ER beta mediates estrogen signaling in inflammatory breast cancer

ERbetamediates estrogen signaling in inflammatory breast cancer

Inflammatory breast cancer (IBC) is a rare and aggressive form of breast cancer. Even with the application of a standard multi-modality treatment approach that incorporates neoadjuvant chemotherapy, radiation, and surgery, the 5-year survival rate for IBC is only about 40–50%. Breast cancer can be typically stratified into different types based on the presence of molecular drivers such as estrogen receptor (ERα), progesterone receptor (PR), or human epidermal growth factor receptor 2 (HER2), which inform the treatment choice.

For IBC, there is a substantially higher incidence of ERα negativity compared with other forms of breast cancer that can reach up to 60%. A specific targetable driver signaling pathway has not been identified so far. About one in three patients already have distant metastasis at the time of diagnosis, contributing to the aggressiveness and poor outcomes associated with IBC.

Despite the absence of ERα from the majority of IBC tumors, estrogen signaling has been implicated in the progression of the disease through ERα-independent pathways. ERβ is a ligand-activated transcription factor that mediates the effects of estrogen, along with ERα in different tissues during growth and development by regulating the transcription of target genes. Tumor suppressive effects of ERβ have been documented in diverse cancer types such as thyroid, kidney, prostate, glioblastoma, ovarian and breast cancer.

Reference : ERβ as a mediator of estrogen signaling in inflammatory breast cancer, Oncotarget DOI 10.18632/oncotarget.28425