"We are excited and grateful for this grant," said Chen. "It signals that we are on the right track. In the past five years, we have focused on developing a potential treatment for breast cancer. With this grant we can move ahead on testing whether the combination approach will significantly improve the existing treatment in an aggressive subtype of breast cancer."
Scientists have learned that human prolactin (PRL), a hormone normally produced in the brain and mainly responsible for mammary gland development and milk production, may be involved in breast cancer development.
"The involvement of PRL in breast cancer is likely due to, in some cases, the fact that mutated breast cells produce PRL as their own survival-growth factor, which keeps most growth signal at "on" position," said Chen. "This self-sustained, vicious growth ability eventually leads to cancer formation."
To "turn off" these growth signals induced by PRL, scientists set out to develop a counteragent -- an antagonist. Working with his colleagues and graduate students at the Oncology Research Institute, Chen has demonstrated that a mutated PRL, called PRL antagonist (G129R), is able to bind specifically to breast cancer cells and block the effect of PRL, inhibiting tumor growth in mice. What's more, the PRL antagonist has synergistic effects with the breast cancer drug Herceptin, which has only 30 percent response
Contact: Wen Y. Chen