Shift work and jet lag may make tumors grow faster by ‘turning on’ genes, new research suggests.
Disrupting the circadian rhythms that fuel our sleeping and waking cycles may ‘turn on’ genes that encourage cancer cells to multiply and ‘turn off’ the ones that block tumor growth, according to the new University of Pennsylvania study.
That means that simply keeping sleep schedules steady may help to cut cancer risks.
And the researchers even believe that timing cancer treatments correctly could make them more effective.
Night shift work and jet lag may throw off our biological clocks in a way that blocks tumor-fighting activity in the body – and even suppresses treatment effects, a new study finds
Long before cell phone screens, fluorescent lights and the 24-hour news cycle, the human schedule was dictated by light and dark.
And try as we might to overcome nature with technology, our bodies still operate according to circadian rhythms, waves of sleeping and waking that regulate many of the body’s other processes.
These rhythms flow in a 24 hour cycle and are sometimes referred to as the internal clock.
But they are triggered by fluctuations in certain hormones that are, in turn, responsive to environmental cues, most notably light.
So when we force ourselves to stay up late into the night, or to do waking behaviors during dark hours, the body winds up fighting itself and the processes that would naturally occur at night.
We may not know all the mechanisms at play between biological rhythms and illnesses, but some links have been clearly identified.
For example, women who do shift work are at five to 20 percent greater risk of developing breast cancer than the general population.
The same hormones that tell our body when to sleep also have effects on tumors.
Our levels of melatonin, for example, swell when the sun goes down. This increase makes us feel sleepy and tells the body to go to bed.
Melatonin also has cancer-fighting properties.
Knowing this, the U Penn researchers wanted to see how they could manipulate the sleep cycle, genes and cell division, the process that happens out of control in tumors.
A hormone sometimes used to treat inflammation, called dexamethasone has the remarkable ability to speed up and throw off daily rhythms at the cellular level.
When they exposed cells to the hormone, they found that they tended to skip ahead from the stage when the cell itself would typically grow in size to the stage at which it starts making more DNA in preparation for cell division.
In other words, the disruption accelerates cell division and, therefore, tumor growth.
That process relies on a domino effect: the sleep disruption kicks on a gene that activates on protein that activates another protein that acts like a key in the ignition for cell division.
But scientists have already developed a drug that blocks the activity of that second protein, which is used in tumor fighting.
So, their theory was that if timing could make the tumor-fueling protein more aggressive, maybe it could make the protein-blocker more effective, too.
They were right: treating cancerous cells with the drug, called PD-0332991, in the morning was more effective than treating the cells at night.
But when they messed with the circadian rhythms of either the Petri dish cells or mice on the regimen, the drug lost some of its power again.
‘We suggest that chronic disruption of the normal circadian rhythm tips the balance between tumor-suppressive and tumor-progressive gene expression to favor tumor growth,’ said Dr Amita Sehgal, study co-author and neuroscience professor at U Penn.
‘Better understanding the molecular effects of jet lag, shift work, and other sources of chronic disruption may lead to strategies to minimize the increased cancer risk associated with these behaviors, and to better treatment strategies, including timing delivery of cancer therapy for maximum benefit.’
In fact, the team’s findings suggest that ‘chornotherapy’ or time-based cancer treatment might be able to supercharge drugs and techniques used to fight tumors.