroenterology, Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA. buffalosoldierms@gmail.com. · Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. mikeheif@gmail.com. · Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. mireillewojtanek@gmail.com. · Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. KevinAdrian@bridgewatermcg.com. · Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. bdecant0823@gmail.com. · Division of Gastroenterology, Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA. bdecant0823@gmail.com. · Division of Gastroenterology, Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA. s-rao@northwestern.edu. · Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. mouellet@unmc.edu. · Toronto General Hospital, 200 Elizabeth St., Toronto, ON M5G 2C4, Canada. ming.tsao@uhn.ca. · Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. dbentrem@northwestern.edu. · Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. pgrippo@uic.edu. · Division of Gastroenterology, Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA. pgrippo@uic.edu. ·Nutrients · Pubmed #30213082.

ABSTRACT: Pancreatic cancer remains a daunting foe despite a vast number of accumulating molecular analyses regarding the mutation and expression status of a variety of genes. Indeed, most pancreatic cancer cases uniformly present with a mutation in the

2 Article TGFβ Signaling in the Pancreatic Tumor Microenvironment Promotes Fibrosis and Immune Evasion to Facilitate Tumorigenesis. 2016

Principe, Daniel R / DeCant, Brian / Mascariñas, Emman / Wayne, Elizabeth A / Diaz, Andrew M / Akagi, Naomi / Hwang, Rosa / Pasche, Boris / Dawson, David W / Fang, Deyu / Bentrem, David J / Munshi, Hidayatullah G / Jung, Barbara / Grippo, Paul J. ·University of Illinois College of Medicine, Urbana-Champaign, Illinois. · Department of Medicine, University of Illinois at Chicago, Chicago, Illinois. · Department of Medicine, University of Illinois at Chicago, Chicago, Illinois. Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois. · Department of Surgical Oncology, Division of Surgery, The University of Texas MD Anderson Cancer Center, Houston, Texas. · Comprehensive Cancer Center of Wake Forest University, Winston-Salem, North Carolina. · Department of Pathology and Laboratory Medicine, Jonsson Comprehensive Cancer Center, David Geffen School of Medicine at UCLA, Los Angeles, California. · Department of Pathology, Northwestern University, Chicago, Illinois. · Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois. · Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois. Department of Medicine, Northwestern University, Chicago, Illinois. · Department of Medicine, University of Illinois at Chicago, Chicago, Illinois. pgrippo@uic.edu bjung@uic.edu. ·Cancer Res · Pubmed #26980767.

ABSTRACT: In early pancreatic carcinogenesis, TGFβ acts as a tumor suppressor due to its growth-inhibitory effects in epithelial cells. However, in advanced disease, TGFβ appears to promote tumor progression. Therefore, to better understand the contributions of TGFβ signaling to pancreatic carcinogenesis, we generated mouse models of pancreatic cancer with either epithelial or systemic TGFBR deficiency. We found that epithelial suppression of TGFβ signals facilitated pancreatic tumorigenesis, whereas global loss of TGFβ signaling protected against tumor development via inhibition of tumor-associated fibrosis, stromal TGFβ1 production, and the resultant restoration of antitumor immune function. Similarly, TGFBR-deficient T cells resisted TGFβ-induced inactivation ex vivo, and adoptive transfer of TGFBR-deficient CD8(+) T cells led to enhanced infiltration and granzyme B-mediated destruction of developing tumors. These findings paralleled our observations in human patients, where TGFβ expression correlated with increased fibrosis and associated negatively with expression of granzyme B. Collectively, our findings suggest that, despite opposing the proliferation of some epithelial cells, TGFβ may promote pancreatic cancer development by affecting stromal and hematopoietic cell function. Therefore, the use of TGFBR inhibition to target components of the tumor microenvironment warrants consideration as a potential therapy for pancreatic cancer, particularly in patients who have already lost tumor-suppressive TGFβ signals in the epithelium. Cancer Res; 76(9); 2525-39. ©2016 AACR.

3 Article HDAC3 mediates smoking-induced pancreatic cancer. 2016

Edderkaoui, Mouad / Xu, Shiping / Chheda, Chintan / Morvaridi, Susan / Hu, Robert W / Grippo, Paul J / Mascariñas, Emman / Principe, Daniel R / Knudsen, Beatrice / Xue, Jing / Habtezion, Aida / Uyeminami, Dale / Pinkerton, Kent E / Pandol, Stephen J. ·Departments of Medicine and Biological Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. · Veterans Affairs Greater Los Angeles Healthcare System & University of California at Los Angeles, CA, USA. · Department of Gastroenterology, Nanlou Division, The PLA General Hospital, Beijing, China. · Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. · Department of Medicine, University of Illinois-Chicago, Chicago, IL, USA. · Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA. · Center for Health and the Environment, University of California, Davis, CA, USA. ·Oncotarget · Pubmed #26745602.

ABSTRACT: Smoking is a major risk factor for developing pancreatic adenocarcinoma (PDAC); however, little is known about the mechanisms involved. Here we employed a genetic animal model of early stages of PDAC that overexpresses oncogenic Kras in the pancreas to investigate the mechanisms of smoking-induced promotion of the disease in vivo. We confirmed the regulation of the interactions between the tumor microenvironment cells using in vitro cellular systems. Aerial exposure to cigarette smoke stimulated development of pancreatic intraepithelial neaoplasia (PanIN) lesions associated with a tumor microenvironment-containing features of human PDAC including fibrosis, activated stellate cells, M2-macrophages and markers of epithelial-mesenchymal transition (EMT). The pro-cancer effects of smoking were prevented by Histone Deacetylase HDAC I/II inhibitor Saha. Smoking decreased histone acetylation associated with recruitment of and phenotypic changes in macrophages; which in turn, stimulated survival and induction of EMT of the pre-cancer and cancer cells. The interaction between the cancer cells and macrophages is mediated by IL-6 produced under the regulation of HDAC3 translocation to the nucleus in the cancer cells. Pharmacological and molecular inhibitions of HDAC3 decreased IL-6 levels in cancer cells. IL-6 stimulated the macrophage phenotype change through regulation of the IL-4 receptor level of the macrophage. This study demonstrates a novel pathway of interaction between cancer cells and tumor promoting macrophages involving HDAC3 and IL-6. It further demonstrates that targeting HDAC3 prevents progression of the disease and could provide a strategy for treating the disease considering that the HDAC inhibitor we used is FDA approved for a different disease.

4 Article Characterization of Mouse Models of Early Pancreatic Lesions Induced by Alcohol and Chronic Pancreatitis. 2015

Xu, Shiping / Chheda, Chintan / Ouhaddi, Yassine / Benhaddou, Hajar / Bourhim, Mouloud / Grippo, Paul J / Principe, Daniel R / Mascariñas, Emman / DeCant, Brian / Tsukamoto, Hidekazu / Pandol, Stephen J / Edderkaoui, Mouad. ·From the *Veterans Affairs Greater Los Angeles Healthcare System, University of California at Los Angeles, Los Angeles, CA; †Department of Gastroenterology, Nanlou Division, The PLA General Hospital, Beijing, China; ‡Departments of Medicine and Biological Sciences, Cedars-Sinai Medical Center, Los Angeles, CA; §Faculty of Sciences Dhar el Mehraz, University Mohamed Ben Abdellah, Fez, Morocco; ∥Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University; ¶Department of Medicine, University of Illinois-Chicago, Chicago, IL; and #Southern California Research Center for ALPD and Cirrhosis, Keck School of Medicine University of Southern California, Los Angeles, CA. ·Pancreas · Pubmed #26166469.

ABSTRACT: OBJECTIVE: We describe the first mouse model of pancreatic intraepithelial neoplasia (PanIN) lesions induced by alcohol in the presence and absence of chronic pancreatitis. METHODS: Pdx1-Cre;LSL-K-ras mice were exposed to Lieber-DeCarli alcohol diet for 6 weeks with cerulein injections. The PanIN lesions and markers of fibrosis, inflammation, histone deacetylation, epithelial-to-mesenchymal transition (EMT), and cancer stemness were measured by immunohistochemistry and Western. RESULTS: Exposure of Pdx1-Cre;LSL-K-ras mice to an alcohol diet significantly stimulated fibrosis and slightly but not significantly increased the level of PanIN lesions associated with an increase in tumor-promoting M2 macrophages. Importantly, the alcohol diet did not increase activation of stellate cells. Alcohol diet and cerulein injections resulted in synergistic and additive effects on PanIN lesion and M2 macrophage phenotype induction, respectively. Cerulein pancreatitis caused stellate cell activation, EMT, and cancer stemness in the pancreas. Pancreatitis caused histone deacetylation, which was promoted by the alcohol diet. Pancreatitis increased EMT and cancer stemness markers, which were not further affected by the alcohol diet. CONCLUSIONS: The results suggest that alcohol has independent effects on promotion of PDAC associated with fibrosis formed through a stellate cell-independent mechanism and that it further promotes early PDAC and M2 macrophage induction in the context of chronic pancreatitis.

5 Article Evaluating dietary compounds in pancreatic cancer modeling systems. 2013

Mascariñas, Emman / Eibl, Guido / Grippo, Paul J. ·Department of Surgery, Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. ·Methods Mol Biol · Pubmed #23359157.

ABSTRACT: With the establishment of outstanding rodent models of pancreatic neoplasia and cancer, there are now systems available for evaluating the role diet, dietary supplements, and/or therapeutic compounds (which can be delivered in the diet) play in disease suppression. Several outstanding reports, which demonstrate clear inhibition or regression of pancreatic tumors following dietary manipulations, represent a noticeable advancement in the field by allowing for the contribution of diet and natural and synthetic compounds to be identified. The real goal is to provide support for translational components that will provide true chemoprevention to individuals at higher risk for developing pancreatic cancer. In addition, administration of molecules with proven efficacy in an in vivo system will screen likely candidates for future clinical trials. Despite this growing enthusiasm, it is important to note that the mere one-to-one translation of findings in rodent models to clinical outcomes is highly unlikely. Thus, careful consideration must be made to correlate findings in rodents with those in human cells with full disclosure of the subtle but often critical differences between animal models and humans. Additional concern should also be placed on the approaches employed to establish dietary components with real potential in the clinic. This chapter is focused on procedures that provide a systematic design for evaluating dietary compounds in cell culture and animal models to highlight which ones might have the greatest potential in people. The general format for this text is a stepwise use of fairly well-known approaches covered briefly but annotated with certain considerations for dietary studies. These methods include administration of a compound or a diet, measuring the cellular and molecular effects (histology, proliferation, apoptosis, RNA and protein expression, and signaling pathways), measuring the level of certain metabolites, and assessing the stability of active compounds. Though this chapter is divided into in vitro and in vivo sections, it is not an implication as to the order of experiments but an endorsement for utilizing human cells to complement work in a rodent modeling system. The notion that cell culture can provide the basis for further in vivo work is an attractive starting point, though the lack of a response in a single cell type should not necessarily prevent diet studies in rodents. The advantage of cell culture over animal models is the human origin of these cells and the ease and directness of manipulating a single cell type (particularly when exploring mechanism of action in that cell). Of course, the full effect of a diet, diet supplement, or therapeutic can only be wholly appreciated in an intact living organism with similar anatomical and physiological relevance. Thus, both approaches are considered in this chapter as each can provide unique strengths to determining the effectiveness of various dietary compounds or supplements on pancreatic neoplasia and cancer.