AR expression and its prognostic implications vary according to breast cancer subtype.

We will review the prognostic effect of AR expression, and discuss recent preclinical studies that have shed light on AR signaling and its interactions with other signaling pathways according to breast cancer subtype.

ABSTRACT: Androgen-stimulated growth of the molecular apocrine breast cancer subtype is mediated by an androgen receptor (AR)-regulated transcriptional program.

Here we report a positive feed-forward loop that enhances breast cancer growth involving AR, AR coregulators, and downstream target genes.

In the absence of an androgen signal, TCF7L2 interacts with FOXA1 at AR-binding sites and represses the basal expression of AR target genes, including MYC.

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Although Breast carcinoma had many targeted biomarkers for its treatment, however, it is a heterogeneous disease with different outcomes and need new markers especially for the triple negative group when estrogen receptor, progesterone receptors and Her2/neu are negative.

Androgen receptor is a new target with unclear role.

Finally, we will discuss AR inhibitors that have been evaluated in early-phase clinical trials and that are under development.

We will also discuss novel mechanistic insights and combinatorial therapeutic strategies that have been developed in preclinical studies with the potential to translate into effective clinical strategies for AR breast cancer.

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