Scientists from the Stanford School of Medicine have developed a remarkable experimental method that targets the BCL6 protein, which enables tumor survival in certain aggressive blood cancers. In the study, this protein, which normally contributes to the survival of cancer cells, was transformed into part of a mechanism that leads the cell to death via a molecule called TCIP3.
The study focuses on diffuse large B-cell lymphoma, one of the most common types of Non-Hodgkin lymphoma. In this type of cancer, the BCL6 protein helps cancer cells multiply and survive by silencing genes associated with cell death. This system, which normally functions temporarily in the immune response, can pave the way for disease progression by remaining constantly active in cancer cells.
TCIP3 CHANGED THE DIRECTION OF THE PROTEIN
The TCIP3 developed by the researchers was designed as a double-sided molecule that brings two different structures together. One end of the molecule binds to BCL6, while the other end captures regulatory proteins called P300 and CBP. As a result of this contact, BCL6's gene-silencing function weakens, and the suppressed cell death genes are reactivated.
X-ray analyses showed that TCIP3 not only brings these proteins closer together but also creates a more stable structure at the molecular level. It was reported that lymphoma cells died rapidly even at low doses in laboratory experiments.

In animal experiments, mice transplanted with human lymphoma cells were given TCIP3 twice a day. According to the reported results, the tumors in the treated mice disappeared completely by the end of the 11th day. It was stated that no significant toxicity or increased inflammation was observed during the experimental process.
Although the findings are promising, the method has not yet been tested in humans. For TCIP3 to proceed to clinical trials, its chemical form must be improved, its safety must be verified in different animal models, and its potential side effects must be examined in detail.
Researchers believe that the idea of making cancer-feeding proteins work toward cell death instead of just suppressing them could open new doors for other resistant cancer types. Some autoimmune diseases associated with BCL6 are also indicated as future areas of research for this approach.
News Source: 12punto