Acceleration of papilloma growth in mice fed high‐fat diets during promotion of two‐stage skin carcinogenesis

Birt, Diane F.; Pelling, Jill C.; Tibbels, Michelle G.; Schweickert, Lori A.

doi:10.1080/01635588909514014

Cited by 12 publications

(7 citation statements)

References 7 publications

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“…In those investigations we observed that the higher ratios of dietary corn oil to coconut decreased tumor incidence (1,2). Our studies differ from those of other researchers, where the higher amount of fat increased tumor incidence (25). These differences can be attributed to the protocol design.…”

Section: Discussioncontrasting

confidence: 74%

Comparison of ultraviolet light‐induced skin carcinogenesis and ornithine decarboxylase activity in Sencar and Hairless SKH‐1 mice fed a constant level of dietary lipid varying in corn and coconut oil

Berton

Fischer

Conti

et al. 1996

Nutrition and Cancer

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To investigate the effect of various levels of corn oil and coconut oil on ultraviolet (UV) light-induced skin tumorigenesis and ornithine decarboxylase (ODC) activity, Sencar and SKH-1 mice were fed one of three 15% (weight) fat semipurified diets containing three ratios of corn oil to coconut oil: 1.0%:14.0%, 7.9%:7.1%, and 15.0%:0.0% in Diets A, B, and C, respectively. Groups of 30 Sencar and SKH-1 mice were fed one of the diets for three weeks before UV irradiation; then both strains were UV irradiated with an initial dose of 90 mJ/cm2. The dose was given three times a week and increased 25% each week. For Sencar mice (irradiated 33 wks for a total dose of 48 J/cm2), tumor incidence reached a maximum of 60%, 60%, and 53% for Diets A, B, and C, respectively, with an overall average of one to two tumors per tumor-bearing animal. For the SKH-1 mice (irradiated 29 wks for a total dose of 18 J/cm2), all diet groups reached 100% incidence by 29 weeks, with approximately 12 tumors per tumor-bearing mouse. No significant effect of dietary corn oil/coconut oil was found for tumor latency, incidence, or yield in either strain. The effect of increasing corn oil on epidermal ODC activity in chronically UV-irradiated Sencar and SKH-1 mice was assessed. Three groups of mice from each strain were fed one of the experimental diets and UV irradiated for six weeks. Sencar mice showed no increase in ODC activity until six weeks of treatment, when the levels of ODC activity in the UV-irradiated mice fed Diet A were significantly higher than those in mice fed Diet B or Diet C: 1.27, 0.55, and 0.52 nmol/mg protein/hr, respectively. In the SKH-1 mice, ODC activity was increased by the first week of UV treatment, and by three weeks of treatment a dietary effect was observed; ODC activity was significantly higher in mice fed Diet C (0.70 nmol/mg protein/hr) than in mice fed Diet A (0.18 nmol/mg protein/hr). Although there was no significant effect of dietary corn oil/coconut oil on UV-induced tumor incidence, the data indicate that chronically UV-irradiated hairless SKH-1 mice are more susceptible to UV-induced skin carcinogenesis than Sencar mice and that this susceptibility is correlated with increased in ODC activity, a parameter of cell proliferation.

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Section: Discussioncontrasting

confidence: 74%

Comparison of ultraviolet light‐induced skin carcinogenesis and ornithine decarboxylase activity in Sencar and Hairless SKH‐1 mice fed a constant level of dietary lipid varying in corn and coconut oil

Berton

Fischer

Conti

et al. 1996

Nutrition and Cancer

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“…ob/ob mice lack leptin and are therefore obese. As obesity is linked to increased cancer susceptibility, including skin cancer (6,11,14), it could have disguised the beneficial effect of the lack of leptin in ob/ob mice. We therefore tested whether lipodystrophic ZIP mice (28,29), for which we confirmed both leptin levels below 5% of those in controls (Table 1) and the lack of visible adipose tissue, would be less susceptible to skin carcinogenesis than their normal littermates.…”

Section: Resultsmentioning

confidence: 99%

“…Skin carcinogenesis is enhanced in genetically obese Ay mice (11,14) and in normal mice made obese by feeding a high fat diet (6). Here, we tested the hypothesis that leptin, which is increased in obesity (22)(23)(24)(25) and which has a direct stimulatory effect on skin cells in vivo (39,40) and in vitro (40-42), was responsible for the effects of obesity on the susceptibility to skin carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

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Susceptibility to Induced and Spontaneous Carcinogenesis Is Increased in Fatless A-ZIP/F-1 but not in Obese ob/ob Mice

Ablamunits

Cohen²,

Brazee³

et al. 2006

Cancer Research

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Obesity is typically associated with increased tumor susceptibility, whereas caloric restriction, a regimen resulting in leanness, inhibits carcinogenesis. The link between adiposity and malignancies suggests that adipose tissue may influence carcinogenesis. An adipose tissue hormone, leptin, could be procarcinogenic because it stimulates proliferation in various tissues and tumor cell lines. Leptin may contribute to the correlation between adiposity and malignancies as its levels are usually increased in obese subjects and reduced by caloric restriction. We hypothesized that leptin deficiency, despite obesity, would inhibit carcinogenesis in leptin-null ob/ob mice and tested this hypothesis in two models: (a) two-stage skin carcinogenesis initiated by 7,12-dimethylbenz(a)anthracene and promoted by phorbol 12-myristate 13-acetate (PMA) and (b) p53 deficiency. Contrary to a typical association between obesity and enhanced carcinogenesis, obese ob/ob mice developed induced skin papillomas and spontaneous p53-deficient malignancies, mostly lymphomas, similarly to their lean littermates. Surprisingly, lipodystrophic (ZIP) mice that had very little both adipose tissue and leptin were highly susceptible to carcinogenesis. Hyperphagia, hyperinsulinemia, and hyperglycemia are unlikely to have contributed significantly to the enhancement of carcinogenesis in ZIP mice because similarly hyperphagic, hyperinsulinemic, and hyperglycemic ob/ob mice had normal susceptibility to carcinogenesis. Our data suggest that, in contrast to a well-known correlation between obesity and cancer, the direct effect of adipose tissue may rather be protective. (Cancer Res 2006; 66(17): 8897-902)

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“…The association between DIO and cancer has been shown in multiple tissues and cell types, including breast, colon, pancreas, liver, lung, and leukocytes 10–14 . Studies have been conducted using the two‐stage skin carcinogenesis model to determine the impact of a high‐fat diet on epithelial carcinogenesis 8,15,16 . Administration of an ad libitum high‐fat diet (46% vs. 11% fat) led to significant differences in body weight and more rapid development of skin tumors; however, no differences in the number of tumors were reported between these diet groups 16 .…”

Section: Cr Diet‐induced Obesity and Cancermentioning

confidence: 99%

Dietary energy balance modulation of epithelial carcinogenesis: a role for IGF‐1 receptor signaling and crosstalk

Moore

Checkley

DiGiovanni

2011

Annals of the New York Academy of Sciences

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Obesity affects more than one third of the U.S. population and is associated with increased risk and/or disease severity for several chronic diseases, including cancer. In contrast, calorie restriction (CR) consistently inhibits cancer across species and cancer types. Differential effects on globally active circulatory proteins, particularly insulin-like growth factor-1 (IGF-1), provide a plausible mechanistic explanation for the energy balance-cancer link. Diet-induced changes in circulating IGF-1 modulate IGF-1R/EGFR activation and downstream signaling to Akt and mTOR. These dietary energy balance effects on signaling ultimately modulate the levels and/or activity of cell cycle regulatory proteins, regulating proliferation, and modulating susceptibility to tumor development. Selective targeting of mTORC1 potently inhibits tumorigenesis in several model systems producing CR mimetic effects. Targeting this and other pathways modulated by dietary energy balance may lead to the development of strategies for cancer chemoprevention and for reversing the effects of obesity on cancer development and progression.

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Acceleration of papilloma growth in mice fed high‐fat diets during promotion of two‐stage skin carcinogenesis

Cited by 12 publications

References 7 publications

Comparison of ultraviolet light‐induced skin carcinogenesis and ornithine decarboxylase activity in Sencar and Hairless SKH‐1 mice fed a constant level of dietary lipid varying in corn and coconut oil

Comparison of ultraviolet light‐induced skin carcinogenesis and ornithine decarboxylase activity in Sencar and Hairless SKH‐1 mice fed a constant level of dietary lipid varying in corn and coconut oil

Susceptibility to Induced and Spontaneous Carcinogenesis Is Increased in Fatless A-ZIP/F-1 but not in Obese ob/ob Mice

Dietary energy balance modulation of epithelial carcinogenesis: a role for IGF‐1 receptor signaling and crosstalk

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