Skin cancer was not a potent selective force in the evolution of protective pigmentation in early hominins.

2014 Skin cancer was not a potent selective force in the evolution of protective pigmentation in early hominins. Greaves [1] proposed that skin cancer was a potent selective force for the evolution of dark pigmentation in early hominins. Blum [2,3] questioned the role of skin cancer in the evolution of skin pigmentation because it only rarely causes death to individuals of reproductive age. Since Blum's studies, much more data on skin cancer rates has been amassed, and a clearer picture of skin cancer aetiol-ogy has emerged. Individuals with lightly pigmented skin, especially those with a tendency to freckle who carry specific polymorphisms of the melanocortin 1 receptor gene (MC1R), are most susceptible to skin cancers of all types [4,5]. Other polymorphisms of pigmentation genes also have been associated with elevated risk of skin cancer in people of European descent [6]. Development of the most common skin cancers, namely, squamous cell carcinoma (SCC) and basal cell carcinoma (BCC), is associated with chronic sun peak exposure and generally develops in the seventh decade of life. Cutaneous malignant melanoma (CMM) is much rarer, is associated with sunburns, particularly in childhood, and can appear as early as the third or fourth decades of life because of the roughly 20 year lag between damaging exposures and the appearance of disease [4]. This still allows for reproduction and the persistence of familial predisposition to CMM [7]. Greaves' case for skin cancer as a potent agent for natural selection of dark skin pigmentation presupposes that ancestral hominins had skin that was pale or light, and that people in Africa who are entirely lacking eumelanin in their integument owing to OCA2 albinism are a suitable model for the ancestral state. OCA2 albinism predisposes individuals to extreme ultraviolet ratiation (UVR)-induced damage to DNA and is associated with severe and often fatal skin cancers (mostly SCC) in the middle of their potential reproductive careers in the third and fourth decades of life [8,9]. Excessively high rates of skin cancer develop in individuals with OCA2 albinism when compared with other very light-skinned people with MC1R variants, probably because of the protective non-pigmentary effects of MC1R, specifically the fewer number of p53 clones that develop after UVR exposure [10]. Early hominins never had naked pale skin comparable in function to that of individuals with OCA2 albinism. All living cattarhine primates have intact pig-mentary systems and can develop facultative pigmentation through tanning or …