A handful of large studies of cancer risk factors have found that working the night shift, as nearly 15 percent of Americans do, boosts the chances of developing cancer.
MIT biologists have now found a link that may explain this heightened risk: in a study of mice, they found that two of the genes that control cells’ circadian rhythms also function as tumor suppressors. Disrupting these genes allows tumors to become more aggressive.
The researchers exposed mice to two different schedules. One group lived with a normal routine of 12 hours of light followed by 12 hours of darkness, while the other mice went onto a “jet lag” schedule: every two to three days, they were exposed to an additional eight hours of light. This mimics the biological-clock disruption that occurs when humans work night shifts or travel through multiple time zones. When this happens, the two genes that control the circadian clock, Bmal1 and Per2, don’t get the light cues that cause levels of the proteins they encode to oscillate throughout the day.
“Cells need the light cue, which is like a reset button for the clock,” says Thales Papagiannakopoulos, a former postdoc at MIT’s Koch Institute for Integrative Cancer Research, who worked with Koch Institute director Tyler Jacks on this study.
Under the jet lag scenario, tumors grew faster and were more aggressive than those in the mice living with a normal light/dark schedule. When the researchers kept the mice on a normal schedule but knocked out Bmal1 or Per2, tumors also grew faster. “If you disrupt these genes in every cell of the body, the light cues that you normally receive do not apply,” says Papagiannakopoulos. “It’s a way of taking a molecular hammer and just breaking this clock.”