[1] Siegel RL, Miller KD, Jemal A. Cancer statistics, 2020. CA Cancer J Clin. 2020; 70(1): 7-30.
[2] Chen H, Qin S, Wang M, et al. Association between cholesterol intake and pancreatic cancer risk: evidence from a meta-analysis. Sci Rep. 2015; 5: 8243.
[3] Wang J, Wang WJ, Zhai L, et al. Association of cholesterol with risk of pancreatic cancer: a meta-analysis. World J Gastroenterol. 2015; 21(12): 3711-3719.
[4] Hanahan, D.; Weinberg, R.A. Hallmark of cancer: The next generation. Cell. 2011; 144(5): 646-674.
[5] Qin C, Yang G, Yang JS, et al. Metabolism of Pancreatic Cancer: Paving the Way to Better Anticancer Strategies. Mol Cancer. 2020; 19(1): 50.
[6] Philip B, Roland CL, Daniluk J, et al. A high-fat diet activates oncogenic Kras and COX2 to induce development of pancreatic ductal adenocarcinoma in mice. Gastroenterology. 2013; 145(6): 1449-1458.
[7] Zhong S, Li L, Zhang YL, et al. Acetaldehyde dehydrogenase 2 interaction with LDLR and AMPK regulate foam formation. J Clin Invest. 2019; 129(1): 252-267.
[8] Xia YR, Klisak I, Sparkes RS, et al. Localization of the gene for high-density lipoprotein binding protein (HDLBP) to human chromosome 2q37. Genomics. 1993; 16(2): 524-525.
[9] Romain Cohen, Cindy Neuzillet, Annemilai Tijeras-Raballand, et al. Targeting cancer cell metabolism in pancreatic adenocarcinoma. Oncotarget. 2015; 6(19): 16832-16847.
[10] Louie SM, Roberts LS, Mulvihill MM, et al. Cancer cells incorporate and remodel exogenous palmitate into structural and oncogenic signaling lipids. Biochim Biophys Acta 2013; 1831: 1566-1572.
[11] Kuemmerle NB, Rysman E, Lombardo PS, et al. Lipoprotein lipase links dietary fat to solid tumor cell proliferation. Mol Cancer Ther. 2011; 10: 427-436.
[12] Provenzano PP, Cuevas C, Chang AE, et al. Enzymatic targeting of the stroma ablates physical barriers to treatment of pancreatic ductal adenocarcinoma. Cancer Cell. 2012; 21(3):418-429.
[13] Hidalgo M. Pancreatic cancer. N Engl J Med. 2010; 362(17):1605-1617.
[14] Tadros S, Shukla SK, King RJ, et al. De Novo Lipid Synthesis Facilitates Gemcitabine Resistance through Enoplasmic Reticulum Stress in Pancreatic Cancer. Cancer Res. 2017; 77(20): 5503-5517.
[15] Guillaumond F, Bidaut G, Ouaissi M, et al. Cholesterol uptake disruption, in association with chemotherapy, is a promising combined metabolic therapy for pancreatic adenocarcinoma. Proc Natl Acad Sci U S A. 2015; 112: 2473-2478.
[16] Horton JD, Goldstein JL, Brown MS, et al. SREBPs: Activators of the complete program of cholesterol and fatty acid synthesis in the liver. J Clin Investig. 2002; 109: 1125-1131.
[17] Yoshiaki Sunami, Artur Rebelo and Jorg Kleeff. Lipid Metabolism and Lipid Droplets in Pancreatic Cancer and Stellate Cells. Cancers (Basel). 2017; 10(1).
[18] Wen LY, Ling W, Wen QH, et al. Vigilin is overexpressed in hepatocellular carcinoma and is required for HCC cell proliferation and tumor growth. Oncol Rep. 2014; 31(5): 2328-2334.
[19] Mistafa O, Stenius U. Statins inhibit Akt/PKB signaling via P2X7 receptor in pancreatic cancer cells. Biochem Pharmacol. 2009; 78: 1115-1126.
[20] Liao J, Chung YT, Yang AL, et al. Atorvastatin inhibits pancreatic carcinogenesis and increases survival in LSL-KrasG12D-LSL-Trp53R172H-Pdx1-Cre mice. Mol Carcinog. 2013; 52: 739-750.
[21] Huang BZ, Chang JI, Li E, et al. Influence of statins and cholesterol on mortality among patients with pancreatic cancer. J Natl Cancer Inst. 2017; 109: 2.
[22] Osmak M. Statins and cancer: current and future prospects. Cancer Lett 2012; 324: 1-12.
[23] Tadros S, Shukla SK, King RJ, et al. De novo lipid synthesis facilitates gemcitabine resistance through endoplasmic reticulum stress in pancreatic cancer. Cancer Res. 2017; 77: 5503-5517.