The protein, called Bcl-xL, has the ability to help keep cells alive, but does so by interfering with programmed cell death, or apoptosis, a process that can rid the body of unwanted or damaged cells.
Because of its protective function in the body, the protein potentially could be used to selectively shield cells from toxic therapies if it were not for the increased risk of tumor development.
The study compared the effect of urethane, a lung-specific carcinogen, on two sets of mice: wild-type mice, which have two functional genes that express Bcl-xL, and transgenic mice that have only one functional gene expressing Bcl-xL. Because they have only one of the genes, the transgenic mice produce less Bcl-xL.
After exposure to urethane, 40% of wild-type mice developed seven or more lung tumors, while no transgenic mice developed more than seven tumors. Furthermore, wild-type mice on average had larger tumors than transgenic mice.
The research team then examined liver cell damage resulting from a regimen that mimicked a three-day alcoholic binge. In this case, wild-type mice fared better than transgenic mice. Transgenic mice showed higher serum levels of a marker for liver injury and greater evidence of damage in tissue examined microscopically.