Nutrition and fetal origins of breast cancer: consumption of high saturated fat diet by rats during pregnancy and female offspring's susceptibility to mammary carcinogenesis

• Grant number: 10/11742-0
• Support Opportunities: Scholarships in Brazil - Doctorate
• Effective date (Start): January 01, 2011
• Effective date (End): April 30, 2014
• Field of knowledge: Health Sciences - Nutrition - Nutrition Biochemistry
• Principal Investigator: Thomas Prates Ong
• Grantee: Fábia de Oliveira Andrade
• Host Institution: Faculdade de Ciências Farmacêuticas (FCF). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated scholarship(s): 12/03330-9 - Morphological and global gene expression analysis of mammary tissue of young female rats treated in utero with high-saturated fatty acid diet, BE.EP.DR

Abstract

Breast cancer is the leading death cause by cancer among women in Brazil and worldwide. Diet is associated with the etiology of 30-50% of all breast cancers and the consumption of animal fat has been associated with increased risk of cancer. As described for non-communicable chronic diseases such as cardiovascular disease, the hypothesis that breast cancer could present a fetal origin has been proposed. The maternal diet during pregnancy may be particularly important for alteration of the fetal environment and therefore susceptibility to breast cancer in adulthood. Diet, environmental exposures and maternal endocrine changes may increase the risk of breast cancer by inducing in the fetus epigenetic changes, such as DNA methylation and histone acetylation, which alter its susceptibility to breast cancer initiating factors. Exposures to high-fat diet in the intrauterine period, during the developmental phase of the breast, have been considered to epigenetically reprogram gene expression in mammary gland, resulting in TEBs ("Terminal End Buds") with altered susceptibility to malignant transformation. Genes that may be affected in this regard include those which normally protect cells from malignant transformation. In this sense genes for cyclin D1, c-myc and RASSF-1, whose involvement in carcinogenênese breast have been described, can be highlighted. The aim of this study is to evaluate whether consumption of high saturated fat diet by female rats during pregnancy increases the susceptibility of female offspring to chemically induced mammary carcinogenesis and possible cellular, molecular and epigenetic mechanisms involved. (AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

ANDRADE, FABIA DE OLIVEIRA; DE ASSIS, SONIA; JIN, LU; FONTELLES, CAMILE CASTILHO; BARBISAN, LUIS FERNANDO; PURGATTO, EDUARDO; HILAKIVI-CLARKE, LEENA; ONG, THOMAS PRATES. Lipidomic fatty acid profile and global gene expression pattern in mammary gland of rats that were exposed to lard-based high fat diet during fetal and lactation periods associated to breast cancer risk in adulthood. Chemico-Biological Interactions, v. 239, p. 118-128, SEP 5 2015. (12/03330-9, 10/11742-0, 11/23259-4)

ANDRADE, FABIA DE OLIVEIRA; FONTELLES, CAMILE CASTILHO; ROSIM, MARIANA PAPALEO; DE OLIVEIRA, TIAGO FRANCO; DE MELO LOUREIRO, ANA PAULA; MANCINI-FILHO, JORGE; ROGERO, MARCELO MACEDO; MORENO, FERNANDO SALVADOR; DE ASSIS, SONIA; BARBISAN, LUIZ FERNANDO; et al. Exposure to lard-based high-fat diet during fetal and lactation periods modifies breast cancer susceptibility in adulthood in rats. JOURNAL OF NUTRITIONAL BIOCHEMISTRY, v. 25, n. 6, p. 613-622, JUN 2014. (12/03330-9, 10/11742-0, 11/23259-4)

Academic Publications

(References retrieved automatically from State of São Paulo Research Institutions)

ANDRADE, Fábia de Oliveira. Nutrition and developmental origin of breast cancer: consumption of lard-based high-fat diet by rats during gestation/lactation and the offspring\'s susceptibility to mammary carcinogenesis. 2014. Doctoral Thesis - Universidade de São Paulo (USP). Conjunto das Químicas (IQ e FCF) (CQ/DBDCQ) São Paulo.