SOX11+ breast tumours display reactivated embryonic developmental signalling and organogenetic features and are at elevated risk of developing metastases, so may benefit from more aggressive therapies.
Inactivation of a multifunctional RNA-binding protein can lead to the acquisition of pro-metastatic phenotypes, possibly by stabilizing large-scale transcriptomic changes that provide a selective advantage during cancer progression.
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.
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.
Cellular acidity, capacity for net acid extrusion, and expression of acid-base transporters in human breast carcinomas independently predict variation in proliferative activity, lymph node metastasis, and patient survival.