Mammary ductal epithelial cell hyperproliferation and hyperplasia induced by a nutritional stress diet containing four components of a Western-style diet

Khan, Naheed L.; Yang, Kan; Newmark, Harold L.; Wong, George; Telang, Nitin T.; Rivlin, Richard S.; Lipkin, Martin

doi:10.1093/carcin/15.11.2645

Cited by 27 publications

(15 citation statements)

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“…The findings reported here are an extension of this earlier study. The previous findings in mammary gland of rodents (8)(9)(10) are similar to proliferative changes in colonie epithelium of rodents fed a Western-style diet (3,4,11). The findings further support the likelihood that common etiological factors increase breast and colon cancer incidences in human populations and suggest that these cancers share common etiological dietary factors (12).…”

Section: Introductionsupporting

confidence: 78%

“…(13) The complete AIN-76A diet was the control diet. As described in our previous studies (3,4,8,11), to simulate a human Western-style diet, the AIN-76A diet was modified to contain high levels of fat and phosphate and decreased calcium and vitamin D, which, on a nutrient density basis, is comparable to levels in human populations at increased risk for breast and colon cancer. Details of the diets are given in Table 1 (for further details see Refs.…”

Section: Dietsmentioning

confidence: 99%

“…In a series of experimental models of mammary carcinogenesis, dietary fat influenced the development and growth of mammary tumors; these included models of spontaneous carcinogen-induced benign and malignant rodent mammary tumors (7). In an earlier study in which female C57BL/6J mice were fed a Western-style diet for 20 weeks without carcinogen, increased growth and duplication of mammary terminal ducts were induced and the mammary gland's proliferative compartment of epithelial cells was expanded (8). The findings reported here are an extension of this earlier study.…”

Section: Introductionmentioning

confidence: 99%

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Model of mouse mammary gland hyperproliferation and Hyperplasia Induced by a western‐style diet

Xue

Newmark

Yang

et al. 1996

Nutrition and Cancer

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Mammary glands of female C57BL/6J mice were analyzed after they were fed a Western-style diet or control AIN-76A diet. The Western-style diet contained several risk factors found in human diets in geographic regions having increased risk for breast cancer: high fat and phosphate and low calcium and vitamin D. After they were fed these diets for 8, 14, and 20 weeks, mice were sacrificed, and mammary glands were removed for morphometric and radioautographic measurements. Although after the animals were fed the Western-style diet for 8 weeks the number of terminal ducts per mouse mammary gland (NTDMG) was similar in the Western-style and control diet groups, after they were fed the Western-style diet for 14 weeks (p < 0.05) and 20 weeks (p < 0.01) the NTDMG significantly increased compared with the control group. Moreover, there was a significant increase (p < 0.01) in the tritiated thymidine labeling index of mammary terminal ductal epithelial cells after 14 and 20 weeks of Western-style diet administration. Thus the Western-style diet induced increased epithelial cell proliferation and increased NTDMG in female mice when fed during young adult growth and development. The findings raise the possibility that the ingestion of a diet with Western-style fat and phosphate content and with low calcium and vitamin D may induce similar changes during the early development of the human mammary gland.

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Section: Introductionsupporting

confidence: 78%

Section: Dietsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Model of mouse mammary gland hyperproliferation and Hyperplasia Induced by a western‐style diet

Xue

Newmark

Yang

et al. 1996

Nutrition and Cancer

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“…This is particularly true of vitamin D compounds, since the high stress western style diet associated with colon and breast cancer is also associated with low levels of vitamin D and calcium (26). Thus, increased autocrine negative TGF␤ activity mediated by vitamin D 3 compounds in MCF-7 E cells may provide a novel mechanism for blocking malignant progression by chemopreventive approaches.…”

mentioning

confidence: 99%

Regulation of Transforming Growth Factor-β Type II Receptor Expression in Human Breast Cancer MCF-7 Cells by Vitamin D3and Its Analogues

Wu¹,

Fan²,

Li³

et al. 1998

Journal of Biological Chemistry

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In view of the tumor suppressor role of the transforming growth factor-␤ (TGF␤) type II receptor (RII), the identification and characterization of agents that can induce the expression of this receptor are of potential importance to the development of chemoprevention approaches as well as treatment of cancer. To date, the identification of exogenous agents that control RII expression has been rare. We demonstrated that proliferation of MCF-7 early passage cells (MCF-7 E), which express RII and are sensitive to TGF␤ growth inhibition activity, was significantly inhibited by vitamin D 3 and its analogue EB1089. In contrast, proliferation of MCF-7 late passage cells (MCF-7 L), which have lost cell surface RII and are resistant to TGF␤, was not affected by these two compounds. TGF␤-neutralizing antibody was able to block the inhibitory effect on MCF-7 E cells by these compounds, indicating that treatment induced autocrine-negative TGF␤ activity. An RNase protection assay showed approximately a 3-fold induction of the RII mRNA, while a receptor cross-linking assay revealed a 3-4-fold induction of the RII protein. In contrast, there was no change in either RII mRNA or protein in the MCF-7 L cells. Transforming growth factor-␤ (TGF␤)1 comprises a family of hormone-like polypeptides that affects cell growth, adhesion, and differentiation (1). They act as growth inhibitors for most epithelial cells and some cancer cells. Two pathways are primarily involved in mediating effects of TGF␤ on cell growth and differentiation. One pathway involves blockade of cell cycle transit, while the other involves alteration of the extracellular matrix environment.TGF␤s elicit their effects by binding to cell surface receptors. Three major types of receptors have been shown to be present in most TGF␤-responsive cell lines. They are designated as type I (RI), type II (RII), and type III (RIII), respectively. RIII is a 280 -330-kDa glycoprotein that has no functional signaling domain but rather serves as a ligand storage protein and presents TGF␤ to the signaling receptors (2). RI and RII, which are glycoproteins of ϳ55 and 85 kDa, respectively, form a heteromeric receptor complex. Both are serine/threonine kinases, and each appears to be indispensable for TGF␤ signaling (3-5). The direct involvement of both RI and RII in conferring TGF␤ effects indicates that loss of either of the functional receptors would contribute to loss of autocrine TGF␤ activity. Loss of negative autocrine TGF␤ activity results in a growth advantage caused by an imbalance in positive and negative regulators, possibly leading to tumor formation and progression (6, 7). Recent evidence has shown a loss of RII is often associated with the failure to respond to autocrine and exogenous TGF␤. We have previously demonstrated that re-expression of this receptor in an RII-deficient breast cancer cell line (late passage MCF-7) leads to restoration of TGF␤ sensitivity and reduced malignancy in athymic nude mice (6). In addition, it has been shown that mutational inactivation of...

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“…In other organs, Western-style diets also have induced epithelial cell hyperproliferation and hyperplasia in mammary gland [38,39] , and hyperproliferati on in pancreas [40] and prostate gland [41] in short-term studies; increasing dietary calcium and vitamin D alone also inhibited the development of those lesions [25] .…”

Section: Preclinical Studiesmentioning

confidence: 99%

Update of preclinical and human studies of calcium and colon cancer prevention

Lipkin¹

1999

WJG

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Mammary ductal epithelial cell hyperproliferation and hyperplasia induced by a nutritional stress diet containing four components of a Western-style diet

Cited by 27 publications

References 0 publications

Model of mouse mammary gland hyperproliferation and Hyperplasia Induced by a western‐style diet

Model of mouse mammary gland hyperproliferation and Hyperplasia Induced by a western‐style diet

Regulation of Transforming Growth Factor-β Type II Receptor Expression in Human Breast Cancer MCF-7 Cells by Vitamin D3and Its Analogues

Update of preclinical and human studies of calcium and colon cancer prevention

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