Scientists know that most cancer cells use glucose to fuel their uncontrolled growth and now an international team of researchers has identified a protein which if switched off could stop the disease in its tracks.
Explained lead academic Dr Concetta Bubici from Brunel University London: "The protein PARP 14 is over-produced in virtually every human cancer but not in normal cells.
"What we have discovered is that its role in cancer is to allow cells to harness glucose in a different way from healthy ones which in turn powers their rapid, uncontrolled growth while also protecting them from the normal cycle of programmed cell death.
"Almost all cells in the human body have a strictly limited life. In stimulating over-production of PARP 14, cancer cells effectively are not only turbo-charged through being able to use glucose to grow and divide which takes a lot of energy but also become immune from the natural checks and balances of the cell death cycle known as apoptosis.
Added Dr Salvatore Papa from the Institute of Hepatology London: "We discovered that too much PARP 14 effects other proteins in the body called kinases that control apoptosis.
"So if we can find a way of stopping this over production of PARP 14 we can cure cancer."
A further benefit of such a new therapy would be to make cancer more vulnerable to existing chemotherapy which the team expect will continue to be used .
Controlling or inhibiting proteins and enzymes in the body is now an integral part of modern medicine widely used to for conditions from stomach ulcers to depression and already has an important role in preventing the recurrence of breast cancer.
But the team warn that much more research needs to be done before doctors are able to prescribe a drug which will inhibit PARP 14.
PARP 14 Q& A
What's so exciting about this discovery of the role of PARP 14?
The research offers a new way of attacking cancers after discovering exactly the role of excess PARP14 in how cancer cells fuel their rapid and uncontrolled growth
If we can find a way of returning PARP 14 levels to that found in healthy cells, cancerous ones will, in effect, be put on a starvation diet.
Cancer cells are able to use the basic fuel of cells -- glucose -- in a different way to healthy cells in the presence of excess PARP 14.
Is that the only way controlling PARP 14 levels could effect cancer?
No. Excess PARP 14 has two further consequences. Most human cells have a life cycle (the main exception being most brain cells) and then they are replaced. Cells on the gut wall are regenerated every five days others have a life span of as much as 15 years.
Excess PARP 14 interferes with this natural process significantly extending cancer cell life. The mechanism for this is by interfering with the action of proteins called kinases.
It's the discovery of this mechanism by the international team which is so exciting as offers the opportunity to target excess PARP14. The search for a specific inhibitor is the next aim for the team and other scientists.
Reducing PARP14 also makes cancer cells more susceptible to existing chemotherapy treatments so they expect any new therapy would go hand in hand with chemo. A further consideration is that cancer cell growth is not the only aim of cancer treatments. Killing every single cancer cell and preventing their spread or metastasis to other parts of the body are also equally important.
Wouldn't reducing sugar consumption have a similar effect?
No. The body produces glucose as fuel for healthy cells from many different foods and glucose is absolutely essential for life.
Could any new therapy be used to cure all cancers?
The role of excess PARP 14 is very new science. The team found evidence of excess PARP14 in a wide range of cancers from solid tumours to blood cancers. However it would not be good science to claim it is a universal mechanism until further research is complete.
What is the likely timescale before a new therapy is available widely to cancer patients?
This is almost impossible to predict because of the huge range of variables involved. But the prospects are very exciting indeed.
Cite This Page: