摘要
Breast cancer （BC） is a leading cause of mortality among women in the world. To date, a number of molecules have been established as disease status indicators and therapeutic targets. The best known among them are estrogen receptor-α （ER-α）, progesterone receptor （PR） and H ER-2/neu. About 15%-20% BC patients do not respond effectively to thera pies targeting these classes of tumor-promoting factors. Thus, additional targets are strongly and urgently sought after in therapy for human BCs negative for ER, PR and HER-2, the so-called triple-negative BC （TNBC）. Recent clinical work has revealed that CC chemokine ligand 5 （CCL5） is strongly associated with the progression of BC, particularly TNBC. How CCL5 contributes to the development of TN BC is not well understood. Experimental animal studies have begun to address the mechanistic issue. In this article, we will review the clinical and laboratory work in this area that has led to our own hypothesis that targeting CCL5 in TNBCs will have favorable therapeutic outcomes with minimal adverse impact on the general physiology.
Breast cancer （BC） is a leading cause of mortality among women in the world. To date, a number of molecules have been established as disease status indicators and therapeutic targets. The best known among them are estrogen receptor-α （ER-α）, progesterone receptor （PR） and H ER-2/neu. About 15%-20% BC patients do not respond effectively to thera pies targeting these classes of tumor-promoting factors. Thus, additional targets are strongly and urgently sought after in therapy for human BCs negative for ER, PR and HER-2, the so-called triple-negative BC （TNBC）. Recent clinical work has revealed that CC chemokine ligand 5 （CCL5） is strongly associated with the progression of BC, particularly TNBC. How CCL5 contributes to the development of TN BC is not well understood. Experimental animal studies have begun to address the mechanistic issue. In this article, we will review the clinical and laboratory work in this area that has led to our own hypothesis that targeting CCL5 in TNBCs will have favorable therapeutic outcomes with minimal adverse impact on the general physiology.
