Chronic Ethanol Feeding Accelerates Hepatocellular Carcinoma Progression in a Sex-Dependent Manner in a Mouse Model of Hepatocarcinogenesis
Article first published online: 21 OCT 2011
Copyright © 2011 by the Research Society on Alcoholism
Alcoholism: Clinical and Experimental Research
Volume 36, Issue 4, pages 641–653, April 2012
How to Cite
Brandon-Warner, E., Walling, T. L., Schrum, L. W. and McKillop, I. H. (2012), Chronic Ethanol Feeding Accelerates Hepatocellular Carcinoma Progression in a Sex-Dependent Manner in a Mouse Model of Hepatocarcinogenesis. Alcoholism: Clinical and Experimental Research, 36: 641–653. doi: 10.1111/j.1530-0277.2011.01660.x
- Issue published online: 27 MAR 2012
- Article first published online: 21 OCT 2011
- Received for publication March 22, 2011; accepted August 9, 2011.
Fig. S1. (A) Changes in body weight (BW) ofcontrol (C) male mice compared to those maintained on EtOH-DW (40to 48 weeks; E), initiated with DEN (3 weeks; D) or initiated withDEN (3 weeks) followed by EtOH-DW (40 to 48 weeks;D + E). *p < 0.05 48 versus 40 weeks,n = minimum of 8/group. (B) Changes in BW of Cfemale mice compared to E, D, or D + E.n = minimum of 8/group.
Fig. S2. Representative immunoblots of alcoholdehydrogenase and acetaldehyde dehydrogenase expression in liverlysates from control (C) male and female mice compared to thosemaintained on EtOH-DW (E), initiated with DEN (D) or initiated withDEN followed by EtOH-DW (D + E).
Table S1. Pathological scoring criteria employed in blind scoring histology slides after H&E and Picrosirius red staining.
Table S2. Mean pathological scores followingblind scoring for steatosis, necrosis, inflammation and fibrosis incontrol male and female mice (C), and mice maintained on ethanol(E) DEN-initiated (D) or DEN-initiated followed by ethanol(D + E).
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