Format

Send to

Choose Destination
Physiol Genomics. 2018 Mar 1;50(3):215-234. doi: 10.1152/physiolgenomics.00105.2017. Epub 2018 Jan 26.

Rat models of 17β-estradiol-induced mammary cancer reveal novel insights into breast cancer etiology and prevention.

Author information

1
McArdle Laboratory for Cancer Research, Department of Oncology, School of Medicine and Public Health, University of Wisconsin-Madison , Madison, Wisconsin.
2
University of Wisconsin Carbone Cancer Center, School of Medicine and Public Health, University of Wisconsin-Madison , Madison, Wisconsin.
3
Department of Population Health Sciences, School of Medicine and Public Health, University of Wisconsin-Madison , Madison, Wisconsin.

Abstract

Numerous laboratory and epidemiologic studies strongly implicate endogenous and exogenous estrogens in the etiology of breast cancer. Data summarized herein suggest that the ACI rat model of 17β-estradiol (E2)-induced mammary cancer is unique among rodent models in the extent to which it faithfully reflects the etiology and biology of luminal types of breast cancer, which together constitute ~70% of all breast cancers. E2 drives cancer development in this model through mechanisms that are largely dependent upon estrogen receptors and require progesterone and its receptors. Moreover, mammary cancer development appears to be associated with generation of oxidative stress and can be modified by multiple dietary factors, several of which may attenuate the actions of reactive oxygen species. Studies of susceptible ACI rats and resistant COP or BN rats provide novel insights into the genetic bases of susceptibility and the biological processes regulated by genetic determinants of susceptibility. This review summarizes research progress resulting from use of these physiologically relevant rat models to advance understanding of breast cancer etiology and prevention.

KEYWORDS:

ACI rat; BN rat; breast cancer; diet; environment; estradiol; estrogen; genetics; hormones; mammary cancer

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Atypon Icon for PubMed Central
Loading ...
Support Center