A study led by researchers at Memorial Sloan Kettering Cancer Center (MSK) and Weill Cornell Medicine discovered a new relationship between cancer cells and the immune system, and shows how cancer can selfishly hijack a normally helpful immune pathway.
Usually, activation of this key immune pathway -; called the STING pathway -; triggers a strong inflammatory response that protects the body from foreign and unhealthy cells. But prolonged activation of the same pathway leads to a desensitization and ultimately to a "rewiring" of cellular signaling, which aids and abets cancer's spread, the researchers found.
"There's been millions of dollars invested in drugs that activate the STING pathway to fight cancer, and so far in clinical trials, they have not shown significant anti-cancer efficacy," Dr. Bakhoum said. "In the lab, these drugs held a lot of promise -; but in one trial of 47 patients, there were only two whose cancers even showed a partial response.
When cell division goes haywire Central to the research is a phenomenon known as chromosomal instability. Cooperation between cancer cells and the immune system is driven by STING A previous collaboration between researchers at MSK and Weill Cornell Medicine, which was also published in Nature, showed the complex chain of events triggered by chromosomal instability leads to changes in cells that drive cancer metastasis.
Related StoriesThe results from mouse models of cancer were then validated in healthy cells and tumor samples from human patients. "One of our most important findings was that altering the level of chromosomal instability or the activation of STING dramatically changes responses in the environment in and around the tumor," Dr. Laughney said.
"When you look at the effects that elicit a response in the cancer microenvironment, all the ligands on those chromosomally unstable cancer cells were associated with a specific cellular stress response -; one that happens to involve STING," she said.
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