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Pancreatic Neoplasms: HELP
Articles by Mu Xu
Based on 5 articles published since 2010
(Why 5 articles?)
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Between 2010 and 2020, Mu Xu wrote the following 5 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Obesity and Pancreatic Cancer: Overview of Epidemiology and Potential Prevention by Weight Loss. 2018

Xu, Mu / Jung, Xiaoman / Hines, O Joe / Eibl, Guido / Chen, Yijun. ·From the Department of Surgery, University of California, Los Angeles, Los Angeles, CA. ·Pancreas · Pubmed #29346216.

ABSTRACT: Currently, there are no effective preventive strategies for pancreatic cancer. Obesity has been increasingly recognized as a strong but modifiable risk factor of pancreatic cancer. In this article, we aim to review the literature regarding weight loss on prevention of pancreatic cancer. Epidemiological and laboratory studies have shown that obesity is associated with increased incidence of pancreatic cancer and potentially worse cancer outcome. Whereas the underlying pathomechanisms remain unclear, chronic inflammation, insulin resistance, and altered intestinal microbiota are all implicated in the carcinogenic effect of obesity. Weight loss, especially the durable and significant weight loss after bariatric surgery, has been shown to reduce the risks of multiple cancers and may become a good intervention for pancreatic cancer prevention.

2 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.

3 Article Robust Early Inflammation of the Peripancreatic Visceral Adipose Tissue During Diet-Induced Obesity in the KrasG12D Model of Pancreatic Cancer. 2016

Hertzer, Kathleen M / Xu, Mu / Moro, Aune / Dawson, David W / Du, Lin / Li, Gang / Chang, Hui-Hua / Stark, Alexander P / Jung, Xiaoman / Hines, Oscar Joe / Eibl, Guido. ·From the Departments of *Surgery and †Pathology and Laboratory Medicine,David Geffen School of Medicine at UCLA, Los Angeles, CA; and ‡Department of Biostatistics, Fielding School of Public Health at UCLA, Los Angeles, CA. ·Pancreas · Pubmed #26495779.

ABSTRACT: OBJECTIVES: Obesity increases the incidence of multiple types of cancer. Our previous work has shown that a high-fat, high-calorie diet (HFCD) leads to visceral obesity, pancreatic inflammation, and accelerated pancreatic neoplasia in KrasG12D (KC) mice. In this study, we aimed to investigate the effects of an HFCD on visceral adipose inflammation with emphasis on potential differences between distinct visceral adipose depots. METHODS: We examined the weight and visceral obesity in both wild-type and KC mice on either control diet (CD) or HFCD. After 3 months, mice were killed for histological examination. Multiplex assays were also performed to obtain cytokine profiles between different adipose depots. RESULTS: Both wild-type and KC mice on an HFCD exhibited significantly increased inflammation in the visceral adipose tissue, particularly in the peripancreatic fat (PPF), compared with animals on a CD. This was associated with significantly increased inflammation in the pancreas. Cytokine profiles were different between visceral adipose depots and between mice on the HFCD and CD. CONCLUSIONS: Our results clearly demonstrate that an HFCD leads to obesity and inflammation in the visceral adipose tissue, particularly the PPF. These data suggest that obesity-associated inflammation in PPF may accelerate pancreatic neoplasia in KC mice.

4 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.

5 Article Long-term Survival After Pancreatic Cancer: Hope Has Arrived. 2015

Xu, Mu / Hines, O Joe. ·Department of Surgery, David Geffen School of Medicine, University of California, Los Angeles. ·JAMA Surg · Pubmed #26061772.

ABSTRACT: -- No abstract --