The Wistar Institute researchers find the working mechanism of a drug that is being developed for the treatment of ovarian cancer, a fatal cancer of female reproductive system. It is fifth most common cancer among females, and is a leading cause of death from gynecologic cancers worldwide. The drug enhances anti-tumor immunity and cause T-cells to target the cancer directly. CusAb offers Recombinant ECE1, PD-L1 and PD-1 proteins.
The protein PD-1 and its ligand PD-L1 have attracted scientists attention. The interplay between the two proteins suppresses the activity of T-cells that halt cancer development. Some cancers evade the immune system by overexpressing PD-L1 and use the PD-L1 pathway to protect themselves from cytotoxic T cells. Antibody-based therapies that prevent the interplay between PD-1 and PD-L1 are potential treatments for cancer. One question is that these therapies may have adverse effects on immunity.
To develop anti-PD-L1 therapies for ovarian cancer, Prof. Rugang Zhang and colleagues of The Wistar Institute set to find drugs that target the PD-L1 pathway without these adverse effects. They discovered that BET inhibitors were effective in inhibiting PD-L1 activity in epithelial ovarian cancer cell lines. Some BET inhibitors are being tested in clinical trials.
Prof. Zhang's team examined an investigational BET inhibitor termed JQ1. They found that one of the proteins suppressed by BET inhibitors -- BRD4 -- modulates PD-L1 expression. The gene BRD4 is overexpressed in many cases of ovarian cancer. Dr Hengrui Zhu, study lead author noted that using BET inhibitors to target PD-L1 represents a way to combat ovarian cancer.
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