BCC is the most common form of skin cancer in White individuals in temperate climates, accounting for 80% of NMSC. BCCs are slow growing and invade local tissues; metastasis is extremely rare.
The registration of BCC is poor in many countries despite its high incidence. One reason is that BCCs may be treated by different clinical specialists with methods, such as cryotherapy, that may preclude histological confirmation. These limitations are refl ected in the reported annual incidence rates in Europe, which range from 50 to 130 per 100 000. The annual incidence in Australia is much higher, ranging from 800 to 1500 per 100 000. The difference in incidence provides evidence for the causative role of ultraviolet (UV) radiation. The mean age at diagnosis is 60 years, although over the last 10 years there has been a notable increase in BCC among younger individuals, especially females in the 20 - 40-year age group.
As with other skin cancers, exposure to UV radiation is the most important risk factor for developing BCC. BCC mainly affects individuals who have a tendency to sunburn, such as those with fair skin and light eye colour. The exact relationship between sun exposure and the development of BCC is unclear, and certainly more complex than for SCC. For example, relatively sun-protected areas such as behind the ear are affected disproportionately more than heavily sun-exposed areas such as the helix of the ear.
In addition, patients who develop BCC tend to have less photodamage (including actinic keratoses, solar lentigines and photoageing) compared with patients who develop SCC. These observations suggest that intermittent sun exposure in childhood and early adulthood is more relevant, as for melanoma, than cumulative UV exposure as with SCC. Less common risk factors include exposure to radiation, arsenic and immunosuppression. Identical twin pairs have been reported to develop BCC at a similar age and at similar sites, suggesting genetic susceptibility plays a strong role. Other epigenetic factors which are yet to be determined are also likely to play a role.
The discovery in 1994 of the PTCH gene on chromosome 9q was a major genetic breakthrough in the molecular pathogenesis of BCC. Germ-line mutations in this gene lead to an autosomal dominant transmission of the Gorlin syndrome, which is characterized by multiple BCCs from an early age, broad nasal bridge with hypertelorism, jaw cysts, palmar pits and bifid ribs. Somatic mutations that amplify the PTCH-sonic hedgehog signalling network, a major cell cycle regulatory pathway, have since been discovered to be important events in sporadic BCC. Other polymorphisms may also play a role, including the melanocortin-1 receptor (MC1R) gene, glutathione methyl transferase (GSTT) gene and DNA repair genes.
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