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. Author manuscript; available in PMC: 2023 Mar 1.
Published in final edited form as: Cancer Prev Res (Phila). 2022 Sep 1;15(9):581–594. doi: 10.1158/1940-6207.CAPR-22-0113

Figure 3.

Figure 3.

The protumor effects of obesity are reversed by weight loss via calorie restriction, but not a nonrestricted low-fat diet. (A) Tumor cross-sectional area (mm2) was calculated following biweekly palpations and is shown here over time for all control, obese, nonrestricted low-fat diet (LFD), low-fat calorie-restricted (LFCR), Mediterranean-style calorie-restricted (MCR), and intermittent calorie-restricted (ICR) mice. The ICR group is not visible on the graph because its growth curve is almost identical to the LFCR growth curve. (B) Tumor weight was measured ex vivo at the study endpoint in all mice. (C) Incidence of lung metastasis in each diet group was determined by examining the lungs of 6 mice/group for micrometastases. (D) Lung metastasis burden for each mouse was calculated as the percentage of lung sections positive for at least 1 micrometastasis, 6 mice/group assessed. (E) Tumor expression of genes related to the epithelial-to-mesenchymal transition were measured by quantitative RT-PCR array in all groups except control (n=3–5 mice/group). Expression levels in all 4 weight loss groups, relative to the obese group, of the 37 genes that differed between all CR mice combined and the obese group, the nonrestricted LFD group, or both (P<0.05) are shown. *P<0.05, ***P<0.001 relative to the obese mice. #P<0.05, ##P<0.01, ###P<0.001, relative to the nonrestricted LFD mice.