Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Pancreatic Neoplasms: HELP
Articles by Morgan R. Barron
Based on 7 articles published since 2010
(Why 7 articles?)
||||

Between 2010 and 2020, M. Barron wrote the following 7 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Clinical Trial Does PET with CT Have Clinical Utility in the Management of Patients with Intraductal Papillary Mucinous Neoplasm? 2015

Roch, Alexandra M / Barron, Morgan R / Tann, Mark / Sandrasegar, Kumar / Hannaford, Katheryn N / Ceppa, Eugene P / House, Michael G / Zyromski, Nicholas J / Nakeeb, Attila / Schmidt, C Maximillian. ·Department of Surgery, Indiana University School of Medicine, Indianapolis, IN. · Department of Radiology and Imaging Science, Indiana University School of Medicine, Indianapolis, IN. · Department of Surgery, Indiana University School of Medicine, Indianapolis, IN. Electronic address: maxschmi@iupui.edu. ·J Am Coll Surg · Pubmed #26095551.

ABSTRACT: BACKGROUND: Intraductal papillary mucinous neoplasms (IPMNs) are well-established pancreatic precancerous lesions. Indications for resection are outlined in the 2012 International Consensus Guidelines (ICG). Because of the low specificity of the ICG, many patients will undergo potentially unnecessary surgery for nonmalignant IPMNs. Several retrospective studies have reported that positron emission tomography (PET) with CT (PET/CT) is highly sensitive and specific in detecting malignant IPMNs. We hypothesized that PET/CT complements the ICG in identification of malignant IPMNs. STUDY DESIGN: From 2009 to 2013, patients with a suspected clinical or cytopathologic diagnosis of IPMN were prospectively enrolled in a clinical trial at a single center. Results of preoperative PET/CT on determination of IPMN malignancy (ie, high-grade dysplastic and invasive) was compared with surgical pathology. PET/CT uptake was considered increased if the standardized uptake value was ≥3. RESULTS: Of the 67 patients enrolled, 50 patients met all inclusion criteria. Increased PET/CT uptake was associated with significantly more malignant and invasive IPMNs (80% vs 13%; p < 0.0001 and 40% vs 3%; p = 0.004). When patients were divided into branch duct and main duct IPMNs, increased PET/CT uptake was also associated with more malignancy (60% vs 0%; p = 0.006 for branch duct IPMN and 100% vs 23%; p = 0.003 for main duct IPMN). Patients with ICG criteria (eg, worrisome features and high-risk stigmata) and increased PET/CT uptake had more malignant and invasive IPMNs than patients with ICG criteria, but no increased uptake (78% vs 17%; p = 0.001 and 33% vs 3%; p = 0.03). The sensitivity and specificity of the ICG criteria for detecting malignancy were 92% and 27%, respectively, and PET/CT was less sensitive (62%) but more specific (95%). When PET/CT was added to ICG criteria, the association resulted in 78% sensitivity and 100% specificity. CONCLUSIONS: The addition of PET/CT to preoperative workup improves the performance of the ICG for predicting malignant risk in patients with IPMN.

2 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

3 Article Does preoperative cross-sectional imaging accurately predict main duct involvement in intraductal papillary mucinous neoplasm? 2014

Barron, M R / Roch, A M / Waters, J A / Parikh, J A / DeWitt, J M / Al-Haddad, M A / Ceppa, E P / House, M G / Zyromski, N J / Nakeeb, A / Pitt, H A / Schmidt, C Max. ·Department of Surgery, Indiana University School of Medicine, Indianapolis, IN, USA. ·J Gastrointest Surg · Pubmed #24402606.

ABSTRACT: Main pancreatic duct (MPD) involvement is a well-demonstrated risk factor for malignancy in intraductal papillary mucinous neoplasm (IPMN). Preoperative radiographic determination of IPMN type is heavily relied upon in oncologic risk stratification. We hypothesized that radiographic assessment of MPD involvement in IPMN is an accurate predictor of pathological MPD involvement. Data regarding all patients undergoing resection for IPMN at a single academic institution between 1992 and 2012 were gathered prospectively. Retrospective analysis of imaging and pathologic data was undertaken. Preoperative classification of IPMN type was based on cross-sectional imaging (MRI/magnetic resonance cholangiopancreatography (MRCP) and/or CT). Three hundred sixty-two patients underwent resection for IPMN. Of these, 334 had complete data for analysis. Of 164 suspected branch duct (BD) IPMN, 34 (20.7%) demonstrated MPD involvement on final pathology. Of 170 patients with suspicion of MPD involvement, 50 (29.4%) demonstrated no MPD involvement. Of 34 patients with suspected BD-IPMN who were found to have MPD involvement on pathology, 10 (29.4%) had invasive carcinoma. Alternatively, 2/50 (4%) of the patients with suspected MPD involvement who ultimately had isolated BD-IPMN demonstrated invasive carcinoma. Preoperative radiographic IPMN type did not correlate with final pathology in 25% of the patients. In addition, risk of invasive carcinoma correlates with pathologic presence of MPD involvement.

4 Article MT1-MMP cooperates with Kras(G12D) to promote pancreatic fibrosis through increased TGF-β signaling. 2011

Krantz, Seth B / Shields, Mario A / Dangi-Garimella, Surabhi / Cheon, Eric C / Barron, Morgan R / Hwang, Rosa F / Rao, M Sambasiva / Grippo, Paul J / Bentrem, David J / Munshi, Hidayatullah G. ·Department of Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. ·Mol Cancer Res · Pubmed #21856775.

ABSTRACT: Pancreatic cancer is associated with a pronounced fibrotic reaction that was recently shown to limit delivery of chemotherapy. To identify potential therapeutic targets to overcome this fibrosis, we examined the interplay between fibrosis and the key proteinase membrane type 1-matrix metalloproteinase (MT1-MMP, MMP-14), which is required for growth and invasion in the collagen-rich microenvironment. In this article, we show that compared with control mice (Kras(+)/MT1-MMP(-)) that express an activating Kras(G12D) mutation necessary for pancreatic cancer development, littermate mice that express both MT1-MMP and Kras(G12D) (Kras(+)/MT1-MMP(+)) developed a greater number of large, dysplastic mucin-containing papillary lesions. These lesions were associated with a significant amount of surrounding fibrosis, increased α-smooth muscle actin (+) cells in the stroma, indicative of activated myofibroblasts, and increased Smad2 phosphorylation. To further understand how MT1-MMP promotes fibrosis, we established an in vitro model to examine the effect of expressing MT1-MMP in pancreatic ductal adenocarcinoma (PDAC) cells on stellate cell collagen deposition. Conditioned media from MT1-MMP-expressing PDAC cells grown in three-dimensional collagen enhanced Smad2 nuclear translocation, promoted Smad2 phosphorylation, and increased collagen production by stellate cells. Inhibiting the activity or expression of the TGF-β type I receptor in stellate cells attenuated MT1-MMP conditioned medium-induced collagen expression by stellate cells. In addition, a function-blocking anti-TGF-β antibody also inhibited MT1-MMP conditioned medium-induced collagen expression in stellate cells. Overall, we show that the bona fide collagenase MT1-MMP paradoxically contributes to fibrosis by increasing TGF-β signaling and that targeting MT1-MMP may thus help to mitigate fibrosis.

5 Article Visualization of mouse pancreas architecture using MR microscopy. 2011

Grippo, Paul J / Venkatasubramanian, Palamadai N / Knop, Richard H / Heiferman, Daniel M / Iordanescu, Gheorghe / Melstrom, Laleh G / Adrian, Kevin / Barron, Morgan R / Bentrem, David J / Wyrwicz, Alice M. ·Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA. p-grippo@northwestern.edu ·Am J Pathol · Pubmed #21683673.

ABSTRACT: Pancreatic diseases, which include diabetes, pancreatitis, and pancreatic cancer, are often difficult to detect and/or stage, contributing to a reduced quality of life and lifespan for patients. Thus, there is need for a technology that can visualize tissue changes in the pancreas, improve understanding of disease progression, and facilitate earlier detection in the human population. Because of low spatial resolution, current clinical magnetic resonance imaging (MRI) at low field strength has yet to fully visualize the exocrine, endocrine, vascular, and stromal components of the pancreas. We used high field strength magnetic resonance microscopy (μMRI) to image mouse pancreas ex vivo without contrast agents at high spatial resolution. We analyzed the resulting high-resolution images using volume rendering to resolve components in the pancreas, including acini, islets, blood vessels, and extracellular matrix. Locations and dimensions of pancreatic components as seen in three-dimensional μMRI were compared with histological images, and good correspondence was found. Future longitudinal studies could expand on the use of in vivo μMRI in mouse models of pancreatic diseases. Capturing three-dimensional structural changes through μMRI could help to identify early cellular and tissue changes associated with pancreatic disease, serving as a mode of improved detection in the clinic for endocrine and exocrine pathologies.

6 Article Three-dimensional collagen I promotes gemcitabine resistance in pancreatic cancer through MT1-MMP-mediated expression of HMGA2. 2011

Dangi-Garimella, Surabhi / Krantz, Seth B / Barron, Morgan R / Shields, Mario A / Heiferman, Michael J / Grippo, Paul J / Bentrem, David J / Munshi, Hidayatullah G. ·Division of Hematology/Oncology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA. s-dangi-garimella@northwestern.edu ·Cancer Res · Pubmed #21148071.

ABSTRACT: One of the hallmarks of human pancreatic ductal adenocarcinoma (PDAC) is its pronounced type I collagen-rich fibrotic reaction. Although recent reports have shown that the fibrotic reaction can limit the efficacy of gemcitabine chemotherapy, the underlying mechanisms remain poorly understood. In this article, we show that the type I collagen allows PDAC cells to override checkpoint arrest induced by gemcitabine. Relative to cells grown on tissue culture plastic, PDAC cells grown in 3-dimensional collagen microenvironment have minimal Chk1 phosphorylation and continue to proliferate in the presence of gemcitabine. Collagen increases membrane type 1 matrix metalloproteinase (MT1-MMP)-dependent ERK1/2 phosphorylation to limit the effect of gemcitabine. Collagen also increases MT1-MMP-dependent high mobility group A2 (HMGA2) expression, a nonhistone DNA-binding nuclear protein involved in chromatin remodeling and gene transcription, to attenuate the effect of gemcitabine. Overexpression of MT1-MMP in the collagen microenvironment increases ERK1/2 phosphorylation and HMGA2 expression, and thereby further attenuates gemcitabine-induced checkpoint arrest. MT1-MMP also allows PDAC cells to continue to proliferate in the presence of gemcitabine in a xenograft mouse model. Clinically, human tumors with increased MT1-MMP show increased HMGA2 expression. Overall, our data show that collagen upregulation of MT1-MMP contributes to gemcitabine resistance in vitro and in a xenograft mouse model, and suggest that targeting MT1-MMP could be a novel approach to sensitize pancreatic tumors to gemcitabine.

7 Article Alteration of strain background and a high omega-6 fat diet induces earlier onset of pancreatic neoplasia in EL-Kras transgenic mice. 2011

Cheon, Eric C / Strouch, Matthew J / Barron, Morgan R / Ding, Yongzeng / Melstrom, Laleh G / Krantz, Seth B / Mullapudi, Bhargava / Adrian, Kevin / Rao, Sambasiva / Adrian, Thomas E / Bentrem, David J / Grippo, Paul J. ·Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. ·Int J Cancer · Pubmed #20725998.

ABSTRACT: Diets containing omega-6 (ω-6) fat have been associated with increased tumor development in carcinogen-induced pancreatic cancer models. However, the effects of ω-6 fatty acids and background strain on the development of genetically-induced pancreatic neoplasia is unknown. We assessed the effects of a diet rich in ω-6 fat on the development of pancreatic neoplasia in elastase (EL)-Kras(G12D) (EL-Kras) mice in two different backgrounds. EL-Kras FVB mice were crossed to C57BL/6 (B6) mice to produce EL-Kras FVB6 F1 (or EL-Kras F1) and EL-Kras B6 congenic mice. Age-matched EL-Kras mice from each strain were compared to one another on a standard chow. Two cohorts of EL-Kras FVB and EL-Kras F1 mice were fed a 23% corn oil diet and compared to age-matched mice fed a standard chow. Pancreata were scored for incidence, frequency, and size of neoplastic lesions, and stained for the presence of mast cells to evaluate changes in the inflammatory milieu secondary to a high fat diet. EL-Kras F1 mice had increased incidence, frequency, and size of pancreatic neoplasia compared to EL-Kras FVB mice. The frequency and size of neoplastic lesions and the weight and pancreatic mast cell densities in EL-Kras F1 mice were increased in mice fed a high ω-6 fatty acid diet compared to mice fed a standard chow. We herein introduce the EL-Kras B6 mouse model which presents with increased frequency of pancreatic neoplasia compared to EL-Kras F1 mice. The phenotype in EL-Kras F1 and FVB mice is promoted by a diet rich in ω-6 fatty acid.