Skin cancer is a malign tumour, highly metastatic, that has undergone a spectacular increase in all of its clinical forms in the last 40 years, with a threefold increase in its incidence. Besides genetic predisposition, intense exposure to sunlight by light skinned patients, together with antecedents of sunburn during childhood, constitute the principal risk factor for its appearance.
Many clinical and histological observations suggest a clear interaction between the immune system of the host and skin cancer. In the disease's progression, in the passage from a phase of horizontal growth to an invasive phase of vertical growth - the determinant factor in prognosis - factors intervene that are only partially understood.
Angiogenesis, or the development of new vessels, is necessary to maintain the growth, invasion and metastatic capacity of a tumour. VEGF and bFGF are outstanding amongst the pro-angiogenic cytokines secreted by the skin cancer cells; these favour endothelial proliferation and the invasive capacity of the tumour. Similarly, it has been found that the presence of Th1 cytokines in the tumourous environment prevents the disease's progression and favours regression, while a Th2 pattern favours invasion and increases the potential for metastasis.
The decline in the immune response of the host might be mediated by the synthesis of immuno-suppresser cytokines by the tumourous cells (IL-10, TGF-_, VEGF) and by the expression on its surface of Fas-L molecules, which make skin cancer a privileged tissue from an immunological point of view.
CITATION An Sist Sanit Navar. 2000 Jan-Apr;23(1):67-84
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