News Fighting the growth of skin cancer cells By Professor Gareth Inman at the Cancer Research UK Beatson Institute and the Institute of Cancer Sciences, University of Glasgow. DEBRA is funding research led by Professor Gareth Inman to investigate Squamous Cell Carcinoma (SCC) an aggressive form of skin cancer which affects children and adults living with a form of EB known as Recessive Dystrophic Epidermolysis Bullosa (RDEB). Professor Gareth Inman at The Old Firm Dinner Recessive Dystrophic Epidermolysis Bullosa (RDEB) is an inherited disorder that results in fragile skin that blisters easily, heals slowly and is prone to excessive scarring. Another serious complication is that a high proportion of people with RDEB will develop a skin cancer called squamous cell carcinoma (SCC), which is often fatal. All cell functioning is regulated by signals being passed within and between cells. We and others have recently shown that a specific signalling system, involving a molecule called Transforming Growth Factor- β (TGF-β), is severely disrupted in the skin of people with RDEB and may act to contribute to inflammation, scarring and cancer development. We have found that TGF-β produced by patient’s cancer cells can act to promote the growth and movement of the cancer cells themselves possibly contributing to tumour growth and spread. Inhibiting TGF-β signalling can block cancer growth and movement in more than half of the samples we have tested and may, therefore, be able to be developed into a potential new therapeutic approach. In some samples, however, inhibiting TGF-β signalling can promote can cell growth. We now need to understand which patients could benefit from therapies that target TGF-β signalling and which would not and how TGF-β signalling can promote cancer cell growth and movement. Understanding this may enable us to develop therapeutic strategies for patient benefit. This research is vital in helping to identify new ways of slowing down the growth of skin cancer cells for people with RDEB and will provide a significant opportunity for future drug and therapeutic development. So far we have stopped growth in over 50 per cent of RDEB patient skin cancer cells in the lab. Now we need to find out how we can improve and exploit these findings for patient benefit. My team and I are really eager to get started.