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Pancreatic Neoplasms: HELP
Articles by Andrea I. Schmidt
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Andrea Schmidt wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Metformin Decreases the Incidence of Pancreatic Ductal Adenocarcinoma Promoted by Diet-induced Obesity in the Conditional KrasG12D Mouse Model. 2018

Chang, Hui-Hua / Moro, Aune / Chou, Caroline Ei Ne / Dawson, David W / French, Samuel / Schmidt, Andrea I / Sinnett-Smith, James / Hao, Fang / Hines, O Joe / Eibl, Guido / Rozengurt, Enrique. ·Department of Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA. · Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA. · Klinik für Allgemein- und Viszeralchirurgie, Universitätsklinikum Freiburg, Freiburg, Germany. · Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA. · Department of Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA. GEibl@mednet.ucla.edu. ·Sci Rep · Pubmed #29651002.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is a particularly deadly disease. Chronic conditions, including obesity and type-2 diabetes are risk factors, thus making PDAC amenable to preventive strategies. We aimed to characterize the chemo-preventive effects of metformin, a widely used anti-diabetic drug, on PDAC development using the Kras

2 Article Direct growth-inhibitory effects of prostaglandin E2 in pancreatic cancer cells in vitro through an EP4/PKA-mediated mechanism. 2017

Schmidt, Andrea / Sinnett-Smith, James / Young, Steven / Chang, Hui-Hua / Hines, O Joe / Dawson, David W / Rozengurt, Enrique / Eibl, Guido. ·Department of Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA; Klinik für Allgemein- und Viszeralchirurgie, Universitätsklinikum Freiburg, Freiburg, Germany. · Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA. · Department of Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA. · Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA. · Department of Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA. Electronic address: GEibl@mednet.ucla.edu. ·Surgery · Pubmed #28222855.

ABSTRACT: BACKGROUND: There is strong evidence linking inflammation and the development of pancreatic ductal adenocarcinoma. Cyclooxygenase-2 (COX-2) and COX-2-derived PGE METHODS: Human pancreatic ductal adenocarcinoma cell lines, Panc-1 and MIA PaCa-2, were treated with PGE RESULTS: PGE CONCLUSION: Our study provides evidence that PGE

3 Article E-cadherin expression in obesity-associated, Kras-initiated pancreatic ductal adenocarcinoma in mice. 2015

Stark, Alexander P / Chang, Hui-Hua / Jung, Xiaoman / Moro, Aune / Hertzer, Kathleen / Xu, Mu / Schmidt, Andrea / Hines, O Joe / Eibl, Guido. ·Department of Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA. · Department of Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA. Electronic address: Geibl@mednet.ucla.edu. ·Surgery · Pubmed #26297056.

ABSTRACT: BACKGROUND: The epithelial-mesenchymal transition (EMT) is critical in the development of invasive epithelial malignancies. EMT is accelerated by inflammation and results in decreased E-cadherin expression. Diet-induced obesity is an inflammatory state that accelerates pancreatic carcinogenesis; its effect on EMT and E-cadherin expression in the development of pancreatic ductal adenocarcinoma is unclear. METHODS: Conditional Kras(G12D) mice were fed a control diet or a high-fat, high-calorie diet for 3 or 9 months (n = 10 each). Immunohistochemistry with anti-E-cadherin antibody was performed. E-cadherin expression was characterized by staining intensity, location, and proportion of positive cells. In vitro expression of E-cadherin and Slug in primary pancreatic intraepithelial neoplasia (PanIN) and cancer cells was determined by Western blot. RESULTS: The HFCD led to increased weight gain in both 3- (15.8 vs 5.6 g, P < .001) and 9-month (19.8 vs 12.9 g, P = .007) mice. No differences in E-cadherin expression among various stages of preinvasive PanIN lesions were found--regardless of age or diet. In invasive cancer, E-cadherin expression was aberrant, with loss of membranous staining and prominent cytoplasmic staining, associated with strong, cytoplasmic expression of β-catenin. In vitro expression of E-cadherin was greatest in primary PanIN cells, accompanied by absent Slug expression. Cancer cell lines demonstrated significantly decreased E-cadherin expression in the presence of upregulated Slug. CONCLUSION: Despite increased pancreatic inflammation and accelerated carcinogenesis, the high-fat, high-calorie diet did not induce changes in E-cadherin expression in PanIN lesions of all stages. Invasive lesions demonstrated aberrant cytoplasmic E-cadherin staining. Loss of normal membranous localization may reflect a functional loss of E-cadherin.