Stanford researchers develop molecule that forces cancer cells to kill themselves

Promising study turns oncogenes against cancer's natural survival mechanisms

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In context: Every day, billions of cells in the human body die thanks to a natural process known as apoptosis. When apoptosis doesn't work by design, cells get cancerous and can cause a life-threatening illness. Now, researchers at Stanford University are working on a novel way to treat, and possibly kill for good, a specific type of cancer.

The researchers' recently published study describes a way to re-activate apoptosis in mutated cells, which would amount to forcing cancer to self-destruct through a bioengineered, bonding molecule.

Gerald Crabtree, one of the study's authors and a professor of development biology, said he had the idea while hiking through Kings Mountain, California, during the pandemic period. The new compound would have to bind two proteins which already exist in the cancerous cells, turning apoptosis back on and making the cancer kill itself.

"We essentially want to have the same kind of specificity that can eliminate 60 billion cells with no bystanders," Crabtree said, so that no cell gets destroyed if it isn't the proper target of this new killing mechanism. The two proteins in question are known as BCL6, an oncogene which suppresses apoptosis-promoting genes in the B-cell lymphoma, and CDK9, an enzyme that catalyzes gene activation instead.

Mutated BCL6 proteins block a signal that should normally bring cancerous cells to activate apoptosis. Traditional, non-destructive cancer treatments have been targeting oncogenes to try and shut the cancer down, while the new study proposes a mechanism to exploit them instead. "You take something that the cancer is addicted to for its survival and you flip the script and make that be the very thing that kills it," Crabtree said.

The researchers tested the new molecule designed to bond BCL6 and CDK9 in diffuse large cell B-cell lymphoma cells in a lab environment, where the compound proved to be effective at killing the cancerous cells. Then they tested the compound in healthy mice to see if it had any toxic effect on normal cells, which it didn't. However, the molecule seemed to target a specific type of immune cells (B cells) which also contained a non-mutated version of the BCL6 protein.

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The team is now testing the molecule on mice affected by diffuse large B-cell lymphomas, to see if the method is effective at killing cancer in living animals. The technique relies on the natural supply of BCL6 and CDK9 in cells, which means it will likely work only on cancerous lymphomas. After testing the new molecule with 859 different types of cancer cells in the lab, the researchers confirmed that it was able to kill only diffuse large cell B-cell lymphoma cells.