Miércoles 31 de Mayo de 2006, Ip nº 155

Tumours 'sabotage immune system'
Scientists have shown how tumours can manipulate the immune system to stop it attacking cancer cells.
They have found that late-stage cancers produce a protein which switches the role of normally helpful immune cells.

Instead, of aiding the mobilisation of the immune systems defences, these cells start to inhibit attempts by the immune system to attack the cancer.

The study, by the Fred Hutchinson Cancer Research Center in Seattle, is published in Nature Immunology.

Tumours produce many types of abnormal proteins, which play different roles in their development.

Some enable the cancer to grow rapidly, but others appear to neutralise the effect of the immune system.

The Seattle team found one of these proteins changes the role of otherwise helpful immune cells, called T helper cells, which in the early stages of the disease play a key role in the body's efforts to destroy cancer cells.

In response to the tumour-derived soluble form of the protein the cells divide and take on a suppressor role, reducing the anti-cancer potency of the immune system.

Boosting cancer fight

Exactly how the T helper cells become suppressor cells is not yet known.

Lead researcher Dr Thomas Spies said: "Once cancer cells have established themselves as a growing, solid tumour they produce massive amounts of the protein and shed it into the bloodstream.

"It profoundly alters the composition of T cells in the body of the cancer patient such that the capacity of the immune system response against tumour cells is severely impaired."

Dr Spies said the protein was of potential clinical interest.

He said: "If one could prevent a tumour from producing the soluble protein it could be beneficial in terms of helping sustain the immune system's normal capacity to mount an anti-tumour response."

Professor John Trowsdale, of the charity Cancer Research UK, said: "The work sheds light on ways in which the body's immune system could be used to tackle cancerous cells."

  28/05/2006. BBC News.