Scientists at Dana-Farber Cancer Institute have conducted a study trying to explain how is the breast cancer treatment resistance mechanism working.
The researchers observed that breast cancer forms that present ER genes mutation will become resistant to tamoxifen and aromatase inhibitors, which are regular treatments for these forms of breast cancer. Unfortunately, such a resistance to treatment means increased mortality.
Estrogen is “nourishing” breast cancer tumors
It has been already proven that some forms of breast cancer tumors are feeding with estrogen. Thus, one of the most successful treatments in such case is to stop estrogen production. For that, drugs such as tamoxifen and aromatase inhibitors are used to influence the endocrine glands hormones secretion.
Unfortunately, 33% of the patients with ER-positive breast cancer (with ER genes mutations) don’t respond to treatment for a long period of time as such breast cancer forms build resistance to tamoxifen and aromatase inhibitors, leading to metastasis and, eventually, death.
DNA studying revealed new information about how such resistance builds
In 2013, another group of scientists observed for the first time that ER genes mutations are the culprits for ER-positive breast cancer treatment resistance.
However, the recent study conducted by the Dana-Farber’s scientists reveals something new. That, the mutations of the ER genes are not only building the resistance to treatment but also cause the breast cancer tumors to metastasize.
“That tells us that even though the drug therapies are selecting tumors that can grow without estrogen, the mutations also confer a metastatic advantage to the tumor,” stated Dr. Brown, one of the study’s authors.
Researching further for a way to avoid treatment resistance and metastasis, the scientists observed in cell cultures and lab animals that their previously developed CDK7 gene inhibitor (THZ1) is slowing tumors growth and is canceling the breast cancer treatment resistance occurrence, but only when administered along with estrogen inhibitors.