Stress DOES have an impact on cancer: Anxiety switches on a gene that speeds up the spread of the disease Study found that stress triggers a 'master switch' gene called ATF3 This corrupts the immune system, giving cancer an fast-track around body Discovery could help develop drugs to dampen the 'stress gene' 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 say 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. Professor 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. The 'stress gene' could one day function as a drug target to combat cancer spread 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. Prof 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.' Meanwhile, 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. 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.'