Approximately 90% of breast and ovarian cancers express the prolactin receptor and these tumors are stimulated by prolactin. More importantly, prolactin can cross-activate many of the same pathways activated by HER2/neu and the ER, which may be responsible for a tumor’s resistance to Herceptin and/or tamoxifen therapy. Therefore, Prolanta serves as novel candidate for breast cancer therapy, either as a stand-alone agent or as part of a combinational approach for a larger proportion of patients. Preclinical data illustrate that combining Prolanta therapy with Herceptin, Tykerb, or tamoxifen results in an even more effective breast cancer treatment than either product alone.
Approximately 50% of breast cancer patients are estrogen receptor (ER) positive. These tumors are stimulated by and partially dependent upon estrogen. Tamoxifen, an inhibitor of estrogen action, can be effective in breast cancer patients that are ER positive, yet often their tumors cease
to be ER positive.
Approximately 20% to 30% of breast cancer patients have tumors that are stimulated by the HER2/neu pathway. However, less than one-third of these patients are successfully treated with Herceptin, which inhibits the