The findings, published in Nature Medicine, suggest it may soon be possible to prevent this condition, giving people the strength to survive treatment and improve their chances of recovery.
The team of researchers from the Centre for Immunology at St Vincent's Hospital and the University of New South Wales and the Garvan Institute of Medical Research published their findings in Nature Medicine and found that most common cancers produce large amounts of a molecule known as MIC-1, which in turn targets receptors in the brain that switch off appetite. Antibodies against MIC-1 make it possible to switch appetite back on.
Conversely, when normal and obese mice are treated with MIC-1, they eat less and lose a lot of weight, suggesting that MIC-1 may also form the basis of a treatment for severe obesity.
Professor Sam Breit at the Centre for Immunology originally cloned the MIC-1 gene. Working with Professor Herbert Herzog, Director of the Neuroscience Research Program at Garvan the reached their findings and determiend this molecule's effect on metabolism and the brain control of appetite.
"This work has given us a better understanding of the part of the brain that regulates appetite. Our bodies send complex chemical signals to our brains, which interpret them and send back responses, in this case 'eat' or 'don't eat'. Our research indicated that MIC-1 is a previously unrecognized molecule sending a 'don't eat' signal to the brain," said Professor Herzog.
Professor Sam Breit said, "Injecting mice with MIC-1 protein also made them stop eating, suggesting that it may be possible to use this to advantage for treating patients with severe obesity."
The study showed that if a human cancer making a lot of MIC-1 is grafted onto a mouse, that mouse lost weight dramatically. Researchers say this new evidence gives hope for cancer patients and the health officials that treat them.
