According to the estimates of American Cancer Society, about one million Americans are newly diagnosed with skin cancer every year.
As a leading researcher at the National Institute of Health (NIH), Dr. Kenneth Kraemer (MD '69) studies skin cancer, the most common cancer among fair-skinned Americans. Kraemer's interest in skin cancer began years ago when he was pursuing his M.D. degree at Tufts.
His relationship with Tufts goes more than skin-deep. "Tufts has been very good to me and my family," Kraemer said. "My son David went to Tufts as an undergraduate, and my wife completed her Masters in education at Tufts.
"I became a dermatologist due to Tufts," Kraemer added. "I was in a special program where you could do medical research while pursuing your degree -- I did virus work for first two years. I was always interested in medical research."
After receiving his M.D. in dermatology from Tufts Medical School in 1969, Kraemer moved to New York, where he practiced dermatology in the Harlem Hospital for two years. It was there that he became interested in something called xeroderma pigmentosum (XP).
XP is a rare genetic disorder characterized by the skin's extreme sensitivity to any ultraviolet (UV) radiation source, including sunlight, the major environmental source of UV. UV is capable of damaging DNA, the warehouse of genetic information. It was the link between XP and UV that got Kraemer interested in DNA repair.
In normal individuals, molecular "handymen" work to find and mend the damaged DNA. However, XP patients lack these handymen, so the damaged DNA remains unrepaired. As a result, uncontrollable cell division (cancer) can occur.
A recipient of several awards from the Society for Investigative Dermatology and the U.S. Public Health Service, Kraemer has established his own research group at NIH, which focuses on DNA repair, as well as the molecular, cellular, and clinical features of diseases such as XP and familial melanoma.
Kraemer is also the co-organizer for the DNA Repair Interest Group, which uses technology to spread science. Through the group's website, http://videocast.nih.gov, thousands from across the world access seminars and lectures delivered by leading scientists without having to leave the comfort of their desks.
Recently, Kraemer published his findings on melanins, the pigments long thought to be protection for the skin. According to Kraemer's study, however, melanin may at times actually be destroying the skin -- resulting in skin burns and cancers.
This, Kraemer found, is especially true for fair-skinned individuals, especially blondes and redheads. Melanins normally protect the nucleus and DNA inside the skin from dangerous UV. However, pheomelanin -- the kind of melanin present in blondes and redheads -- can sometimes turn reactive and harmful.
Eumelanin -- the type of melanin present in dark-skinned individuals -- is less reactive than pheomelanin, and makes the risk of getting skin cancer about 50 to 100 times less likely for dark-skinned individuals, and about 10 times less likely for Asians.
Kraemer's finding explained the increased incidence of skin cancer in blondes and redheads. "We had thought that melanins are always beneficial," Kraemer said. This study, however, proved that melanins could have "some beneficial and some harmful effects."
The study used mice to find the relationship between melanin and skin cancer. Yellow mice represented the skin of blondes and redheads, and black mice represented that of dark-skinned individuals. A third class of mice, albinos, simulated an unprotected skin devoid of any kind of skin pigments.
In mice, the melanins are concentrated around hair follicle, the cells that produce hair. "When we exposed the mice at the hair follicles with UV, it was seen that more damage occurred in the skin of the pigmented mice than the albino mice," Kraemer said. "That came as a surprise to us."
While the broad similarities between mice and human skin helped to make a correlation between melanin and skin cancer, the differences between them made the study easier. In human skin, the cells that produce melanin, called melanocytes, are spread throughout the skin's layers, whereas in mice, melanocytes are only in the follicle.
This difference simplified the experiment tremendously, since the researchers did not have to worry about shielding incoming UV and deducing the origin of the damage. Secondly, mouse epidermis is only about two to three cells thick, whereas a human's is about six cells thick.
"This experiment was made possible by the absence of melanin outside of the hair follicles in mouse skin," Kraemer said.
According to the Center for Disease Control and Prevention, both tanning and burning can increase a person's risk for skin cancer -- and most Americans do not consistently protect themselves from UV rays. According to its statistics, approximately 43 percent of white children under the age of 12 have had at least one sunburn during the past year
"In protective tanning, the melanin level goes up in the skin," he said. Tanning of the skin, however, indicates damage, and burning indicates skin cell death. Cell death may be good -- the layer of dead skin cells containing melanin can act as a natural sun screen at low UV doses.
When burn-resistant mutant cells are already present, however, this event could lead to further mutations in the skin cells, causing skin cancer. "Some people never burn, some people never tan," Kraemer said. "It's an inherited characteristic of the skin. We don't know why, exactly, this is so."
Kraemer's study corroborated the previous reports that pheomelanin could react with UV. UV-irradiated melanin may therefore generate active oxygen species like super oxide and hydroxyl radicals -- the chemical equivalent of bullets -- which are capable of causing DNA breaks.
According to the study, this could mean that, in pheomelanin-containing individuals, melanin may act as a microscopic X-ray source, resulting in skin burns and possibly skin cancer.
