'Missing link' Discovered
In Fight Against Cancer
By Robert Matthews
Medical scientists believe that they have found the "missing link" between the causes of cancer and the body's immune system.
Following the breakthrough researchers think that they can explain why tumours can sometimes evade the body's defences and how existing anti-inflammatory drugs could help to fight against the disease. According to this new view of cancer, these defences could be boosted by regular doses of a common drug such as aspirin.
With around one in three people in Britain developing cancer at some stage in their life, finding ways of treating or preventing the disease has been the target of medical science for decades. But while the causes of most forms of cancer are now well-recognised, only in a few cases - such as with Tamoxifen and breast cancer - have efforts to fight the disease been successful.
In theory, the body's own immune system should seek out and destroy any cancerous cells. Such cells are constantly being created because of genetic damage but are usually dealt with. Why this does not always happen has, however, so far been a mystery. Now scientists in Britain have, for the first time, tied the spread of cancer to the failure of the immune system to stop the disease.
The link emerged following a lecture given last year by Prof Angus Dalgleish, an expert on cancer and immunology at St George's Hospital, London, to cancer researchers at Leicester Royal Infirmary. He explained that studies of the immune systems of patients with colon cancer had found unusually low levels of so-called Th1-type immunity, which is involved in fighting microbes.
This suggested that the cancer thrived when Th1 (thymus-derived helper cell type 1) levels were low - when, for example, the immune system was fighting inflammatory diseases. In the audience was Dr Ken O'Byrne, from Leicester Royal Infirmary, who was studying how tumours spread through new blood vessels around them. He told The Telegraph: "A whole lot of things suddenly fell into place."
According to Dr O'Byrne, the picture of cancer that emerges is of a disease that starts with healthy cells being attacked for many years by irritants such as the chemicals in tobacco smoke. This causes long-term inflammation which, in turn, prompts the body's immune system to switch into healing mode, lowering its Th1 level to allow repairs to be carried out.
Dr O'Byrne said: "The trouble is that we need Th1 to detect and deal with invaders like viruses and bacteria, and also with normal cells that have turned cancerous. But if Th1 levels have fallen, it means that any cells that have become cancerous have a better chance of evading our immune system." Worse still, the wound-healing process triggered by inflammation is also linked to increase in the so-called Th2 response, which is responsible for creating new blood vessels around damaged tissue.
Dr O'Byrne said: "This is fine if the tissue really does need repair. But if it's actually made from cancer cells, then these new blood vessels just allow the tumour to grow and spread around the body." Long-term tissue inflammation thus leads to a "double whammy" effect, said Dr O'Byrne: "Not only does the lower Th1 level allow cancer cells to go undetected, but the increased Th2 level actually helps them to grow and spread."
According to Dr O'Byrne, this new view of cancer explains why the disease is so often linked to inflammatory disorders. "Evidence has been accumulating for years that conditions like ulcerative colitis and chronic hepatitis are linked to cancer in later life. Now we can explain why. It is the response of the immune system to these inflammatory conditions which allows cancer cells to thrive." More importantly, said Dr O'Byrne, it points to new ways of tackling the disease. "It suggests that drugs that fight inflammation and raise Th1 levels could help fight cancer, or even prevent it. Aspirin is an obvious case in point."
According to Prof Dalgleish, there is already evidence that taking aspirin long-term does help prevent cancer. He said: "There are many reports that patients taking aspirin over many years really do have a lower rate of many cancers, including colorectal, oesophageal and lung cancer - just as this new approach would predict." Prof Dalgleish is now working with Dr O'Byrne on a series of papers for leading medical journals outlining the implications of the new view of cancer.
He said: "What we need now is a big clinical trial to test this new approach, with thousands of patients over several years." The findings so far have already caught the attention of other leading cancer experts. Prof Robert Hawkins of the Christie Hospital, Manchester, said: "It is a very interesting proposal that needs to be pursued."
Prof Adrian Harris of the Imperial Cancer Research Fund unit at the Churchill Hospital, Oxford, said that by linking cancer with inflammation the new approach may lead to more ways of stopping the spread of cancer. He said: "To spread, tumours have got to get a blood supply and also escape immune surveillance, so this new approach gives two routes for dealing with that."
Prof Dalgleish said that a combination of anti-inflammatory drugs and Th1 boosting agents could have a dramatic impact on the war against cancer: "At the very least we may be looking at such a combination helping to prevent and treat over half of all cancers." He said that he was already sufficiently convinced of the link to have begun a regular course of anti-inflammatory medication: "I now take at least 300mg of dissolvable aspirin each day."
Prof Dalgleish said, however, that such a course should only be undertaken under medical supervision.

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