Researchers at Fox Chase Cancer Center have zeroed in on a crucial gene, thought to be the reason for the spread of breast cancer and resistance to long-term estrogen deprivation. The gene may be beneficial in ascertaining the risk factors of breast cancer reappearance, and would enable a good idea to specialists about potential treatment options.
The research targeted breast cancer cells which had developed resistance to a particular class of anti-hormone drug called aromatase inhibitors. These inhibitors cause the closure of an enzyme aromatase, which causes the body to produce estrogen outside the ovaries. These drugs offer the most effective hormone therapies for women whose estrogen in the body propels the growth of cancer cells.
Fox Chase Cancer Center biochemist Joan S. Lewis-Wambi, Ph.D said, "Unfortunately, one of the drawbacks to extended use of an AI may be that some of the cancer cells develop resistance to the drug and are able to grow and spread independent of estrogen. Our laboratory has developed several AI-resistant breast cancer cell lines and have found that these cells are very invasive compared to AI-sensitive breast cancer cells. Analyses of gene activity in these AI-resistant cells have shown that they express high levels of genes associated with invasiveness and metastasis."
The researchers also found a solution, to employ molecules called "small interfering RNAs" which would quash the gene called CEACAM6 (carcinoembryonic antigen-related cell adhesion molecule6). Lewis-Wambi concluded, "Overall, these findings identify CEACAM6 as a unique mediator of the aggressiveness and spread of AI-resistant breast cancer. This suggests that it might be an important biomarker for metastasis and a possible target for novel treatments for patients with metastatic breast cancer."