In a laboratory study published in the journal Cancer Research, Scott & White Healthcare anatomic pathologist Arundhati Rao, M.D. is a co-investigator looking at the ways in which estrogen can interfere with how chemotherapy does its job in destroying breast cancer cells. The most common type of breast cancer is "estrogen-receptor positive" breast cancer.
Velusamy Rangasamy and Ajay Rana, Ph.D., are also the lead authors on the study and are based at Loyola University Medical Center in Chicago where Dr. Rana is a professor of pharmacology.
"What we know is that not all breast tumors are the same and if a tumor is estrogen-receptor positive, it's possible that chemotherapy isn't going to be as effective as it could be," said Dr. Rao. "This is why we see some breast cancer patients on chemo that isn't working like it should. With this additional information regarding estrogen, it could help us create more targeted therapies in the future."
"These findings are important because efficiently killing estrogen receptor positive (ER+) breast cancer cells with currently available chemotherapy is a challenging task and many times these ER+ breast tumors don't respond to classical chemotherapy," said Dr. Rana. "Our research identified an alternative cellular protein which can serve as a viable target for ER+ breast cancer treatment."
Dr. Rao went on to say that "with this research we found that in order to make cancer drugs work better, we may need to give patients a different drug and this could possibly shorten the duration of their chemotherapy course if we knew more."
"Our work suggests that any drugs/agents that will activate this protein will sensitize the ER+ breast cancer cells toward commonly used chemotherapies. We have been working to find the drugs/agents that can activate this protein and kill the ER+ cancer cells," said Dr. Rana.
Dr. Rana explained that "these findings are encouraging but further research is needed to find how this cellular pathway could be utilized to target estrogen positive breast cancer cells."
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