BCL6 remarks
Researchers at the Stanford School of Medicine have reversed the traditional “protein suppression” approach in cancer treatment. The team developed a two-sided molecule called TCIP3 that turns the BCL6 protein, which feeds aggressive blood cancers, into a trigger that destroys the tumor.
In diffuse large B-cell lymphoma, cancer cells survive thanks to BCL6, which constantly silences cell death genes.
TCIP3 steps
One end of TCIP3 binds to BCL6, while the other end binds to the regulatory proteins P300 and CBP. This union reopens the suppressed death genes through the added acetyl tags, driving the cell to suicide. X-ray analyses showed that the molecule locks the two proteins together almost like glue.
Evaluation note
In mice transplanted with human lymphoma cells, the treatment administered twice a day completely eliminated tumors on day 11; no significant toxicity was observed. Further studies are needed before human trials; however, the method is said to hold promise for other cancers and for autoimmune diseases such as rheumatoid arthritis and myasthenia gravis.