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Cancer Moles Pictures

Think twice before you set out to get a suntan this summer.

IT IS DIFFICULT to imagine today, but for hundreds of years in Europe and the U.S., a suntan branded one as an inferior person. A bronzed face and hands were a sign of the lower classes--those who labored under the sun.

The Caucasian ideal of male and female beauty during that time was of milky white, alabaster skin. Like the individuals who populate Georges Seurat's famous 1884 painting, "A Sunday on La Grande Jatte," people hugged the shade and avoided the sun.

Then came Coco Chanel, the 1920s French fashion designer who gave women's apparel a freer, more comfortable style. Everything Chanel did set a standard. So, when she returned one day from a Palm Beach vacation with a suntan the bronzed look suddenly went from shunned to chic.

The passion for suntans further was nurtured by improvements in transportation that allowed seaside and mountain vacations and by the popularity of motion pictures. More leisure time, a burgeoning interest in outdoor activities, and the growth of suburbs with their lawns, gardens, and swimming pools all contributed to what has become an annual ritual to achieve the golden-brown tint of success, sexiness, beauty, and health.

Well, the latter is not necessarily true. For five decades, physicians have seen growing numbers of the three common skin cancers: basal cell carcinoma, squamous cell carcinoma, and malignant melanoma. In 1978, doctors diagnosed between 400,000 and 500,000 new cases of skin cancer; this year, over 1,000,000 new cases are expected. More than 90% of these cancers are thought to be caused by overexposure of the skin to ultraviolet (UV) radiation in sunlight. (Burn scars and radiation therapy for acne are also linked to non-melanoma skin cancers.)

Those most vulnerable to skin cancer are people with red or blond hair, light-color eyes, and fair skin that tends to freckle and burn, rather than tan. Knowing why this is so and how UV light causes cancer is to understand why people of all races--particularly those with light or pale skin--should protect themselves and their children from prolonged sun exposure.

Humans need a certain amount of sunlight for emotional and physical health. It is necessary for the production of vitamin D in the skin, for example. However, experiments in the 1920s and 1930s revealed that the UV radiation in sunlight leads to cancer.

Invisible to the human eye, UV radiation follows the violet band of the rainbow. Ultraviolet light ranges in wavelength from 200 to 400 nanometers (nm). Scientists divide this range into three groups: UVA (320-400 nm); UVB (290-320 nm), and UVC (200-290 nm).

When a beam of sunlight strikes the Earth, it first penetrates the atmosphere. About 30 miles above the planet's surface, it enters the ozone layer. When it comes out the other side, some 12 miles up, about half the UV radiation in the beam has been stripped away, absorbed by ozone molecules.

As a result, nearly no UVC and very little UVB--the most energy-packed UV wavelengths --reach the Earth's surface. What does reach the surface--and the people working and playing on it--is some UVB, the rays that cause sunburn and are most responsible for cancer, and most of the UVA, the longest of the ultraviolet wavelengths. UVA--the predominant radiation emitted by tanning lamps--is linked to premature wrinkling of the skin and to skin cancer.

Humans are protected from UV rays by their skin, which is composed of two main layers--the epidermis and dermis. The epidermis is the topmost and thinnest. It consists of multiple layers of cells that are in a state of constant turnover. Cells at the bottom of the stack divide, pushing the cells above them toward the surface. As these cells move outward, they flatten and gradually replace their internal organelles with large amounts of the protein keratin. In fact, most of the cells in the epidermis are known as keratinocytes. By the time these cells reach the skin's surface, they have become mere scales of keratin that eventually flake off.

Scattered among the innermost keratinocytes are the melanocytes. These cells make melanin pigment and do the actual work of protecting the body from UV radiation. They also give the skin color. Moles are islands of melanocytes.

The number of melanocytes in a person's skin helps determine his or her skin type, which is a measure of tanning ability. It is usually represented as a six-point scale and reflects the relative number of melanocytes in the skin. A dark African-American who never sunburns from normal exposure has a high proportion of melanocytes and has skin type six; someone who rarely develops sunburn and tans dark brown has skin type three; and someone who never tans and always burns has skin type one and a low proportion of melanocytes.

Beneath the epidermis lies the dermis, a relatively thick layer that consists largely of collagen and elastic fibers. These fibers give the skin its pliability and resilience. The dermis contains hair follicles, sweat and oil glands, blood and lymph vessels, and some melanocytes. When UVA penetrates the dermis, it can damage the collagen and elastic fibers, leading to wrinkling and premature aging. Most tanning equipment utilized today predominately emits UVA radiation, causing growing concern among dermatologists.

UV radiation and cancer

Scientists have discovered how UV radiation leads to cancer, particularly squamous cell carcinoma. With sun or tanning-bed exposure, UVB rays penetrate the epidermis, while the longer-wavelength UVA rays continue on into the dermis. This exposure triggers pigment production by melanocytes, which might be thought of as parasols for skin cells. Each melanocyte has many long, elaborately branched projections that extend among surrounding keratinocytes. The cells send the additional pigment out into the projections to absorb the UV and shade the keratinocytes and dermis. Unfortunately for most Caucasians with skin types one, two, and three, they develop this protection only in part.

Prolonged unprotected sun exposure can lead to the reddening and inflammation characteristic of a mild sunburn, which is a first-degree burn. Still longer sun exposure triggers severe inflammation and blistering, the hallmarks of a second-degree burn.

Sunburn represents the visible harm wrought by UVB rays. Unseen is the damage done to keratinocytes within the epidermis. This damage leads to cancer, and it can happen even in the absence of sunburn. To understand why, it is necessary to journey into the very core of an epidermal keratinocyte. Think of this cell as a box. At the center of the box is a sphere, the cell nucleus. Packed inside the nucleus like tangled spaghetti are the cell's chromosomes. Each is a strand of DNA crated with proteins.

To visualize the DNA that lies at the core of each chromosome, imagine stretching out one of these strands and scraping away the proteins. This exposes a naked strand of DNA. Now view the strands a long, flexible ladder twisted into a helical pattern for its entire length.

Like other ladders, this DNA ladder--known as the DNA double helix--has two sidepieces that run its length and "rungs" that join the sidepieces together. Focus now tin the rungs in one short length of the ladder. Instead of being a solid piece, each rung consists of two halves joined in the middle. At this close-up view, a strand of DNA appears somewhat like two combs facing one another with the tips of their teeth touching.

To understand how UV damages DNA, visualize each tooth in these combs as one of four colors: amber (A), tan (T), green (G), and cherry red (C), representing the four bases in DNA--adenine, thyme, guanine, and cytosine. The colors, or bases, are always paired the same way. That is; A and T are always paired, as are C and G. Thus, if five neighboring teeth on the left are TCGGC, the teeth they are touching will be AGCCG.

Damage characteristic of UV can arise where two Cs occur in a row on one of the "combs." UVB breaks the normal chemical bond that joins the Cs to their Gs, creating a new and abnormal bond that joins the two Cs.

This produces a glitch in that keratinocyte's genetic code. While skin cells usually can repair such damage using DNA repair enzymes, the repair system sometimes fails. This failure ultimately leads to permanent damage to the DNA--a gene mutation known as a thymine dimer. Thymine dimers are caused only by UV light. Thus, when scientists detect thymine dimers in tumor cells, it signals that the cell was exposed to UV radiation.

Such mutations can have serious consequences, since genes contain the information needed by cells to make proteins. Damage to a gene may cause it to stop producing its protein, to produce a protein that works improperly, or to overproduce the protein. If that particular protein helps control cell division, the change can lead to cancer.

UV radiation damages genes in another way, notes Fredika Robertson, professor of immunology and an Ohio State University Comprehensive Cancer Center researcher. "For years, thymine dimers were considered to be the classic sign of UV damage to DNA. But now, research is showing that UV radiation produces oxygen radicals that also alter DNA."

Oxygen radicals are substances normally found in low levels in cells, by-products of the chemical reactions that keep the cell healthy. When exposure to UVB produces a flood of these chemicals, however, they become troublemakers that damage DNA.

One gene frequently mutated by UVB is the p53 tumor suppressor gene. Tumor suppressor genes serve as a brake on runaway cell division. More than 90% of squamous cell carcinoma tumors of the skin show mutations in p53. These are usually of the thymine dimer type, implicating UVB as the cause.

The loss of p53 genes in sun-damaged cells is linked to development of actinic keratoses. These hard, discolored patches of skin result from chronic sun exposure and may either clear up or progress on to squamous cell carcinoma.

"We want to learn which type of DNA damage is most critical for skin cancer development and which comes first," indicates Tatiana Oberyszyn, a research scientist with the Ohio State Comprehensive Cancer Center. "This might enable us to identify markers that would tell us whether a person with actinic keratosis will progress to squamous cell carcinoma."

What of the UVA that has penetrated the dermis? About 10 to 100 times more UVA reaches the Earth's surface than UVB. It stimulates melanocytes and leads to tanning. The tan that is achieved, though, tends to less protective against UVB radiation. Long exposure to UVA damages the elastic and collagen fibers of the dermis, causing premature wrinkling and aging of the skin. High doses and long exposures of UVA have been found to cause cancer in laboratory animals.

Genetic influences

It typically takes decades to accumulate the mutations necessary for skin cancer development. The rate at which they build up depends on traits an individual inherits. These include skin type, ability to tan, and the effectiveness of an individual's DNA repair systems.

There are also differences in the development and behavior of melanoma and squamous cell and basal cell carcinomas. (For this reason, the latter two are often referred to as non-melanoma skin cancers.) For example, basal cell and squamous cell carcinoma develop in keratinocytes, while malignant melanoma does so in melanocytes. Development of basal cell carcinoma is related to the total amount of UV exposure accumulated by a person until a threshold of damage is reached. At that point, one or more small tumors will begin to develop in the sun-exposed area.

"It's not unusual for a patient with basal cell carcinoma to have two, five, or even 10 skin cancers on the face surgically removed, and then a year or so later have one or more new ones develop," explains Ronald Siegle, a skin cancer specialist at The James Cancer Hospital, Columbus, Ohio. "Basal cell carcinomas grow very slowly, and the individuals often continue to get skin cancers their entire lives."

Exactly how malignant melanoma arises remains poorly understood, though research has shown that UVB can cause it, and suppression of the immune system by UV radiation is thought to play a role as well. Strong epidemiological evidence ties the disease to excessive sun exposure, particularly to severe sunburns sustained during childhood. Since 1950, the incidence of malignant melanoma has grown more than six percent a year, while deaths due to the disease have risen by two percent annually. If the rate of increase continues, it is estimated that one in 75 Americans will develop the malignancy. Fortunately for those who do, malignant melanoma is highly curable if caught early. If left untreated, however, it readily invades neighboring tissues and metastasizes to other areas of the body, and the disease becomes deadly.

Preventing skin cancer means avoiding undue exposure to UV radiation. Stay out of the sun between 10 a.m. and 4 p.m., when 60% of the day's UV rays reach the Earth. Stand in the shade or use an umbrella to avoid sun exposure during midday. When in the sun, wear a wide-brimmed hat and tightly woven clothes to shield exposed skin. Complete the ensemble with UV-screening sunglasses, because UV radiation also is linked to cataract development.

Use a sunblock or a broad-spectrum sunscreen with a sun protection factor (SPF) of 15 or greater. Sunblocks contain titanium dioxide, which protects the skin by reflecting UV from the body. Broad-spectrum sunscreens of SPF 15 or greater protect against 94% of UVB rays and a significant portion of UVA rays. These contain the chemical parasol, also known as avobenzone, that absorbs much of the UVA in sunlight.

Siegle cautions that sunscreens provide only limited protection from sun damage. "Some individuals use sunscreens to remain outdoors longer than they might without them. This increases their exposure to UVA, against which even broad-spectrum sun. screens until recently offered only modest protection. Individuals who stay in the sun longer because they are wearing sunscreen actually end up getting much more exposure to UVA light than they might if they had to come out of the sun to prevent getting sunburned."

In short, the best protection from skin cancer is simple: Enjoy the shade and avoid strong sun.

Darrell E. Ward is a senior medical writer concentrating on cancer research and clinical progress, Office of University Communications, Ohio State University, Columbus.

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