Risk factors

It is estimated that 90% of NMSCs are linked to UV exposure and data from epidemiologic studies indicate that greater cumulative lifetime exposure is associated with a higher risk of developing SCC, whereas severe sunburns correlates more with BCC.6

Most cases of BCC are sporadic; however, it occurs frequently in the rare individuals with hereditary disorders such as basal cell nevus syndrome (also known as Gorlin's syndrome) and xeroderma pigmentosum (XP). The patched gene (PTCH), a tumor-suppressor gene, has been shown to be mutated in XP and 50% to 60% of sporadic BCCs. The oncogene bcl-2, which suppresses programmed cell death (ap-optosis), also has been found to be expressed in high levels in patients with BCC.

There is clear evidence linking defects of the immune system to the development of NMSC. For example, it is observed that patients receiving chronic immunosuppressant therapy for organ transplantation have a 50% risk of developing SCC within

20 years of transplantation, and 30% of these cancers are highly aggressive. Additionally, patients with HIV infection are predisposed to melanoma. Data also support the idea that UV radiation exposure induces immunosuppression and that this is associated with carcinogenesis.58 Langerhans' cells are responsible for antigen processing and initiation of the immune cascade in the skin, and it has been demonstrated that

UVB alters their function. UV radiation also induces suppressor T cells and activates biologic response modifiers by initiating cytokine cascades, ultimately leading to a state of immune tolerance and unsuppressed tumor growth.

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