An innovative treatment for B cell lymphoma could hold the key for a new generation of precision cancer therapy, researchers have reported.
A team led by researchers at Stanford University, California, have developed the new treatment in the laboratory, aiming to reverse the resistance that lymphoma cells have to programmed cell death, known as apoptosis.
The treatment involves neutralising the cancer-promoting protein BCL6 that underlies diffuse large cell B-cell lymphoma. The new technique tethers BCL6 to CDK9, which then reactivates pro-apoptosis genes, the researchers have reported in Science.
The researchers say the approach is novel as it aims to switch on inactivated genes – while other targeted approaches seek to switch off cancer drivers. They believe they can use their treatment strategy to “trick” cancer cells into disposing of themselves.
Laboratory tests suggest the treatment is specific to diffuse large cell B-cell lymphoma, the researchers say. It killed only lymphoma cells and had no effect on 859 different kinds of cancer cell.
The team now plan to test the treatment on laboratory mice. The developers are hoping it will avoid treatment resistance, as 13 different apoptosis promoting genes are reactivated in the process.
Researcher Professor Gerald Crabtree said: “It occurred to me, this is the way we want to treat cancer. We essentially want to have the same kind of specificity that can eliminate 60 billion cells with no bystanders, so no cell is killed that is not the proper object of the killing mechanism.”
Researcher Dr Roman Sarott said: “Since oncogenes were discovered, people have been trying to shut them down in cancer. Instead, we’re trying to use them to turn signalling on that, we hope, will prove beneficial for treatment.”
Source:
Sarott RC, Gourisankar S, Karim B, Nettles S, Yang H, Dwyer BG, Simanauskaite JM, Tse J, Abuzaid H, Krokhotin A, Zhang T, Hinshaw SM, Green MR, Crabtree GR, Gray NS. (2024) “Relocalizing transcriptional kinases to activate apoptosis.” Science, 4 October 2024, doi: 10.1126/science.adl5361
Link: https://www.science.org/doi/10.1126/science.adl5361
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