Cancer is the consequence of the recalcitrant multiplication of the
transformed cells. Cancer cells grow and proliferate at a fast pace and do not follow
normal regulation of cell division. Breast cancer is a heterogeneous group of diseases,
which is the second leading cause of death among women. Although androgen is
primarily considered a male steroid hormone, it also has an important role in the female
reproductive system. The literature evidence suggests the role of androgen receptors
(AR) in the normal development of the breast. At puberty, the expression of AR is even
more than ER, suggesting its importance during the process of sexual development; its
activity maintains the ER-induced cell proliferation and normal development of the
breast. Epidemiological studies have suggested a positive correlation between high
endogenous androgens and the risk of breast cancer in both pre- and postmenopausal
women. In both ER and PR-positive breast cancers, AR is expressed in 60-70% of the
cases. AR is also reported to be co-expressed with ER in around 80-90% of breast
cancer cases and is considered an independent prognostic factor of ER-positive breast
cancers. Tumor-microenvironment has a complex role in tumor initiation, progression,
and metastasis. Tumor-infiltrating and resident cells secretes a variety of inflammatory
and anti-inflammatory cytokines, which in turn either inhibit or promote tumor growth.
Immunosuppressive and immuno-inductive effects of androgen have been reported in
various studies. Androgens have been reported to influence the adaptive immune
system more than the innate immune system in many ways. Crosstalk of androgen and
cytokine signaling has many effects in breast cancer epidemiology. So, in this chapter,
we will discuss the various immune-endocrine perspectives of breast cancers.
Keywords: Adaptive immunity, Androgens, Apocrine breast cancer, Cancer immunoediting, Dihydrotestosterone, Innate immunity, T cytotoxic cells, T helper cells.
