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Last Updated: Friday, 10 November 2006, 11:46 GMT
Immune boost tackles skin cancer
Skin cancer cells dividing
The treatment appears to stop skin cancer progressing
The body's own immune system could be used to fight the most serious form of skin cancer, scientists have claimed.

Two US teams have been able to manipulate immune cells to boost the attack on cancer cells.

Research presented to a European cancer research conference in Prague showed longer-term survival in 29 patients.

Experts said the studies were "significant", but much more research was needed before the treatment could be offered to patients.

This is a fundamentally different approach to treating cancer
Dr Alexander Eggermont, chairman of the cancer conference

Malignant melanoma affects around 8,000 people in the UK each year, and there were 1,777 deaths from the condition in 2004.

The average life expectancy after diagnosis of the most serious form of the disease, stage four, is around nine months.

Surgery or high doses of chemotherapy drugs are used to treat the cancer, but while they can reduce the size of tumours they cannot prevent the disease recurring.

The immune system that attacks cancer cells is a finely balanced defence system.

The amount of one kind of T cells, which recognise and attack foreign bodies such as tumour cells is controlled by a second, called Tregs.

Tregs usually act as a break stop the immune attack going into overdrive and turning on the body.

Activation

One study found it was possible to suppress Tregs by blocking the activity of a protein on the cells' surface.

This meant other parts of the immune system were free to attack.

The University of California, Los Angeles researchers treated 25 patients with injections of an antibody to block the protein.

Almost a year-and-a-half later, 24 of the patients are still alive. Three are free of cancer.

In the second study, researchers from the University of Louisville in Kentucky treated seven people with advanced skin cancer with a drug combination of the diphtheria toxin and interleukin 2, to stop the Tregs effect.

Mice studies had already found that the combination led to another part of the immune system armoury called CD8+T lymphocytes being freed up to attack and kill melanoma cells.

The five patients on the higher dose saw their tumours shrink or remained stable. All seven are still alive 12 months after the treatment was given.

Dr Chesney told the cancer conference: "From the results, we conclude that depleting Treg cells in patients with melanoma may allow the immune system to be activated successfully to kill cancer cells.

"These patients have survived longer than the median average life expectancy of a patient with stage four melanoma."

He added: "We also believe that, in the future, immunotherapies that depend on depleting Treg cells may prove to be useful in all types of cancer."

Caution

Dr Alexander Eggermont, professor of surgical oncology at the University of Rotterdam in the Netherlands, chairman of the conference, said: "This is a fundamentally different approach to treating cancer.

"If we can change the rules of the game by keeping the immune system active, we might be able to prevent tumour regrowth."

However, there is a risk in removing the immune system's control mechanism.

There are concerns it could lead to autoimmune diseases - where the body attacks itself - such as hepatitis, colitis or dermatitis.

Rick Bucala, a professor at Yale University School of Medicine said the research could prove "highly significant".

But he said caution was still needed as there was relatively little data on the treatment.

Henry Scowcroft, science information officer at Cancer Research UK, said: "This is very early work with very ill patients, but the results are extremely encouraging.

"There have been several similar findings in recent years. Taken together, these advances suggest that immunotherapy is finally starting to live up to early expectations."


SEE ALSO
Gene therapy rids men of cancer
01 Sep 06 |  Health
Hope over new 'skin cancer patch'
30 Oct 06 |  Edinburgh and East

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