TP53 is a tumor-suppressor gene, meant to keep cells from proliferating out of control. Mutations in the TP53 gene can lead to cancer—and, in fact, mutations in this very gene are often observed in triple-negative breast cancer. ESR2, meanwhile, is a protein found in more than half of all triple-negative breast cancers. In some cases, ESR2 appears to slow the spread of cancer cells, and in others, it appears to speed it up. In a study published on April 16 in the Journal of the National Cancer Institute, a group of scientists reported on the interactions between TP53 and ESR2, and uncovered some interesting results.    

Using laboratory tests, the scientists tested the effects of both overexpressing and deactivating the ESR2 protein, looking to see how these two processes would affect both overall cell growth, as well as the specific genes that are influenced by TP53. They also tested tumor samples from TNBC patients, and performed statistical analysis on data from TNBC patients in the METABRIC study. These steps were taken in order to determine the relationship between TP53 mutation, ESR2 levels, and patient outcome.   

 The results showed that, when there is no mutation in the TP53 gene, ESR2 actually promotes cancer growth, and so is disadvantageous. When there is a mutation in the TP53 gene, however, the ESR2 protein is actually beneficial, since, in that case, it inhibits cancer growth. Importantly, the researchers determined that the drug tamoxifen increases the levels of ESR2. This means that tamoxifen can help TNBC patients who do have the TP53 gene mutation—but would not be beneficial for those who do not have the mutation. These findings are important for the TNBC community, as tamoxifen could represent an alternative treatment to chemotherapy for a majority of patients who exhibit the TP53 mutation.

Read the original study here