Protein linked with lung cancer development

Results: A protein that normally helps defend cells from infection, known as NF-kappaB, can play a critical role in the development of lung cancer, according to MIT cancer biologists. The MIT team found that a particular pair of genetic circumstances is required to activate NF-kappaB in mouse lung tumors: expression of the cancer gene ras, and loss of the tumor suppressor gene p53. They also showed that inhibition of NF-kappaB in mice with that genetic profile can slow tumor growth.

Why it matters: The findings suggest that NF-kappaB could be a promising target for new drugs against lung cancer, which kills more than one million people each year. Any potential treatments targeting NF-kappaB could be useful in the 15 percent of human lung cancer patients who have the specific genetic mutations required to activate NF-kappaB.
 
How they did it: The researchers found that when they inhibited NF-kappaB in mice with lung tumors expressing this genetic profile, tumor growth slowed dramatically. During the three-week period following NF-kappaB inhibition, tumors in treated mice grew, on average, half as much as tumors in untreated mice. In some treated mice, tumors shrank.

Next steps: The researchers could use their mouse model of lung cancer to look for compounds that could selectively and powerfully inhibit NF-kappaB.

Source: "Requirement for NF-kB signaling in a mouse model of lung adenocarcinoma," Etienne Meylan, Tyler Jacks et al. Nature, Oct. 22, 2009.