TRIM37 Overexpression and PLK4 Inhibitor to Come up as Novel Breast Cancer Treatment Regimen

Release Date: 20-Nov-2020

A group of researchers at Johns Hopkins University School of Medicine and the University of Oxford have developed a potential mechanism of action of stopping the cancer cells found in breast cancer by targeting an important key mechanism that is employed by the cancer cells for its division. According to the researchers, the breast cancer cells overexpresses protein called as TRIM37. The treatment of the protein with PLK4 inhibitor disrupted the overall activity of the centriole which is important for the division of the cell. The researchers focused on such activity of the inhibitor and led to a clinical study that targets the inhibitor and the protein for finding an important treatment for cancer.

The researchers involved in the respective study took the cancer cells that have high copy number of 17q23 chromosomal region. It is observed that their cell division process is completely dependent on the centrioles. It was also observed by the researchers indulged into the clinical research study that 40 protein-coding genes located within the 17q23 region there was TRIM37 protein. Therefore, the researchers introduced PLK4 inhibitor so that they could evaluate cell division process in the TRIM37-overexpressing breast cancer cells. It was found by the researchers that breast cancer cells with TRIM37 levels when treated with were not able to divide.  Therefore, marking that TRIM37 overexpression could be targeted to develop an efficient therapy for the breast cancer patients. The same is taken forward by developing a PLK4 inhibitor- Dubbed CFI-400945 combined with AstraZeneca’s PD-L1 inhibitor Imfinzi against triple negative breast cancer. The clinical outcome of the research study is estimated to transform the entire breast cancer therapeutics market in the near future.