Former President Jimmy Carter greets a Nepalese boy in Kathmandu, Nepal, in November 2013, when the Carter Center monitored Nepal’s constituent assembly election, sending observers from 31 countries. (PHOTO BY THE CARTER CENTER)
Former President Jimmy Carter’s skin cancer diagnosis began the way it does for so many others facing the disease. A spot discovered on his liver turned out to be melanoma. Then when doctors ordered an imaging scan, they found four more melanomas on his brain.
Carter, 91, disclosed his diagnosis in August. Four months later, he announced that his latest brain scan found no evidence of melanoma – but no one is using the word “cure.” Tim Turnham, the executive director of the Melanoma Research Foundation, told the New York Times that melanoma has a “frightening ability” to return years into remission.
Most likely in Carter’s case, the melanoma started somewhere in his skin and traveled via his bloodstream or lymph system to his liver and brain, says Ramsay Farah, MD, division chief for dermatology at Upstate Medical University. The majority of cases of melanoma begin in melanocytes in our skin, although these cells that provide our pigment can be located in other parts of the body.
“As the fetus is developing, these melanocytes can migrate to other parts of the body,” he explains. “So even though most of them are in the skin, you find them in the eye, in the gastrointestinal tract, in the lining of the brain. Anywhere you have melanocytes, you can get a melanoma.”
News reports say the 91-year-old Carter underwent radiation therapy and has been taking a new immune therapy drug called Keytruda. He receives his care at Emory University’s Kinship Cancer Institute in Atlanta.
Farah says Keytruda is an antibody that targets a receptor on a cell of the immune system called a T cell. “Normally T cells have some natural breaks on them so that they don’t attack every cell in your body. When the T cells are sleeping, they’re not going to attack the melanoma,” he explains. “This medicine basically awakens the T cell, so it can awaken its brothers and sisters, and they all attack the melanoma.”
While some melanomas run in families, most are caused by exposure to ultraviolet radiation from sunshine or tanning beds.
Who is more likely to develop melanoma?
- Someone with light skin. The pigment in our skin is protective. Melanocytes produce melanin, the chemical that absorbs ultraviolet radiation and protects the cells. People with dark pigment have an incidence of melanoma about 1/20th that of people with light pigment.
- Someone who was exposed to high levels ultraviolet radiation, especially in childhood. Farah says “a lot of the sun damage we see in adults, they acquired it before the age of 12. There is a long latency period for melanoma.”
- Someone who lives in an ozone-depleted region. Earth’s ozone layer filters some of the ultraviolet radiation coming from the sun. The highest rates of melanoma are from areas, such as Queensland, Australia, with a hole in the ozone.
- Someone with lots of moles. Having 50 or more moles increases one’s risk of melanoma, and having suspicious moles also increases the risk.
Farah advocates prevention and vigilant screening so that any melanomas are caught early, before they can spread.
Mole check
See your health care provider if you have moles with any of these characteristics:
A – asymmetry. Use your mind’s eye to cut the mole in half: Are both sides symmetrical?
B – border. Healthy moles have borders that are smooth, as opposed to jagged.
C – color. Shades of tan or brown are normal. Troublesome colors are red, white or blue.
D – diameter. Moles greater than ¼ inch diameter are suspicious.
E – evolution. Sudden growth of a mole, pain or bleeding warrants examination by a health professional.
Some melanomas are hidden, existing in the gastrointestinal tract, an eye or a nail bed. Others, called amelanotic melanomas, have no color but may be felt as bumps on the skin.
Source: Ramsay Farah, MD
Hear Farah’s radio interview at healthlinkonair.org by searching “melanoma.” This article appears in the winter 2016 issue of Cancer Care magazine.
