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= Evolutionary Biology of Melanoma =

Background
Melanoma is a disease in which melanocytes, a type of cell found in the epidermis layer of our skin, becomes cancerous. Malignant melanoma forms when genetically altered melanocytes develop due to interactions between genetic and environmental factors. UV radiation is a major cause of malignant melanoma and high levels of melanin pigmentation provides protective effects against it.

The earliest members of the hominid lineage had mostly unpigmented or lightly pigmented skin covered with dark black hair. Dark, naked pigmentation then occurred in the early evolution of the Homo genus. This dark and/or highly melanised skin evolved 1.2 million years ago with the selection of a very active melanocortin receptor 1 allele. The selective pressure was solar UVB damage to the skin with consequent skin cancer and folate loss or other lethal pathologies [1]. The dark epidermis protected the skin against UV injury. While melanized skin prevents skin damage, it also greatly contributes to individual reproductive success [2].

Evolutionary Theory of Melanoma
The primary belief, although challenged, is that the adaptation of light skin pigmentation in hominids that migrated out of the tropics was an adaptation to maximize vitamin D synthesis. Populations in northern latitudes often don’t get enough UV to synthesize vitamin D naturally in their skin. Therefore, selection has favored genetic solutions to that problem such as pale skin that absorbs UV more efficiently [2]. According to Jablonski and Chaplin, the evolutionary mechanism of melanin levels portray a trade-off between vitamin D synthesis and protection against UV light damage [3].

Either way, the adaptation of pale skin has today become a liability. Many light skinned Europeans have migrated to sunnier climates (e.g. Australia), and now take part in activities that allow increased sun exposure such as holidays in the sun, and tanning beds. With this in mind, skin cancer can be viewed as a consequence of mismatch between ancestral environmental conditions in which we evolved, and our current social and behavioral activities [4].

There are a few notable scientists that have provided insight on the evolutionary ideology of melanoma. In 2014, Professor Mel Greaves of The Institute of of Cancer Research published a paper where he made a case that lethal skin cancer, such as melanoma, could have provided a strong selective force for the emergence of black skin in early hominins. His case proposes that ancestral hominins had skin that was very pale, and that people in Africa who are completely lacking eumelanin in their skin owing to OCA2 albinism are a suitable model for the ancestral state. OCA2 albinism is associated with severe skin cancers in the middle of humans potential reproductive careers, and predisposes individuals to extreme UV radiation induced damage to DNA [4].

This idea, however, was soon challenged by Nina Jablonski and George Chaplin who stated that skin cancer was not a potent selective force in the evolution of protective pigmentation in early hominins. Their main skepticism was the validity of applying the OCA2 albinism model to human evolution. Based on previous articles, they explain that the absence of pigmentation seen in individuals suffering from OCA2 albinism is not comparable to the ancestral state seen in early hominins. This counter argument is supported by two statements. The first is that OCA2 albinism results in complete and irreversible loss of pigmentary function. The second is that even if OCA2 albinism were taken as the model for early hominin skin, skin cancer could have been only a weak selective force. This is because ancestral hominins reproduced early in life, and most reproductive effort would have been completed before skin cancer could affect reproductive success [5].