Oxford American handbook of oncology. Second Edition. Oxford University Press (2015)
Incidence rates are rising faster than for any other cancer worldwide. In 20.3, an estimated 76,690 new cases and 9480 deaths are anticipated in the United States.
The lifetime risk is currently estimated at >1:80 for Caucasians, but as low as 1:1200 among those with pigmented skin. Rates in Australia are the highest in the world and continue to double each decade.
The incidence among women is at least comparable to the incidence in men, although death from melanoma is more common in men.
Sunlight is the main environmental cause of melanoma. Excess exposure to UV radiation, particularly in early life, is strongly associated with subsequent risk of developing melanoma. A history of severe sunburn or intense, intermittent exposure may be particularly relevant.
Genetic risk plays a role, with ~10% of cases having a strong family history of melanoma. A melanoma susceptibility gene CDKN2A on chromosome 9 has been identified as a tumor suppressor gene. Germline mutations are implicated in up to 40% of patients with familial melanoma and may have a role in sporadic cases.
Benign pigmented nevi (Fig. 39.1 and Fig. 39.2) may be precursor lesions to malignant disease, but more frequently these are markers of a more general increased risk within the individual.
Immunosuppression, as occurs in patients after organ transplantation, appears to be associated with an increased risk of developing melanoma (Fig. 39.3 and Fig. 39.4). Currently, there is no evidence that melanoma is more prevalent in the HIV-positive population.
Figure 39.1. Benign pigmented lesion.
Figure 39.2. Benign nevus close-up.
Figure 39.3. Malignant melanoma close-up.
Figure 39.4. Malignant melanoma close-up.