STRESS fuels cancer by triggering a 'master switch' gene, which
allows the disease to spread, according to new research.
The 'unexpected' discovery could lead to the development of
drugs that target the protein and stop tumours spreading to
other organs and causing death.
Stress has long been linked to many forms of the disease
including breast and prostate cancer, but the reason has remained
a mystery.
Doctors have discovered the 'stress gene' ATF3 can make
immune cells behave erratically, giving cancer an 'escape route' to
other areas of the body.
Now a team at Ohio State University says our own bodies help
turn cancer against us by turning on a 'master switch' gene known
as ATF3, which is expressed in response to stressful conditions
in all types of cells.
Usually, it causes normal and benign cells to commit suicide if they
decide they have been irrevocably damaged.
But cancer cells somehow coax immune-system cells recruited to
the site of a tumour to express ATF3.
It is unclear exactly how, but the gene promotes the immune cells
to act erratically and give cancer an escape route to other areas
of the body.
The results published in the Journal of Clinical Investigation
provide important insights into how tumour cells use their signalling
power to co-opt the rest of the body into aiding cancer's survival
and movement to distant organs.
Prof. Tsonwin Hai said: 'If your body does not help cancer cells,
they cannot spread as far. So really, the rest of the cells in the
body help cancer cells to move, to set up shop at distant sites.
And one of the unifying themes here is stress.'
Her researchers first linked the expression of ATF3 in immune-
system cells to worse outcomes among a sample of almost 300
breast cancer patients.
Experiments on mice then found those lacking the gene had less
extensive spread of breast tumour cells to their lungs than ones
that could activate it.
"The cancer cells were always the same, but we had different
hosts. The primary tumors were similar in size, but only in the host
that can express ATF3 - the stress gene - did the cancer cells
metastasize efficiently.
"This suggests that the host stress response can help cancer to
metastasize.
"If the body is in perfect balance, there isn't much of a problem.
When the body gets stressed, that changes the immune system.
And the immune system is a double edged sword," she said.
In general, when cancer cells first appear, the immune system
recognises them as foreign and various immune cells travel to the
site to attack them.
Hai said if further research bear out the results "the stress gene
could one day function as a drug target to combat cancer spread,
or metastasis as it is known medically."
Although the work suggests a drug to dampen ATF3's effect
could lower the risk for metastasis, Prof Hai noted scientists do
not fully understand what the overall effects would be.
She said: "We have this gene for a reason. It is a gene that helps
us adapt to changes. So it is a question of how and when to
target ATF3."
Another new study has found restricting calories for a set
period of time - combined with targeted cancer therapy - can
increase the success of cancer treatment in mice.
The journal Blood reports that we eat, the body metabolises food
to produce energy and assist in the building of proteins.
If we consume less, the amount of nutrients available to the
body's cells are reduced, which slows the metabolic process and
limits the function of certain proteins - including one protein
associated with several cancers.
Dr. Jean-Ehrland Ricci, of the French Institute for Health and
Medical Research in Nice, said: "By understanding the link between
metabolism and the body's natural cancer suppressors and
activators, we can perhaps improve the efficacy of therapy and
improve survival for patients suffering from specific types of
cancer."
Although more research in a clinical setting is needed, the
promising results are believed to apply to humans too.
"We next want to examine what component of a reduced-calorie
diet - fats, sugars, or another food compound - influenced the
lymphoma cells' improved sensitivity to treatment."
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