British scientists have announced a major breakthrough in understanding the spread of cancer – and it should lead to dramatic improvements in survival rates.
The exciting discoveries – explaining why some cancer cells break free and develop into new tumours – will drive future efforts into developing drugs that can find and then kill those itinerant cells.
Researchers from the Beatson Institute in Glasgow have discovered that a protein which suppresses cancer in healthy people changes sides or "flips" in some sufferers, allowing cancerous cells to break away, move and survive elsewhere in the body. The protein, P53, is mutated or flipped in 50 per cent of all tumours, which means that this breakthrough could eventually stop the disease from spreading in thousands of patients a year. While recent advances in treatments for single-site tumours have saved thousands of lives, nine out of 10 cancer deaths are the result of secondary tumours or metastases.
Understanding the basic science behind why some cancers cells can break away from a tumour, move and
then thrive in other parts of the body is the key to improving the survival rates for cancer patients.
The research, published in the peer-reviewed journal Cell last week, was carried out by two teams of experts working side by side in the pioneering Cancer Research UK institute. Professor Karen Vousden, co-author and the P53 expert, said: "This is very exciting because we're talking about huge numbers of people here, not a rare event. We still need to burrow down more deeply but this takes us a nice step along the way; it is an extremely important piece of the cancer spreading jigsaw. Understanding what goes wrong with cells and proteins to allow cancer to spread will make it much easier to fix or stop. Working together with other experts at the institute has allowed us to make this discovery so quickly."
Experts agree that the biggest challenge in cancer treatment is to stop it from spreading to other parts of the body. This is very difficult to replicate in a test tube, which means that advances in this area have been slow.
Working alongside Professor Vousden's team were the integrin experts. Integrins are linking molecules which connect cells to non-cellular tissue such as a membrane or collagen. In cancer patients who have the mutated P53, the integrins are encouraged to behave abnormally. They come into the cancer cell, along with the growth factor receptors, before returning to their original position on the cell wall; all this is co-ordinated by another important protein called rab coupling protein (RCP), the study found. This rapid process is like the "reach and grab" action used to climb up a ladder which pulls the cell along and encourages it to multiply. The cycle is repeated over and over again, promoting the growth of the malignant cells.
Professor Jim Norman, co-author and the integrin and RCP expert, said: "Until now the integrin and P53 fields have sat apart. This research pulls them together. Drugs that simply block the movement of cells won't work; that's like blocking the barn door after the horse is bolted. We now know that we must find drugs that can seek out cells which are inappropriately on the move, and then kill them."