When a tumour invades beyond its initial site of growth and actually develops in distant tissues ( a process called metastasis) this usually results in poorer chances of long-term survival for the patient. Thus preventing this initial invasion is a goal in anti-cancer medicine. In recessive dystrophic epidermolysis bullosa (RDEB) the major cause of premature death is the development of squamous cell carcinoma (SCC) that, unusually for skin-derived SCC becomes metastatic. In order for tumour cells to invade they require cell surface molecules, called integrins, to enable them to attach to the protein matrix outside of the cells (the so called extracellular matrix- ECM) which provides traction for cell movement. The tumour cell must also utilize from the ECM, or generate themselves, enzymes which degrade the ECM to enhance their ability to move through (invade) this matrix.

When SCC develops in RDEB the researchers have found that the presence of an integrin, which is not usually present in normal resting skin, is significantly increased. This same integrin, called a vb 6, promotes invasion and enzyme production in invasive SCC cells derived from oral cancers. This invasion can be inhibited in the laboratory by blocking the function of a vb 6 with antibodies, that prevent binding of the integrin to the ECM, or chemicals that act to disturb the biochemical signals that a vb 6 generates when it is working. Thus, the researchers believe that the a vb 6 molecules that are increased in SCC from RDEB are also promoting invasion in a similar fashion.