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New research suggests that shiftwork and jet lag can accelerate tumor growth by "activating" genes.
According to the new study from the University of Pennsylvania, disrupting the circadian rhythms that fuel our sleep and waking cycles can "activate" genes that encourage cancer cells to multiply and "disable" those that block growth tumor.
This means that maintaining stable sleep schedules can help reduce the risk of cancer.
And researchers are even convinced that scheduling cancer treatments could make them more effective.
Long before cell phone screens, fluorescent lights and the 24-hour news cycle, the work program of the man was dictated by light and darkness.
And if we try to defeat nature with technology, our body still works with circadian rhythms, waves of sleep and waking that regulate many other body processes.
These rhythms circulate on a 24-hour cycle and are sometimes called internal clock.
But they are triggered by fluctuations in certain hormones that respond to environmental signals, including light.
Thus, when we force ourselves to stay awake late at night or to wake up during the dark hours, the body ends up fighting and the processes that would occur naturally at night.
We may not know all the mechanisms involved between biological rhythms and diseases, but some links have been clearly identified.
For example, women who work shifts are at a higher risk of developing breast cancer by 5% to 20% than the general population.
The same hormones that tell our body when to sleep also affect tumors.
Our melatonin levels, for example, increase when the sun goes down. This increase makes us sleepy and invites the body to go to bed.
Melatonin also has anticancer properties.
Knowing this, the U Penn researchers wanted to see how they could manipulate the sleep cycle, genes and cell division, a process that occurs uncontrollably in tumors.
Dexamethasone, a hormone sometimes used to treat inflammation, has the remarkable ability to accelerate and release daily rhythms at the cellular level.
When they exposed the cells to the hormone, they found that they tended to move from the stage where the cell itself was usually growing to the stage where it starts to produce more and more. DNA for cell division.
In other words, rupture accelerates cell division and, consequently, tumor growth.
This process relies on a domino effect: sleep disturbance triggers a gene that activates on a protein that activates another protein that acts as a key in igniting cell division.
But scientists have already developed a drug that blocks the activity of this second protein, used in the fight against tumors.
So, their theory was that if the timing could make the protein that feeds the tumor more aggressive, maybe it could also make the protein blocker more efficient.
They were right: treating the cancer cells with the drug, called PD-0332991, in the morning was more effective than treating the cells at night.
But when they made fun of the circadian rhythms of the Petri dishes or the diet mice, the drug again lost power.
"We suggest that a chronic disruption of the normal circadian rhythm tilts the balance between the expression of tumor suppressor and progressive tumor genes in order to promote tumor growth," said Dr. Amita Sehgal, co-author. author of the study and professor of neuroscience at U Penn.
& # 39; A better understanding of the molecular effects of jet lag, shift work and other sources of chronic disruption could help develop strategies to minimize the increased cancer risk associated with these behaviors, as well as better treatment strategies, including the timing of cancer treatment. & # 39;
In fact, the team's findings suggest that "chornotherapy" or a time-based cancer treatment might be able to overload drugs and techniques used to fight tumors.
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