New Target Discovered for ‘Triple-Negative’ Breast Cancer
Researchers at University of Virginia are working on variability of triple negative breast cancer. They have found a method for inhibition of triple-negative breast cancer by finding out unknown routes for restriction of uncoordinated growth.
Researchers have found a new target for triple-negative breast cancer on November 21, 2017. Triple-negative breast cancer is an aggressive and difficult-to-treat form of cancer. Unlike other breast cancer subtypes, its cells test negative for estrogen and progesterone receptors, as well as for a gene called human epidermal growth factor receptor 2 (HER2), which is involved in the development of breast cancer. Therefore, it is unable to respond to therapies inhibiting cancer-growing signals that come from estrogen, progesterone, and HER2.
Triple-negative breast cancer is highly variable in patients and among tumour cells of a patient, which makes it difficult to understand and treat. Other subtypes of breast cancer are homogeneous, which are easy to predict and treat. Treatment options available for triple-negative breast cancer includes surgery, radiation therapy, and chemotherapy, which cause side effects and rarely lead to remission.
“We’re interested in the variability that’s characteristic of triple-negative breast cancer. We believe this variability gives clues to how the cancer arises, and clues to treatment possibilities that would exploit the way the tumors are regulated or misregulated as the cells communicate with each other,” said Kevin Janes, Associate Professor of Biomedical Engineering Board of Reviewing Editors for Science Signaling.
The results are published in the journal Developmental Cell. Results of the study showed a possible way to rearrange a tumor suppressor protein Growth Differentiation Factor 11 (GDF11), which was found to be inactivated in triple-negative breast cancer cells. Janes and his colleagues have found that GDF11 is unable to mature into a bioactive tumor suppressor, as it should normally do, but instead accumulates within cells in a ‘pre-active’ state.
“Instead of trying to find and target hormones or genes that might promote growth of these tumor cells, as has been successful for other cancer types, we are focusing on a protein in triple-negative tumor cells that normally should inhibit abnormal cell growth, but has been disengaged. This is an exciting realization because we now can look for ways to remobilize the GDF11 precursor and reengage its normal tumor suppressive activity wherever triple-negative cancer cells reside in the body,” Janes said
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