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Major discovery into cancer weight loss

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La Trobe University scientists have discovered the cause of cachexia, the muscle wasting disease that kills up to one third of all cancer patients.

Work on developing drugs to potentially stop the disease has already begun.

Cancer-cachexia is the loss of body weight seen in many advanced cancers and manifests as muscle loss, fat loss and overall metabolic imbalance.

Estimated to account for up to 30% of all cancer deaths, the condition severely restricts treatment options for people with late-stage cancers.

The research found that Fn14, a receptor on a cell’s membrane which is often present on cancer cells, can cause cachexia. (Watch the video report here.)

A large number of people with cancer – between 50 to 80% of those with solid tumours – suffer from this wasting condition. In advanced cachexia, cancer treatment is often withdrawn due to a person’s emaciated state.

Game changing research

It was always thought that weight-loss was due to cancer spreading and consuming the body, with loss of appetite and nutritional complications causing the body to waste away.


However, in game-changing research published in the top international life sciences journal Cell, a 28-member international research team led by the Department of Biochemistry and Genetics at the La Trobe Institute for Molecular Science (LIMS) has shown otherwise.

It found by blocking Fn14 they could stop the cachexia, regardless of the presence of a tumour.

Professor of Biochemistry, Nick Hoogenraad, said ‘These findings, based on about a decade of research, could translate into huge benefits for those fighting serious illness and the potential for effective treatment is now much closer to reality.

‘If we can arrest cachexia it will give people extra time, improved quality of life, make them stronger and allow for therapy to continue. This is a very significant development.’

Colleague and lead author of the Cell paper, Dr Amelia Johnston, said that ‘Fn14 has been known to be involved in cancer, but it was a surprise to us that it caused the wasting condition.’

‘Our treatment is an “antibody” directed against Fn14, and because antibodies are very specific to their target, this means treatment is less likely to come with the unwanted side effects of other therapies such as many chemotherapy drugs.’

The discovery brings the researchers closer to finding a way to stop cachexia and may have potential to also help fight cancer directly. In some cases, treatment with the ‘antibody’ therapy that blocked the cachexia also slowed the growth of the tumours.


Preparation for human trials

‘Our findings are a positive step in the right direction for developing a treatment for cancer-cachexia. We are currently converting the antibody therapy into a treatment appropriate to trial in humans,’ Dr Johnston said.

‘This is being done in collaboration with scientists at the Olivia Newton-John Cancer Research Institute. After we have made an equivalent therapy for human use, clinical trials would be the next step.’

University of Melbourne collaborator, Dr Kate Murphy, helped characterise the laboratory model of the disease used in the research.  She said ‘Cancer cachexia is such a serious complication of cancer and affects patients’ quality of life and ability to undergo punishing chemotherapy treatments. There is no treatment for cachexia, so the ability to develop one would be a huge step forward.’

The 28-member international research team included Professor Nick Hoogenraad, Dr Amelia Johnston and Laura Jenkinson, La Trobe University; Associate Professor John Silke, Walter and Eliza Hall Institute; Professor Gordon Lynch and Dr Kate Murphy, University of Melbourne; and scientists from Melbourne’s Baker Institute.

International collaborators are from the Universities of Lausanne and Zürich, Switzerland; and Harvard, MIT and Biogen Idec in the US.  

The research was originally funded by the Co-operative Research Centre for Biomarker Translation and is currently funded by the NHMRC.

(Source: La Trobe University)



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Dates

Posted On: 12 October, 2015
Modified On: 18 October, 2015

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