Gestational high-fat diet and bisphenol A exposure heightens mammary cancer risk

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Abstract

In utero exposure to bisphenol A (BPA) increases mammary cancer susceptibility in offspring. High-fat diet is widely believed to be a risk factor of breast cancer. The objective of this study was to determine whether maternal exposure to BPA in addition to high-butterfat (HBF) intake during pregnancy further influences carcinogen-induced mammary cancer risk in offspring, and its dose–response curve. In this study, we found that gestational HBF intake in addition to a low-dose BPA (25 µg/kg BW/day) exposure increased mammary tumor incidence in a 50-day-of-age chemical carcinogen administration model and altered mammary gland morphology in offspring in a non-monotonic manner, while shortening tumor-free survival time compared with the HBF-alone group. In utero HBF and BPA exposure elicited differential effects at the gene level in PND21 mammary glands through DNA methylation, compared with HBF intake in the absence of BPA. Top HBF + BPA-dysregulated genes ( ALDH1B1, ASTL, CA7, CPLX4, KCNV2, MAGEE2 and TUBA3E) are associated with poor overall survival in The Cancer Genomic Atlas (TCGA) human breast cancer cohort ( n = 1082). Furthermore, the prognostic power of the identified genes was further enhanced in the survival analysis of Caucasian patients with estrogen receptor-positive tumors. In conclusion, concurrent HBF dietary and a low-dose BPA exposure during pregnancy increases mammary tumor incidence in offspring, accompanied by alterations in mammary gland development and gene expression, and possibly through epigenetic reprogramming.

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Prenatal environmental exposures, epigenetics, and disease.

Frederica Perera, Julie Herbstman (2011)

This review summarizes recent evidence that prenatal exposure to diverse environmental chemicals dysregulates the fetal epigenome, with potential consequences for subsequent developmental disorders and disease manifesting in childhood, over the lifecourse, or even transgenerationally. The primordial germ cells, embryo, and fetus are highly susceptible to epigenetic dysregulation by environmental chemicals, which can thereby exert multiple adverse effects. The data reviewed here on environmental contaminants have potential implications for risk assessment although more data are needed on individual susceptibility to epigenetic alterations and their persistence before this information can be used in formal risk assessments. The findings discussed indicate that identification of environmental chemicals that dysregulate the prenatal epigenome should be a priority in health research and disease prevention. Copyright © 2011 Elsevier Inc. All rights reserved.

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Developmental exposure to estradiol and bisphenol A increases susceptibility to prostate carcinogenesis and epigenetically regulates phosphodiesterase type 4 variant 4.

Shuk-Mei Ho, Wan-Yee Tang, Jessica Belmonte de Frausto … (2006)

Early developmental perturbations have been linked to adult-onset prostate pathology, including excessive exposure to estrogenic compounds; however, the molecular basis for this imprinting event is not known. An important and controversial health concern is whether low-dose exposures to hormonally active environmental estrogens, such as bisphenol A, can promote human diseases, including prostate cancer. Here, we show that transient developmental exposure of rats to low, environmentally relevant doses of bisphenol A or estradiol increases prostate gland susceptibility to adult-onset precancerous lesions and hormonal carcinogenesis. We found permanent alterations in the DNA methylation patterns of multiple cell signaling genes, suggesting an epigenetic basis for estrogen imprinting. For phosphodiesterase type 4 variant 4 (PDE4D4), an enzyme responsible for cyclic AMP breakdown, a specific methylation cluster was identified in the 5'-flanking CpG island that was gradually hypermethylated with aging in normal prostates, resulting in loss of gene expression. Early and prolonged hypomethylation at this site following neonatal estradiol or bisphenol A exposure resulted in continued, elevated PDE4D4 expression. Cell line studies confirmed that site-specific methylation is involved in transcriptional silencing of the PDE4D4 gene and showed hypomethylation of this gene in prostate cancer cells. Importantly, the PDE4D4 alterations in the estrogen-exposed prostates were distinguishable before histopathologic changes of the gland, making PDE4D4 a candidate molecular marker for prostate cancer risk assessment as a result of endocrine disruptors. In total, these findings indicate that low-dose exposures to ubiquitous environmental estrogens affect the prostate epigenome during development and, in so doing, promote prostate disease with aging.

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Migration patterns and breast cancer risk in Asian-American women.

R G Ziegler, R Hoover, M Pike … (1993)

Breast cancer incidence rates have historically been 4-7 times higher in the United States than in China or Japan, although the reasons remain elusive. When Chinese, Japanese, or Filipino women migrate to the United States, breast cancer risk rises over several generations and approaches that among U.S. Whites. Our objective was to quantify breast cancer risks associated with the various migration patterns of Asian-American women. A population-based, case-control study of breast cancer among women of Chinese, Japanese, and Filipino ethnicities, aged 20-55 years, was conducted during 1983-1987 in San Francisco-Oakland, California, Los Angeles, California, and Oahu, Hawaii. We successfully interviewed 597 case subjects (70% of those eligible) and 966 control subjects (75%). A sixfold gradient in breast cancer risk by migration patterns was observed. Asian-American women born in the West had a breast cancer risk 60% higher than Asian-American women born in the East. Among those born in the West, risk was determined by whether their grandparents, especially grandmothers, were born in the East or the West. Asian-American women with three or four grandparents born in the West had a risk 50% higher than those with all grandparents born in the East. Among the Asian-American women born in the East, breast cancer risk was determined by whether their communities prior to migration were rural or urban and by the number of years subsequently lived in the West. Migrants from urban areas had a risk 30% higher than migrants from rural areas. Migrants who had lived in the West for a decade or longer had a risk 80% higher than more recent migrants. Risk was unrelated to age at migration for women migrating at ages less than 36 years. Ethnic-specific incidence rates of breast cancer in the migrating generation were clearly elevated above those in the countries of origin, while rates in Asian-Americans born in the West approximated the U.S. White rate. Exposure to Western lifestyles had a substantial impact on breast cancer risk in Asian migrants to the United States during their lifetime. There was no direct evidence of an especially susceptible period, during either menarche or early reproductive life. Because heterogeneity in breast cancer risk in these ethnic populations is similar to that in international comparisons and because analytic epidemiologic studies offer the opportunity to disentangle correlated exposures, this study should provide new insights into the etiology of breast cancer.

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Author and article information

Journal

Journal ID (nlm-ta): Endocr Relat Cancer

Journal ID (iso-abbrev): Endocr. Relat. Cancer

Journal ID (hwp): ERC

Title: Endocrine-Related Cancer

Publisher: Bioscientifica Ltd (Bristol )

ISSN (Print): 1351-0088

ISSN (Electronic): 1479-6821

Publication date Collection: July 2017

Publication date (Electronic): 09 May 2017

Volume: 24

Issue: 7

Pages: 345-358

Affiliations

[1 ]Department of Environmental Health Cincinnati, Ohio, USA

[2 ]Center for Environmental Genetics University of Cincinnati College of Medicine, Cincinnati, Ohio, USA

[3 ]Cincinnati Cancer Center Cincinnati, Ohio, USA

[4 ]Department of Pathology and Laboratory Medicine University of Cincinnati College of Medicine, Cincinnati, Ohio, USA

[5 ]Department of Pharmacology and Cell Biophysics University of Cincinnati College of Medicine, Cincinnati, Ohio, USA

[6 ]Cincinnati Veteran Affairs Hospital Medical Center Cincinnati, Ohio, USA

Author notes

Correspondence should be addressed to S-M Ho; Email: shuk-mei.ho@ 123456uc.edu

[†]

(S Belcher is now at Department of Biological Sciences, Raleigh, North Carolina, USA)

Article

Publisher ID: ERC170006

DOI: 10.1530/ERC-17-0006

PMC ID: 5488396

PubMed ID: 28487351

SO-VID: d9e2d3c3-ccdf-4f3a-b7bd-438e3a84b944

License:

This work is licensed under a Creative Commons Attribution 3.0 Unported License..

History

Date received : 3 May 2017

Date accepted : 8 May 2017

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Gestational high-fat diet and bisphenol A exposure heightens mammary cancer risk

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Most cited references 51

Prenatal environmental exposures, epigenetics, and disease.

Developmental exposure to estradiol and bisphenol A increases susceptibility to prostate carcinogenesis and epigenetically regulates phosphodiesterase type 4 variant 4.

Migration patterns and breast cancer risk in Asian-American women.

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