دورية أكاديمية
أعرض في EDS

Pubertal high fat diet: effects on mammary cancer development.

التفاصيل البيبلوغرافية
العنوان: Pubertal high fat diet: effects on mammary cancer development.
المؤلفون: Zhao Y, Tan YS, Aupperlee MD, Langohr IM, Kirk EL, Troester MA, Schwartz RC, Haslam SZ
المصدر: Breast cancer research : BCR [Breast Cancer Res] 2013; Vol. 15 (5), pp. R100.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: BioMed Central Ltd Country of Publication: England NLM ID: 100927353 Publication Model: Print Cited Medium: Internet ISSN: 1465-542X (Electronic) Linking ISSN: 14655411 NLM ISO Abbreviation: Breast Cancer Res Subsets: MEDLINE
أسماء مطبوعة: Publication: London, UK : BioMed Central Ltd
Original Publication: London, UK : Current Science, c1999-
مواضيع طبية MeSH: Diet, High-Fat* , Sexual Maturation*, Breast Neoplasms/*etiology , Mammary Neoplasms, Experimental/*etiology, Animals ; Breast Neoplasms/metabolism ; Breast Neoplasms/mortality ; Breast Neoplasms/pathology ; Cell Proliferation ; Cytokines/metabolism ; Female ; Gene Expression Profiling ; Hormones/blood ; Humans ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation Mediators/metabolism ; Intercellular Signaling Peptides and Proteins/genetics ; Intercellular Signaling Peptides and Proteins/metabolism ; Mammary Neoplasms, Experimental/metabolism ; Mammary Neoplasms, Experimental/mortality ; Mammary Neoplasms, Experimental/pathology ; Mice ; Neovascularization, Pathologic/genetics ; Neovascularization, Pathologic/metabolism ; Signal Transduction ; Time Factors ; Tumor Microenvironment
مستخلص: Introduction: Epidemiological studies linking dietary fat intake and obesity to breast cancer risk have produced inconsistent results. This may be due to the difficulty of dissociating fat intake from obesity, and/or the lack of defined periods of exposure in these studies. The pubertal mammary gland is highly sensitive to cancer-causing agents. We assessed how high fat diet (HFD) affects inflammation, proliferative, and developmental events in the pubertal gland, since dysregulation of these can promote mammary tumorigenesis. To test the effect of HFD initiated during puberty on tumorigenesis, we utilized BALB/c mice, for which HFD neither induces obesity nor metabolic syndrome, allowing dissociation of HFD effects from other conditions associated with HFD.
Methods: Pubertal BALB/c mice were fed a low fat diet (12% kcal fat) or a HFD (60% kcal fat), and subjected to carcinogen 7,12-dimethylbenz[a]anthracene (DMBA)-induced tumorigenesis.
Results: HFD elevated mammary gland expression of inflammatory and growth factor genes at 3 and 4 weeks of diet. Receptor activator of nuclear factor kappa-B ligand (RANKL), robustly induced at 4 weeks, has direct mitogenic activity in mammary epithelial cells and, as a potent inducer of NF-κB activity, may induce inflammatory genes. Three weeks of HFD induced a transient influx of eosinophils into the mammary gland, consistent with elevated inflammatory factors. At 10 weeks, prior to the appearance of palpable tumors, there were increased numbers of abnormal mammary epithelial lesions, enhanced cellular proliferation, increased growth factors, chemokines associated with immune-suppressive regulatory T cells, increased vascularization, and elevated M2 macrophages. HFD dramatically reduced tumor latency. Early developing tumors were more proliferative and were associated with increased levels of tumor-related growth factors, including increased plasma levels of HGF in tumor-bearing animals. Early HFD tumors also had increased vascularization, and more intra-tumor and stromal M2 macrophages.
Conclusions: Taken together in this non-obesogenic context, HFD promotion of inflammatory processes, as well as local and systemically increased growth factor expression, are likely responsible for the enhanced tumorigenesis. It is noteworthy that although DMBA mutagenesis is virtually random in its targeting of genes in tumorigenesis, the short latency tumors arising in animals on HFD showed a unique gene expression profile, highlighting the potent overarching influence of HFD.
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معلومات مُعتمدة: P30 ES010126 United States ES NIEHS NIH HHS; U01 ES019472 United States ES NIEHS NIH HHS; U01ES019472 United States ES NIEHS NIH HHS; U01ES012800 United States ES NIEHS NIH HHS; U01ESO19434 United States PHS HHS
المشرفين على المادة: 0 (Cytokines)
0 (Hormones)
0 (Inflammation Mediators)
0 (Intercellular Signaling Peptides and Proteins)
تواريخ الأحداث: Date Created: 20131026 Date Completed: 20140911 Latest Revision: 20211021
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC3978633
DOI: 10.1186/bcr3561
PMID: 24156623
قاعدة البيانات: MEDLINE
الوصف
تدمد:1465-542X
DOI:10.1186/bcr3561