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Pancreatic Neoplasms: HELP
Articles by Caroline Ei Ne Chou
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Caroline Ei Ne Chou wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Deficiency in hormone-sensitive lipase accelerates the development of pancreatic cancer in conditional KrasG12D mice. 2018

Xu, Mu / Chang, Hui-Hua / Jung, Xiaoman / Moro, Aune / Chou, Caroline Ei Ne / King, Jonathan / Hines, O Joe / Sinnett-Smith, James / Rozengurt, Enrique / Eibl, Guido. ·Departments of Surgery, David Geffen School of Medicine, University of California, Los Angeles, 10833 Le Conte Ave, CHS 72-236, Los Angeles, CA, 90095, USA. · CURE: Digestive Diseases Research Center, University of California at Los Angeles, Los Angeles, USA. · Departments of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA. · Departments of Surgery, David Geffen School of Medicine, University of California, Los Angeles, 10833 Le Conte Ave, CHS 72-236, Los Angeles, CA, 90095, USA. GEibl@mednet.ucla.edu. · CURE: Digestive Diseases Research Center, University of California at Los Angeles, Los Angeles, USA. GEibl@mednet.ucla.edu. ·BMC Cancer · Pubmed #30086728.

ABSTRACT: BACKGROUND: Hormone sensitive lipase (HSL) is a neutral lipase that preferentially catalyzes the hydrolysis of diacylglycerol contributing to triacylglycerol breakdown in the adipose tissue. HSL has been implicated to play a role in tumor cachexia, a debilitating syndrome characterized by progressive loss of adipose tissue. Consequently, pharmacological inhibitors of HSL have been proposed for the treatment of cancer-associated cachexia. In the present study we used the conditional KrasG12D (KC) mouse model of pancreatic ductal adenocarcinoma (PDAC) with a deficiency in HSL to determine the impact of HSL suppression on the development of PDAC. METHODS: KC;Hsl RESULTS: Compared to KC;Hsl CONCLUSIONS: HSL deficiency is associated with adipose tissue and pancreatic inflammation and accelerates PDAC development in the KC mouse model.

2 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 f├╝r Allgemein- und Viszeralchirurgie, Universit├Ątsklinikum 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

3 Article Prostaglandin E2 activates the mTORC1 pathway through an EP4/cAMP/PKA- and EP1/Ca2+-mediated mechanism in the human pancreatic carcinoma cell line PANC-1. 2015

Chang, Hui-Hua / Young, Steven H / Sinnett-Smith, James / Chou, Caroline Ei Ne / Moro, Aune / Hertzer, Kathleen M / Hines, Oscar Joe / Rozengurt, Enrique / Eibl, Guido. ·Department of Surgery, David Geffen School of Medicine at UCLA, Los Angeles, California; and. · Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California. · Department of Surgery, David Geffen School of Medicine at UCLA, Los Angeles, California; and GEibl@mednet.ucla.edu. ·Am J Physiol Cell Physiol · Pubmed #26310818.

ABSTRACT: Obesity, a known risk factor for pancreatic cancer, is associated with inflammation and insulin resistance. Proinflammatory prostaglandin E2 (PGE2) and elevated insulin-like growth factor type 1 (IGF-1), related to insulin resistance, are shown to play critical roles in pancreatic cancer progression. We aimed to explore a potential cross talk between PGE2 signaling and the IGF-1/Akt/mammalian target of rapamycin complex 1 (mTORC1) pathway in pancreatic cancer, which may be a key to unraveling the obesity-cancer link. In PANC-1 human pancreatic cancer cells, we showed that PGE2 stimulated mTORC1 activity independently of Akt, as evaluated by downstream signaling events. Subsequently, using pharmacological and genetic approaches, we demonstrated that PGE2-induced mTORC1 activation is mediated by the EP4/cAMP/PKA pathway, as well as an EP1/Ca(2+)-dependent pathway. The cooperative roles of the two pathways were supported by the maximal inhibition achieved with the combined pharmacological blockade, and the coexistence of highly expressed EP1 (mediating the Ca(2+) response) and EP2 or EP4 (mediating the cAMP/PKA pathway) in PANC-1 cells and in the prostate cancer line PC-3, which also robustly exhibited PGE2-induced mTORC1 activation, as identified from a screen in various cancer cell lines. Importantly, we showed a reinforcing interaction between PGE2 and IGF-1 on mTORC1 signaling, with an increase in IL-23 production as a cellular outcome. Our data reveal a previously unrecognized mechanism of PGE2-stimulated mTORC1 activation mediated by EP4/cAMP/PKA and EP1/Ca(2+) signaling, which may be of great importance in elucidating the promoting effects of obesity in pancreatic cancer. Ultimately, a precise understanding of these molecular links may provide novel targets for efficacious interventions devoid of adverse effects.