Effect of high fat diet on body weight and mammary tumor latency in MMTV-TGF-α mice

Cleary, Margot P.; Grande, Joseph P.; Maihle, Nita J.

doi:10.1038/sj.ijo.0802664

Cited by 50 publications

(44 citation statements)

References 44 publications

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“…These studies may suggest that the mammary gland microenvironment can affect cellular growth. In agreement with this hypothesis, studies by Cleary et al 44 have demonstrated that a highfat diet and increased adiposity may accelerate tumor formation in a mouse model of breast cancer.…”

Section: Diet Cholesterol and Cancermentioning

confidence: 57%

Role of Cholesterol in the Development and Progression of Breast Cancer

Llaverı́as

Danilo

Mercier

et al. 2011

The American Journal of Pathology

270

237

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Breast cancer is the most commonly occurring cancer in women in Western societies. 1 It is estimated that 207,090 new cases will be diagnosed and that in the United States, 39,840 women will die of the disease in 2010 (American Cancer Society, Cancer Facts & Figures 2010, http://www. cancer.org/Research/cancer-facts-and-figures-2010, last accessed November 15, 2010. Interestingly, the incidence is about 5 times higher in Western countries than in developing countries. 2 Moreover, relocation and migrational studies have demonstrated that migration from a region with low incidence to a region with high incidence increases breast cancer incidence in the immigrant population. 3 These observations suggest a strong environmental influence on breast cancer development.Diet and obesity are now considered important risk factors for cancer development. 4,5 However, despite major modifications of its metabolism during obesity development and its function in tissue pathogenesis, little is known about the metabolism and role of plasma cholesterol in cancer development. Epidemiological studies have demonstrated that patients with cancer have abnormal levels of high-density lipoprotein (HDL)-cholesterol and low-density lipoprotein (LDL)-cholesterol, 6,7 which are the major lipoprotein carriers of cholesterol in human plasma. In addition, numerous studies have established that transformed cells and tumors exhibit abnormal regulation of several genes that are under the control of cholesterol. The products of these genes include the LDL receptor (LDL-R), hydroxy-methyl-glutaryl coenzyme A reductase (HMG-CoA Reductase), and their regulators, the sterol regulatory element binding proteins. 8 -13 As a consequence, these genes are dysregulated at the transcriptional level during tumorigenesis. These data suggest that transformed cells may require or utilize more cholesterol than normal cells, and this may be associated with their increased rate of proliferation. More recent studies have implicated HDL during tumor formation in breast cancer. 14 -16 However, their precise function remains controversial. The present study was performed to test the hypothesis that dietary cholesterol and plasma cholesterol levels have an important role in the regulation of breast cancer onset and progression.

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Section: Diet Cholesterol and Cancermentioning

confidence: 57%

Role of Cholesterol in the Development and Progression of Breast Cancer

Llaverı́as

Danilo

Mercier

et al. 2011

The American Journal of Pathology

270

237

View full text Add to dashboard Cite

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“…In both cases these obese mice did not develop MT while their lean counterparts had tumor incidence rates comparable to that of the originally described MMTV-TGF-a mice [33]. However, when this transgenic mouse strain was subjected to dietary-induced obesity, mammary tumor latency was shortened for these hormone-responsive tumors [34]. Interestingly, in a second strain of transgenic mice, MMTV-neu, that develop ER-negative tumors, there were few differences in mammary tumor development between dietary-induced obese and lean mice [35].…”

Section: Introductionmentioning

confidence: 76%

Mammary tumor development from T47-D human breast cancer cells in obese ovariectomized mice with and without estradiol supplements

Nkhata

Ray

Doğan

et al. 2008

Breast Cancer Res Treat

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Obesity is a risk factor for postmenopausal breast cancer, particularly for development of estrogen-receptor (ER)-positive tumors. Additionally, obesity is implicated in breast cancer progression. However, few studies address mechanisms of action of how obesity mediates these responses. Our goal was to address how obesity and/or elevated serum leptin affects tumor formation from ER-positive T47-D cells. In Study 1 ovariectomized CD-1 nude female mice were injected with goldthioglucose (GTG) at 0.5 mg/g body weight in saline or the vehicle at 6 weeks of age. At 10 weeks of age mice were inoculated with T47-D cells and implanted with estrogen pellets. In Study 2 mice were injected with 0.3 mg/g GTG or the vehicle. At 10 weeks of age cells were inoculated and mice were implanted with estrogen or placebo pellets. Mice were followed until 30 weeks of age. Some GTG mice became obese and others were non-responders. In Study 1 no mice developed tumors. In Study 2 mice with placebo pellets developed more tumors than mice with estrogen pellets, 50% vs. 13%. GTG-obese mice with placebo pellets had a 100% tumor incidence compared to 50% and 20% for GTG-lean and controls without estrogen. Serum leptin was higher in obese compared to lean mice and adiponectin was not affected by body weight. Adiponectin:leptin ratio was significantly reduced in obese compared to lean mice. Leptin, leptin receptor and signaling protein expression were determined in mammary and tumor tissue. Leptin and STAT3 were most abundant in tumors. These findings suggest that in vivo estrogen suppressed proliferation of T47-D cells but without supplemental estrogen obesity enhanced tumor development. The exact reason for this is not presently clear.

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“…Most studies that find a positive relationship between adiposity and carcinogenesis have not been designed to test whether the relationship between obesity and cancer is causal (4,7,8,(10)(11)(12)(13)(14)16). In such studies, the adiposity was not an independent variable itself and the connection between adiposity and carcinogenesis, thus, might have arisen because both were regulated by the same underlying factor(s).…”

Section: Discussionmentioning

confidence: 99%

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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Effect of high fat diet on body weight and mammary tumor latency in MMTV-TGF-α mice

Cited by 50 publications

References 44 publications

Role of Cholesterol in the Development and Progression of Breast Cancer

Role of Cholesterol in the Development and Progression of Breast Cancer

Mammary tumor development from T47-D human breast cancer cells in obese ovariectomized mice with and without estradiol supplements

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

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