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Marija Trajkovic-Arsic, Evdokia Kalideris and Jens T Siveke

The role of the insulin and insulin-like growth factor system in pancreatic cancer The human pancreas is a complex exocrine and endocrine gland with two vital functions: production of digestive juices and regulation of glucose metabolism. Its

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He-jun Zhao, Xia Jiang, Li-juan Hu, Lei Yang, Lian-dong Deng, Ya-ping Wang and Zhi-peng Ren

Introduction Pancreatic cancer is closely related to diabetes mellitus. Diabetes mellitus is not only a risk factor for pancreatic cancer, but it is also one of the clinical manifestations of pancreatic cancer ( Everhart & Wright 1995 , Chari

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Xiaoxia Che, Fangfang Jian, Chen Chen, Chang Liu, Gedan Liu and Weiwei Feng

was related to the loss of miR-148b in the CAF-derived exosomes. In addition, bone marrow mesenchymal stem cell (BMSC)-derived exosomal miR-126-3p was proven to inhibit pancreatic cancer development by targeting ADAM9 ( Wu et al. 2019 ). Lazar

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Soojin Kim, Daksh Thaper, Samir Bidnur, Paul Toren, Shusuke Akamatsu, Jennifer L Bishop, Colin Colins, Sepideh Vahid and Amina Zoubeidi

questioned whether PEG10 is involved in regulating proliferation of cells. Previous studies have shown that PEG10 plays a role in breast and pancreatic cancer cell proliferation ( Li et al. 2016 , Peng et al. 2017 ). More importantly, Akamatsu et al

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Chanchal Gupta and Kulbhushan Tikoo

pancreatic cancers ( Czyzyk & Szczepanik 2000 ). It has been reported that up to 16% of older breast cancer patients also suffer from diabetes ( Coebergh et al . 1999 ). Many epidemiological studies suggest that women with diabetes have increased risk of

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Custodia García-Jiménez, Jose Manuel García-Martínez, Ana Chocarro-Calvo and Antonio De la Vieja

expression of critical genes such as E2F and cyclins A and E ( Masur et al . 2011 ). Proliferation is also induced through increased expression of epidermal growth factor (EGF) and enhanced EGF receptor signaling in pancreatic cancer cells ( Li et al

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E Mato, C González, A Moral, J I Pérez, O Bell, E Lerma and A de Leiva

for pancreatic cancer ( Arumugam et al . 2009 , Wellner et al . 2009 , Palena et al . 2011 ). It was of interest to note that this effect could be reverted when the ZEB1 gene was knocked down in the selected cells. In these selected cells, the

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Ian L P Beales and Olorunseun O Ogunwobi

cancer cell lines in culture ( Iwase et al . 1997 , Stepan et al . 1999 , Haigh et al . 2003 ), inhibits apoptosis in pancreatic cancer cells ( Todisco et al . 2001 ), and transgenic over-expression of gastrin induces gastric atrophy and promotes

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Xilin Yang, Zezhang Tao, Zhanyong Zhu, Hua Liao, Yueqiang Zhao and Huajun Fan

be related to cancer development. For example, Slc38a1 can induce the migration of human pancreatic cancer cells ( Xie et al . 2013 ). Slc38a1 was found significantly elevated in human hepatocellular carcinoma and preneoplastic liver tissues ( Kondoh

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Jandee Lee, Mi-Youn Seol, Seonhyang Jeong, Hyeong Ju Kwon, Cho Rok Lee, Cheol Ryong Ku, Sang-Wook Kang, Jong Ju Jeong, Dong Yeob Shin, Kee-Hyun Nam, Eun Jig Lee, Woong Youn Chung and Young Suk Jo

expression of KSR1 and KSR2 was associated with coordinated upregulation of Notch signaling. Previous studies using pancreatic cancer cells suggested that the MAPK pathway is able to promote Notch signaling activation by γ-secretase complex