Prolactin activates the enzyme, glutathione-S-transferase, that detoxifies platinum drugs, doxorubicin, cyclophosphamide and etoposide, contributing to the resistance of cancer cells to chemotherapies (LaPensee, Schwemberger et al. 2009). Accordingly, the antagonism of prolactin by Prolanta™ may increase the effectiveness of these chemotherapies , and our own data indicates synergy with taxanes and platinum therapy.
Asai-Sato, M., Y. Nagashima, et al. (2005). "Prolactin inhibits apoptosis of ovarian carcinoma cells induced by serum starvation or cisplatin treatment." Int J Cancer 115(4): 539-44.
Howell, S. J., E. Anderson, et al. (2008). "Prolactin receptor antagonism reduces the clonogenic capacity of breast cancer cells and potentiates doxorubicin and paclitaxel cytotoxicity." Breast Cancer Res 10(4): R68.
LaPensee, E. W., S. J. Schwemberger, et al. (2009). "Prolactin confers resistance against cisplatin in breast cancer cells by activating glutathione-S-transferase." Carcinogenesis 30(8): 1298-304.
Human prolactin is associated with the development of resistance to platinum and taxane therapies (Asai-Sato, Nagashima et al. 2005; Howell, Anderson et al. 2008; LaPensee, Schwemberger et al. 2009; Levina, Nolen et al. 2009).