Switching TNF to the ‘dark side’ – how a cancer killer becomes a cancer promoter

Dr Marcos Vidal's research is revealing how the immune system responds to cancer

Our immune systems are highly trained to recognise and destroy foreign invaders such as bacteria and viruses. But cancer starts from our own cells, so it’s difficult for the immune system to recognise and fight tumours.

However, our immune defences do have some powerful weapons at their disposal, including a molecule called tumour necrosis factor, or TNF. As the name suggests, TNF activates the immune system to help kill cancer cells. But at a certain point in the development of cancer, TNF switches to the ‘dark side’ and starts encouraging tumours to grow and spread.

Now recent research, published in the journal Developmental Cell, from scientists at the Cancer Research UK Beatson Institute in Glasgow explains what causes this change.

Led by Dr Marcos Vidal, the team found that when a certain cancer promoting gene is switched on and another cancer protective gene is switched off, TNF changes from a cancer killer to a cancer promoter. At the moment the team are working with fruit flies, but they plan to find out if the same mechanisms are at work in human cells.

Here’s a short interview with Dr Vidal, explaining more about his work:

[youtube=http://www.youtube.com/watch?v=-MT8IzVmsvA]

Understanding what causes TNF to ‘switch sides’ is an important step in unravelling why the immune system responds (or doesn’t respond) to cancer.

Many scientists around the world, including some funded by Cancer Research UK, are working on immunotherapy – treatments that harness the power of the immune system to destroy cancer cells. This new research helps us to understand more about the complexities of the  immune response to tumours, and will shed light on lifesaving future treatments for cancer.

Kat

Reference:

Cordero, J. et al (2010). Oncogenic Ras Diverts a Host TNF Tumor Suppressor Activity into Tumor Promoter Developmental Cell, 18 (6), 999-1011 DOI: 10.1016/j.devcel.2010.05.014