Insights into the roles and mechanisms of two of the miRNAs upregulated in human breast cancer stem cells in at least some breast cancers are presented.

A novel first-in-class small molecule (ERX-11) that interacts with and disrupts the interactome of the estrogen receptor (ER), blocks the growth of ER-positive breast cancers, including those that are resistant to currently approved hormonal agents.

GDC-0810 is a novel, orally bioavailable SERD that exhibits robust pre-clinical activity in models of ER+ breast cancer, including models of tamoxifen resistance, and those that express the ERα mutations, ER.Y537S and ER.D538G.

Transcription elongation by the elongation factor P-TEFb promotes the epithelial–mesenchymal transition and metastasis of breast cancer cells, implicating inhibition of this factor as a potential treatment for the late stages of this cancer.

Bazedoxifene's SERD activities enable it to resist the impact of activating ESR1 mutations in breast cancer.

Maternal embryonic leucine zipper kinase (MELK) is a new anti-cancer target that is highly selective for basal-like breast cancer.

The transcription factor STAT5 mediates the increased breast cancer risk associated with a late age pregnancy, but intermittent anti-STAT5 treatment can lower this risk and thus prevent breast cancer.

The study of a recurrent breast cancer MAGI3 truncation reveals the role of MAGI3 in regulating the Hippo effector YAP and highlights premature mRNA cleavage and polyadenylation as a mechanism underlying cancer development.

Loss of RUNX1, a key regulator of estrogen receptor-positive luminal breast cells, impairs mammary epithelial differentiation and contributes to luminal breast cancer via genetic interactions with a loss of p53 or RB1.

CCL5-dependent macrophage recruitment drives breast cancer recurrence through collagen deposition in residual tumors.