Sunlight has dual roles in cancer risk
New thesis explores the mechanisms of programmed cell death and melanoma malignum.
Although sunlight is detrimental to the DNA of skin cells, it can also prevent self-destruction of the damaged cells. Sunlight intensity and ultraviolet radiation stimulate the production of a protein that counteracts apoptosis, programmed cell death, and thus increases the risk of skin cancer.
Melanoma malignum is the most serious form of skin cancer and the one most on the rise among the fair-complexioned. Without early treatment, the tumor grows rapidly and soon spreads to other bodily organs. In Sweden alone, 2 100 persons acquire the disease each year, with mortal consequences for 400.
The factor is melanin, the pigment that gives our skin its natural color, but also is a factor in melanoma. When skin is exposed to the sun, melanocytes produce more pigment, causing the skin to tan, or darken. They are resistant to apoptosis, programmed cell death, which is a necessary process. Science does not yet have all the facts on how cell suicide is regulated.
Doctoral candidate Cecilia Bivik, in her thesis on dermatology, shows that the heat and UV radiation of sunlight stimulates the production of protein Hsp70 (70 kilodalton heat shock proteins).
By studying cultures of human pigment cells, she has been able to demonstrate that this protein effectively suppresses programmed cell death. Exposure to sunlight can do the same, increasing the risk that apoptosis will not take place in DNA-damaged cells, opening the way for development of melanoma malignum. Hsp70 might thus be a significant target protein in the battle to curb and treat this disease.
Last updated: 2009-06-03