Cost-effectiveness of upcoming treatments for hepatitis C: we need to get the models right.

نویسندگان

  • Emmanuel A Tsochatzis
  • Catriona Crossan
  • Louise Longworth
چکیده

[1] Huang Q, Tan Y, Yin P, Ye G, Gao P, Lu X, et al. Metabolic characterization of hepatocellular carcinoma using nontargeted tissue metabolomics. Cancer Res 2013;73:4992–5002. [2] Beyoglu D, Imbeaud S, Maurhofer O, Bioulac-Sage P, Zucman-Rossi J, Dufour JF, et al. Tissue metabolomics of hepatocellular carcinoma: tumor energy metabolism and the role of transcriptomic classification. Hepatology 2013;58:229–238. [3] Nishikawa T, Bellance N, Damm A, Bing H, Zhu Z, Handa K, et al. A switch in the source of ATP production and a loss in capacity to perform glycolysis are hallmarks of hepatocyte failure in advance liver disease. J Hepatol 2014;60:1203–1211. [4] Bonuccelli G, Whitaker-Menezes D, Castello-Cros R, Pavlides S, Pestell RG, Fatatis A, et al. The reverse Warburg effect: glycolysis inhibitors prevent the tumor promoting effects of caveolin-1 deficient cancer associated fibroblasts. Cell Cycle 2010;9:1960–1971. [5] Migneco G, Whitaker-Menezes D, Chiavarina B, Castello-Cros R, Pavlides S, Pestell RG, et al. Glycolytic cancer associated fibroblasts promote breast cancer tumor growth, without a measurable increase in angiogenesis: evidence for stromal-epithelial metabolic coupling. Cell Cycle 2010;9:2412–2422. [6] Chan IS, Guy CD, Chen Y, Lu J, Swiderska-Syn M, Michelotti GA, et al. Paracrine hedgehog signaling drives metabolic changes in hepatocellular carcinoma. Cancer Res 2012;72:6344–6350.

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عنوان ژورنال:
  • Journal of hepatology

دوره 61 2  شماره 

صفحات  -

تاریخ انتشار 2014