Affiliations: Department of Pathology, Section on Comparative Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA | Michigan State University, East Lansing, MI, USA
Correspondence:
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Corresponding author: J. Mark Cline, DVM, PhD, DACVP, Associate Professor of Pathology/Comparative Medicine, Comparative Medicine Clinical Research Center, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1040, USA. Tel.: +1 336 716 1564; Fax: +1 336 716 1515; E-mail: jmcline@wfubmc.edu; URL: http://www.wfubmc.edu/pathology/faculty.htm
Abstract: Macaques are Old World anthropoid primates with a high degree of genetic identity to human beings and striking similarities in breast development, reproductive endocrinology, and menstrual cycle characteristics. These animals share critical pathways of hormone metabolism with humans, to a degree that is distinct from rodent models. Macaques also express estrogen receptors alpha and beta, progesterone receptors, and androgen receptors in the normal breast in patterns similar to those described for women. Spontaneously occurring hormone-dependent breast cancers occur in macaques at a similar prevalence to lower-risk populations of women, and these neoplasms exhibit similar growth patterns and key molecular changes seen in human lesions. These similarities lend support to a biomarker approach for modeling breast cancer risk. Estrogen+progestogen treatment of postmenopausal animals produces a proliferative response in the normal breast epithelium which reflects the breast cancer promoting effects of continuous combined hormone replacement therapy. Studies of novel agents such as tibolone, selective estrogen receptor modulators, and alternative progestogens in macaques have also helped to identify hormonal therapies with a more acceptable balance of benefit to risk. Future studies of novel selective estrogens, androgens, and dietary estrogens in the macaque model will further contribute to our understanding of breast cancer risk and prevention.
DOI: 10.3233/BD-2006-24105
Journal: Breast Disease, vol. 24, no. 1, pp. 59-70, 2006
