​You have now entered the readings for Skin Cancer Prevention (the Skin Cancer Early Diagnosis readings are loc​ated here).

There are several articles listed in the coloured area to the left. To proceed with the readings, click on the Next link. This will take you through each of the required readings in turn. Alternatively, you may navigate through the readings in any order you choose by clicking on the titles to the left.

Summary: Sunlight Exposure, Pigmentation Factors, and Risk of Nonmelanocytic Skin Cancer I. Basal Cell Carcinoma 

Basal cell carcinoma (BCC) of the skin is the most common malignancy among white populations in Europe, North America and Australia. Sunlight exposure is generally considered the most important environmental risk factor for developing this tumour.

This study (sunlight_i.pdf) evaluated the relationship between sunlight exposure, pigmentary factors and basal cell carcinoma, because little information is available on the character and timing of sunlight exposure responsible for BCC. The results showed:

• Significantly elevated risks for BCC among subjects with:
  • Light skin colour.
  • Red hair.
  • A tendency to burn, not tan, after sun exposure.
• Subjects whose mothers were of Southern European ethnic origin were at significantly lower risk for BCC than those whose mothers were of English, Celtic and Scandinavian origin.
• Freckling in childhood increased the risk for developing BCC later in life.
• Only recreational childhood exposure showed a significant link to risk of BCC. Subjects who had frequent or severe sunburns in childhood and adolescence, up to 19 years of age, had increased risk compared to those who did not recall being sunburned. This increased risk was evident only among non-tanners. (Subjects were divided into tanners, people who get a brown suntan without burning, and non-tanners, who usually sunburn followed by a tan, or only burn.)
• Sunburn history as an adult, from age 20 on, did not show any risk for BCC.
• Cumulative sun exposure, combining recreational and occupational exposure, did not show an association with BCC.
• There was no association between degree of tanning and risk of BCC.

The results of this study suggest that childhood sunlight exposure may be an important factor in adult risk for BCC. The increased risk seen among people with light skin correlates with results from several previous studies, as does the protective nature of Southern European ancestry. Light hair colour has also been shown to increase risk in several investigations, with red-haired individuals at highest risk.

In addition, the association between freckling and BCC is important, because the findings correlate with another study, and freckling is a well-established risk factor for melanoma and may be a marker for UV light damage to the skin.

The fact that sunburn in childhood, particularly severe sunburn, substantially increased risk for adult BCC, while no such effect was seen for adult sunburn, suggests skin may be more sensitive in childhood to initiating events that eventually lead to malignancy. Again, a similar relationship has been detected for malignant melanoma.

While the findings from this study require confirmation, they indicate:

• The timing and character of sun exposure may be more important than cumulative dose in predicting adult risk for basal cell carcinoma.
• Among sensitive individuals, sun avoidance behaviour in adulthood may not markedly reduce risk for this tumour.

You can refer to the complete journal article for additional details on the:

• Study design, methods and materials.
• Data collected during the study.
• Comments on interpreting the data.

Summary: Sunlight Exposure, Pigmentation Factors, and Risk of Nonmelanocytic Skin Cancer
II. Squamous Cell Carcinoma

Squamous cell carcinoma (SCC) of the skin is a common cancer in white populations, and the incidence appears to be increasing. Sun exposure is thought to be the most important environmental risk factor for the disease, and a number of studies have confirmed this association, without assessing how character, duration and timing of exposure relates to risk. Age is also strongly associated with risk.

The purpose of this study sunlight_ii.pdf was to investigate the relationship of squamous cell carcinoma to individual solar UV exposure, after controlling for phenotype and pigmentary factors. The results show:

• An elevated risk of squamous cell carcinoma among subjects:
  • With light skin and red hair.
  • Who burn rather than tan when first exposed to the sun, and are unable to develop a tan even after a week or more of exposure.
• Subjects whose mothers were of Southern European extraction - Italian, Portuguese, Spanish or Greek - had a reduced risk of SCC compared to those with mothers of English, Celtic and Scandinavian origin.
• Freckling in childhood appears to increase the risk of SCC.
• Two or more very severe burns in childhood, causing pain for two days or longer, markedly increased the risk of SCC.
• A strong trend toward increased risk with chronic occupational exposure in the ten years prior to diagnosis.
• Very severe burns once or more per year in the ten years prior to diagnosis indicated a ten-fold elevation of risk.
• Sunburn frequency in the intermediate decades of adult life (20-29, 30-39, etc.), showed no association with SCC.
• There was no relationship between degree of tanning and risk of SCC.

These results reflect previous study findings, and suggest people with light skin, blond or red hair, who tend to burn rather than tan, are at greater risk of SCC. A propensity to freckle has also been reported as more common in individuals with SCC. Another study found a history of severe sunburn is characteristic of patients with SCC. In addition, one other study reported Southern European origin reduces risk.

Other evidence implies the appearance of squamous cell carcinoma may be related to sunlight exposure just prior to diagnosis. Some actinic keratoses are precursor lesions of SCC, and recent sun exposure is connected to their development. Actinic keratoses sometimes disappear without treatment in people who limit solar exposure, suggesting that the progression to malignancy requires continued exposure to relatively high doses of UV light. If this hypothesis is true, subjects with SCC would likely demonstrate higher UV exposure in the years immediately prior to diagnosis, as was the case in this study.

These results require confirmation in other studies, but suggest late stage solar exposure may be important in accounting for squamous cell carcinoma.

(This study was conducted in conjunction with a companion investigation of basal cell carcinoma of the skin.)

You can refer to the complete journal article for additional details on the:

• Study design, methods and materials.
• Data collected during the study.
• Comments on interpreting the data.

​Summary

More than half of people buy or use sunscreens. However, the public seems to be confused about health messages for sunscreen. Although cancer prevention groups promote sun avoidance and regular sunscreen use, 70% of people participating in a beach survey were there to get or maintain a tan, and only half were using sunscreen sunscreen.pdf.

Studies have shown sporadic sunscreen use, from 10% in one study to less than one-third in another. Two-thirds of skiers surveyed in Alberta used sunscreen, while in Australia, three-quarters of adult patients told their family physician they use sunscreen. Only one-third of U.K. parents regularly protect their children from the midday sun, and half their children burn at least once a year.

Some people use sunscreens to prevent sunburns, some to improve tanning, some to avoid wrinkling, some to prolong time in the sun, and some because they believe sunscreen prevents all skin cancers.

Application

Sunscreens work as soon as applied, although some suggest applying sunscreen 30-60 minutes before going outside. The only reason to apply early is to allow absorption so the sunscreen is less likely to be washed off if someone's going in the water.

The average application rate of sunscreens is one-third that used during testing (i.e., an SPF 15 will act like SPF 5 because not enough sunscreen has been applied). The correct amount is enough to make the skin slightly white, transiently until absorbed.

Frequent application is often suggested, but there's evidence that this may not be necessary if enough has been applied the first time. In one study, one application provided the same level of protection as four applications. For some patients, the cost of sunscreen may limit use, if they think repeated applications are required.

Few public health messages tell people how much sunscreen to apply, and most use about 30% of the amount needed to achieve the sun protective factor (SPF) listed on the container. For example, the way SPF 15 is commonly applied, it has an SPF between 3 and 7. Many organizations continue to recommend SPF 15 despite this knowledge.

SPF

There is considerable disparity between the SPF achieved in laboratory tests with artificial light sources and SPF in sunlight. For instance, an SPF 6 sunscreen only had a protective factor of 4.8 in sunlight.

Ultraviolet A wavelengths between the upper end of UVB at 320 nanometers and visible light at 400 nanometers cause sagging skin from photoaging, but UVA is not a major cause of skin cancer. UVB is the major risk factor for developing skin cancer. Parasol 1789 is the best sunscreen blocker of UVA, and most dermatologists recommend broad spectrum sunscreens with Parasol 1789. However, no transparent sunscreen is completely protective, because they let some ultraviolet energy through. Sunscreens that block all UV light are opaque blockers such as titanium dioxide and zinc oxide.

Sunscreens and the Elderly

Few elderly people are likely to develop new skin cancers from present sun exposure, and should be advised to refrain from excessive sun avoidance - which can negatively impact their quality of life - as long as they prevent sunburn. One study showed sunscreen did not alter vitamin D levels in older people, an earlier concern. In fact, some sun exposure is probably recommended for the elderly, since they face a decrease in vitamin D production capacity from aging.

Skin Reactions

Although sunscreen can be both an irritant and an allergen, allergic reactions are rare. Many people put a large amount of sunscreen on the forehead, which flows into their eyes with perspiration, causing a stinging sensation. Advise people to apply a modest amount of sunscreen in this area and wash their hands afterwards, because rubbing fingers covered with sunscreen near the eyes can also cause irritation.

Why Use Sunscreens?

Broad spectrum sunscreens can prevent sunburns, some aspects of photoaging, and actinic keratoses. Some pre-existing actinic keratoses can regress as well. Squamous cell carcinoma may also be prevented, since actinic keratoses are precursors of this condition. Evidence does not suggest that sunscreens directly prevent basal cell carcinoma or melanoma, although intuitively, consistent use from childhood should reduce the risk of these cancers.

Refer to the complete journal article for more information on sunscreen use and effects and recommended areas for future research sunscreen.pdf​.

​Summary

The incidence of malignant melanoma has risen significantly over the last 30 to 40 years, and continues to increase in the United States, Canada, Australia and Europe, becoming a major public health concern nevi.pdf. A number of studies have identified three categories of major risk factors:

• Environmental - Solar ultraviolet (UV) exposure is the major environmental risk.
• Constitutional - Light skin and hair colour and propensity to burn rather than tan in the sun are genetically based constitutional risk factors.
• Combination - Acquired melanocytic nevi and freckles combine the risks of constitutional susceptibility and environmental UV exposure.

The single greatest predictor of risk for developing melanoma is the total number of nevi. Studies over the last 15 years have revealed a great deal about the way nevi develop and the relationship between nevi and melanoma. The studies can be divided into adult and child investigations to determine the prevalence of nevi by sex and age, and to identify factors associated with a high number of nevi.

Studies of Nevi in Adults

The findings on adult nevi are somewhat contradictory, because many of the studies were conducted over broad age ranges and may have differences in UV exposure and the number of nevi. Highlights include:

• Sunburn frequency up to ten years old showed the strongest relationship with the number of nevi in one study, suggesting childhood sun exposure is connected to nevus prevalence in young adults.
• Sun exposed surfaces had higher counts than less exposed areas.

Different results may arise because people who are most likely to burn avoided the sun.

Studies of Nevi in Children

Recent research focuses on childhood and adolescence since most nevi develop by age 20. Results have shown:

• Boys developed more nevi than girls, and the number of nevi increased with age. Girls showed substantial gains between 13 and 18 in one study.
• Nevus density increased to about age 14.
• Nevi were more common in sun sensitive children, based on predisposition to burn or tan, light eye and hair colour, freckling, and a history of childhood sunburns.
• Higher counts were seen in children with a family history of skin cancer.
• The number of nevi increased among children who lived closer to the equator.

Results among children are clearer than for adults. Nevus density increases up to ages 9-14, and peaks in areas with higher sun exposure, which suggests exposure is involved in nevus development. It's also been suggested sunlight may be involved in the disappearance of nevi in older people. Nevus counts appear to be higher in children with light skin and a propensity to burn. Children with a history of sunburns, particularly with blisters, have higher counts than those who have not burned.

Pre-existing nevi are present in about 50% of adult melanomas, suggesting some nevi may be precursors of melanoma. As a result, reducing nevi in children may substantially lower melanoma rates as they move into adulthood. Regularly covering the skin with clothing, using a high SPF sunscreen containing Parsol 1789, and minimizing sun exposure between 11 am and 3 pm can prevent the development of some nevi.

Refer to the complete journal article for additional details on individual studies nevi.pdf.

The chance of developing a skin cancer in British Columbia, Canada is approximately 1 in 7, over a lifetime. This corresponds to perhaps 1 in 3 for a white population in California, and even higher for a white population in Queensland, Australia. Skin cancer is by far the most common kind of cancer diagnosed in Canada.

The most common skin cancer diagnosed in Canada is basal cell carcinoma. In areas of very high sun exposure such as Queensland, Australia, squamous carcinoma is more common. The chance of developing a malignant melanoma during a lifetime, in North America, is in the order of 1 in 100. This is a startling increase over the figures of, for instance 1935 when the rate was 1 in 1,500. The difference is presumably accounted for in out-of-doors leisure activities.

​Classical carcinogenesis theory has an initiation event, followed by a series of promotional events. The model for this has been clearly demonstrated in animals for the ultraviolet light induction of squamous carcinoma. An initiation event such as a sunburn is far more likely to produce a squamous carcinoma if there are a series of subsequent promotional events, such as further sunburns. Presumably the initial DNA damage can only carry a cell a certain way towards a full expression of a cancer, but multiple other abnormalities must be induced before the final expression of that cancer.

The viral induction of squamous carcinoma, such as that caused by oncogenic papilloma virus infections, may or may not follow such a pathway in, for instance the development of squamous carcinoma of the cervix.

Squamous carcinoma occurring in chronic wounds is presumably on the basis of an induced high mitotic rate, coupled with chronic inflammatory reaction. The exact cellular mechanisms are unknown.

The etiology of basal cell carcinoma and melanomas not nearly so well worked out. There is no good animal model for basal carcinoma. While melanoma has been noted in experimental systems using the fish and the nose of the opossum, the relevance of these findings to man is questionable.

We do know that both basal cell carcinoma and melanoma are most significantly linked to early exposure to ultraviolet light. Squamous carcinoma on the other hand is linked to total lifetime exposure, with the past ten years exposure being very important, and total exposure levels being even more important. Both melanoma and basal cell carcinoma have a rapidly accelerating relative risk with relatively low exposures, followed by a broad plateau.

Indeed, outdoor workers with a very large exposure to ultraviolet light have a slightly lower risk of melanoma than indoor workers episodically significantly exposed to ultraviolet light. In other words the carcinogenesis patterns for basal cell carcinoma and melanoma on one hand, and squamous cell carcinoma on the other are fundamentally different.

Ultraviolet B (UVB), with wavelengths between 280 and 320 nanometers, is felt to be the most significant cause of all three types of skin cancer. UVB, the burning and carcinogenic wavelengths of light, is blocked by window glass. Wavelengths below 280 nanometers (ultraviolet C) are blocked by the ozone layer.

UVB exerts its damage directly on DNA, and that effect is directly related to dosage intensity. UVB can cause such damage at lower levels than that causing clinical sunburns.

Between UVB and visible light is ultraviolet A. Ultraviolet A is 320 to 400 nanometers, the beginning of visible light. Ultraviolet A has two types of energies within it. Between 320 and 340 nanometers is UVA of sufficient similarity to UVB to cause direct DNA damage. UVB and UVA up to 340 nanometers are carcinogenic. Between 340 and 400 nanometers there is pure UVA type damage, which is indirect through an effect of other molecules on DNA. The UVA activates photoactive molecules in the cell that in turn damage the DNA. Pure UVA effect is much less carcinogenic than UVB. Pure UVA can cause tanning and is an important cause of photoaging, and is the specific cause of what has been termed UVA wrinkling and sagging of the skin (see photoaging). In other words, ultraviolet A as a broad band is not just a tanning wavelength, it includes some UVB like activity at one end of its spectrum, and a more pure UVA like activity at the other. The major UVA effect is to cause tanning and UVA photoaging effects such as UVA sagging of the skin.

Good lighting is required to examine the skin for early skin cancers. Standard office ceiling lighting is rarely satisfactory. A wall or floor mounted gooseneck lamp added as a supplement is very helpful.

The areas of skin cancer involvement are usually areas of either maximum sun exposure ie: the face and dorsum of the hands, or areas of intermittent severe sun exposure, back and arms of men and women and the lower legs of women. It is important in female patients to examine the legs, particularly below the knees. Wearing dresses as a child is the probable reason for this increased of melanomas on the legs of women as compared to men.

Ideally, all patients should be examined clothing free. This is not practical in most practice settings. High risk patients should have such an examination, but for the average patient removing the shirt exposes 60% of the body surface area to scrutiny, and a larger percentage of sun-damaged skin. Examining the lower legs of women should be routine in this context.

It is important not to be distracted by one lesion. If one notices a basal cell carcinoma on the face one can stop an examination and miss a melanoma on the back. The risk factors are similar. It is important to do an examination as thorough on a patient with a known or suspect pathology as one would do for a patient that was simply at high risk. In addition, it has been noted that approximately 40% of patients with one melanoma have a dysplastic nevus that is obvious at that same examination. It is important to review melanoma patients for dysplastic nevi at that first examination, and annually thereafter.

Linked are three references that review some risk factors for melanoma. Please print out these references or review them online.

Some ultraviolet light risk factors have been reviewed under carcinogenesis. Hereditary factors can be important.

Fair skin is obviously an inherited risk factor. Darker skinned Caucasians have a significantly lower risk of developing all types of skin cancer than fair skinned Caucasians, assuming that both have an equal amount of light exposure. South Asian skin appears to be quite protective, as is East Asian and, of course, Black skin. Heredity can also be influential in other ways. In a family of similar skin tones, there can be a dramatically different risk of skin cancer. This seems to relate to a genetic susceptibility, although the exact mechanism is not known. A specific example of this is a tendency towards numerous nevi from a given amount of sun exposure. The absolute number of nevi is the single greatest predictor of melanoma risk on a population basis.

An acquired nevus is the result of a single melanocyte that became abnormal and began to divide. These abnormal melanocytes pile up, causing a brown spot. Most nevi, probably at least 9 out of 10, are secondary to sun damage. Some individuals are far more likely to develop a large number of nevi with a specific amount of ultraviolet light.

Another example of heredity is the tendency towards developing abnormal nevi. This has been called the dysplastic nevus syndrome, or the cancer family multiple mole syndrome, and is manifested by not only an increased number of nevi, but by clinical atypia. The nevi in these individuals seem to be more genetically unstable. There is large variation of colour and edge in these nevi, implying subclones of cells that produce variable amounts of melanin, or grow at different rates. These patients and their families are at particularly high risk for developing melanoma.

The congenital nevus is another risk factor for melanoma. It is well known that large congenital nevi, bigger than 2 palms of one's hand, are at significant risk for developing melanoma over a lifetime. The lifetime risk of a 5 cm diameter hairy congenital nevus may be in the order of 5%, but large prospective series have not been published. Smaller congenital nevi appear to have a smaller risk, proportionate to their size. Less than 2% of the population is born with a single mole. All of the others we acquire, mostly from sun damage.

Congenital nevi can be broadly divided into three types. The first is the most common nevus cell nevus. This is generally manifested as a brown raised lesion that is often hairy. It is the congenital nevus with the most data. Most experts agree that a congenital nevus of this morphology should be surgically removed, if that is practical.

The second type of congenital nevus is the congenital blue nevus. The congenital blue nevus is a blue-black plaque on the skin. There is not good epidemiological data but it appears to be more common in East Asians than in Caucasians. The risk of melanoma arising in such lesions is not well understood, but there is some evidence that the risk is high enough to warrant prophylactic removal of such lesions.

The third type of congenital nevus can be called the hamartomatous type. This is a large lesion, found in neonates, with many histologic patterns in each lesion. The hamartomatous type may show soft tissue sarcoma like changes in areas, as well as melanoma changes in other areas. The hamartomatous congenital nevus appears to be at very high risk for developing multiple cancers, and its early removal is recommended.

Many patients inquire about the risk to other family members given that they have had a skin cancer. There is a definite familial association with all types of skin cancer, but the genetics is complicated. Families with an outdoor lifestyle or who have been residents in a very sunny area, will of course have an increased risk compared to the general population.

The skin colour is obviously familial in most cases. Fair skinned individuals are much more likely to develop all types of skin cancer than darkly skinned individuals. Appropriate family counselling must take these factors into account.

Nevoid basal cell carcinoma syndrome is a dominant condition where multiple basal cell carcinomas develop over a lifetime. Hundreds of basal cell carcinomas can develop before age 40. It is associated with hypertelorism and palmar pitting, as well as jaw cysts and other abnormalities. Xeroderma pigmentosum is another condition where there is incomplete DNA repair of UV damage, leading to the early development of all major types of skin cancer. This is evidenced by obviously accelerated photoaging of the skin in the teenage or early adult years, with the development of skin cancers shortly thereafter.

The most clinically significant genetic association is the dysplastic nevus syndrome. The tendency towards developing multiple dysplastic nevi can be inherited as an autosomal dominant trait. This is a common condition. A single dysplastic nevus does not imply the dysplastic nevus syndrome. A patient with an increased number of nevi, many of which are clinically atypical, is at risk for this syndrome. In addition to their personal risk of developing multiple melanomas, there is an increase of melanoma in first-degree relatives. Patients with a melanoma and dysplastic nevi, or simply multiple dysplastic nevi, should be advised to have first degree relatives reviewed in the context of that diagnosis.

It is difficult to recommend a precise follow up for the early diagnosis of new lesions. Approximately 40% of patients with one basal cell carcinoma will develop a second basal cell carcinoma within 5 years. Six percent of patients with one melanoma will develop a second melanoma. Patients with dysplastic nevi and a family history of melanoma have, without regular review, an almost certainty of developing melanoma in their lifetime. Significantly freckled individuals are at high risk for melanoma, as are those with nevi numbering more than 50.

All of these must be taken into account when recommending appropriate follow-up examinations. In general, if a patient has had a skin cancer or a pre-skin cancer, review by a physician once a year would be appropriate. In some individuals with a pace of new lesions would suggest that a more frequent follow-up would be appropriate. Patients with multiple actinic keratoses are frequently seen at 3 to 4 monthly intervals with new lesions being treated at each visit.

Avoiding sunshine can prevent most types of skin cancer. However one should be realistic about sun avoidance in older adults. The squamous carcinoma on the forehead of an elderly individual probably relates more to occupational and childhood exposure than to exposure in the past few years.

It would be unrealistic for the elderly to adopt a significant sun avoidance strategy as most of the damage has already been done. Also, vitamin D production may be impaired by excessive sun avoidance.

It is very different for young adults. Young adults with a pre-cancerous or cancerous lesion are telling us that they are at significant risk for new skin cancers. Avoiding sunshine is entirely reasonable in this case. Sun avoidance is best undertaken by the timing of outdoor activities so as to avoid the mid-day maximum, wearing appropriate clothing, and lastly, if one can not do the first two, using a sunscreen.

Sunscreens certainly prevent sunburns. It is proven that sunscreens can prevent actinic keratoses and there is good evidence that they will prevent some squamous carcinomas. There is no direct evidence that sunscreens prevent basal cell carcinoma or melanoma, although there is good evidence that sunscreens prevent the development of nevi, which is an important precursor of melanoma.

Reference 2 reviews some aspects of the use and misuse of sunscreens. Please print out this reference. It will answer many questions that your patients have of how and why to use sunscreens.

Sunscreens can be discussed in two broad categories. The opaque sunscreens are sunscreens that do not permit light to penetrate the skin. Zinc oxide or titanium dioxide, applied thickly, are in this category. The major advantage of an opaque sunscreen is that it provides a complete block by reflecting ultraviolet light. It is of particular use at times of maximal exposure such as mountain climbing, competition sailing or other such activities.

Transparent sunscreens, on the other hand, are not risk free. Transparency is important from the cosmetic point of view. Few people can or will use a physical blocker in urban areas. However, with the transparency comes some ultraviolet light induced damage. It is not possible to block all ultraviolet light in a transparent sunscreen.

It is naïve to think that sunscreens do not change behaviour. It has been well documented that high SPF sunscreens are associated with increased time in the sun. This is both a benefit and a deficit. Clearly people would like to spend more time doing what they enjoy doing. High SPF sunscreens can permit this. The down side is that there can be a build up of low-grade damage caused by the transparency of that sunscreen. For that reason it is very important, when using a high SPF sunscreen, to use one that provides a very broad block. It is important to block UVA, in addition to UVB.

UVB blocking is the traditional sunscreen block. Many ingredients, added together, can block burning, which is the patient's major concern. Pure UVA, i.e. above 340 nanometers and below 400 nanometers, the cause of UVA sagging and possibly immune suppression, is blocked well by only one ingredient found in transparent sunscreens, Parsol 1789 (dibenzoylmethane). Very few dermatologists would recommend a sunscreen that did not contain this ingredient.

Sun avoidance may obviate the need for chemical sunscreen. Sun avoidance means reducing, whenever possible, activities between 11 am and 3 pm.

Clothing is an important sunscreen. Clothing is chemical free, and is inexpensive. Good clothing is a complete block. An important part of clothing is the use of a hat with a wide brim. This at least provides partial screening for the face. A 7 cm brim is an SPF 20 on the forehead, but only 4 to 8 to the nose. Hats alone are not enough. There are UV blocking clothes on the market which have a specific weave that permits airflow, while blocking ultraviolet light. These clothes tend to be expensive, but they are generally effective.

Glass is an excellent sunscreen for preventing burning. You will not burn through window glass but you will tan through window glass. Theoretically you can wrinkle through window glass.

Tanning salons can be a significant cause of UV damage. Most tanning salons now use UVA tubes rather than UVB tubes. This is a step forward. However, the UVA tubes do emit a small amount of UVB, probably in the order of 1% to 2% of total energy produced. As exposure times are quite long in the UVA light beds, this can be a significant exposure to UVB. UVA alone is only a small contributor to skin cancer risk, but is an important cause of skin sagging.

The use of tanning beds is promoted for colour, and protection. The bronzing creams containing dihydroxyacetone can give a brown colour, at very low risk, should that be desired. The argument for inducing a tan so that there will be fewer sunburns is less easily dealt with. Clearly a suntan does provide some protection; it has been suggested that a dark suntan equals a SPF 4 sunscreen. Equally certain is that the suntan was the direct result of skin injury by the ultraviolet light. A better approach would be to avoid the tanning parlour, and use a high SPF sunscreen at the beach.

The dysplastic nevus syndrome is autosomal dominant. Approximately 50% of the offspring of an affected parent would be expected to have the gene for increased sensitivity to ultraviolet light. It is important to examine family members of patients who have had a melanoma for evidence of the dysplastic nevus syndrome. Approximately 40% of melanoma patients have a clearly very atypical nevus at the time of their presentation of the melanoma.

Photos - click on tab labelled Actinic keratosis.

Actinic keratoses are precancerous lesions that if untreated may progress to invasive squamous carcinoma. Clinically they are manifested by a hyperkeratotic (scaling) lesion often on a pink base. The scale is very adherent. When rubbed the lesion is often tender. Actinic keratoses are frequent in areas of maximum sun exposure. Whereas basal cell carcinomas and melanomas occur most frequently on skin areas receiving intermittent severe sun damage, squamous carcinomas occur in areas of the skin receiving maximum lifetime exposure. These areas include the face, scalp in balding individuals, dorsum of the hands, arms and legs, as well as elsewhere if there has been severe sun damage.

Progression to squamous carcinoma is usually slow, extending over many years. While some actinic keratoses can disappear spontaneously, it is generally a good practice to treat these lesions. The use of sunscreens can prevent the development of actinic keratoses, and by inference, squamous carcinomas.

​Dysplastic leukoplakia is the equivalent of actinic keratoses on non-moist skin. Hyperkeratotic skin, when wet, turns white. A patch of white skin on a moist area such as the mouth or vaginal mucosa is suggestive of thickened skin. Skin can become thickened from many causes. This spectrum of causation extends from a hypertrophic response to trauma, to benign human papilloma virus infection, through to dysplastic leukoplakia that is precancerous.

Dysplastic leukoplakia can be secondary to an oncogenic human papilloma virus, or can be secondary to other carcinogens such as, in the case of the oral mucosa, chronic exposure to chewing tobacco. A biopsy is necessary to diagnose dysplastic leukoplakia. If untreated, dysplastic leukoplakia can lead to squamous carcinoma. See squamous carcinoma photos.

Photos - click on tab labelled Congenital nevus

Congenital nevi, compared to normal skin and compared to banal acquired nevi, are at increased risk for developing melanoma. As a congenital nevus is, essentially, a large accumulation of abnormal melanocytes, this is not unexpected. The risk of melanoma appears to be related to size, i.e. the number of melanocytes. Congenital nevi less than 1 cm diameter appear to have a melanoma risk of less than 1%, whereas nevi of twice the size of the palm probably have a lifetime risk in the order of 5%.

Changes in a congenital nevus that would indicate a potentially worrisome alteration include spatial regression (depressed white areas) and inflammation, as well as a rapidly changing localized colour change or the development of a firm nodule.

Congenital nevi are often excised if small to medium in size. If very large, such as the entire bathing trunk area, excision is practically impossible. In that case yearly review may be indicated. A good close up photograph is often helpful to the patient when doing self examination.

A note on history taking: It is often more useful to ask the patient if they were told that the lesion was present at birth, rather than if the lesion was present at birth. Present since they can remember does not indicate that they have a congenital nevus.

Café au lait lesions (see benign lentigo, click on the tab labelled Lentigo) must be separated from a flat congenital lesion. 26% of children have one café au lait lentigo, whereas only 2% have a congenital nevus. Café au lait lesions have no malignant potential. If in doubt, a small biopsy will define the diagnosis.

Photos - click on tab labelled Dysplastic (Atypical)

Banal common nevi evolve through a process from a junctional nevus to a compound nevus to a dermal nevus. Junctional nevi are the result of a single abnormal melanocyte that begins to proliferate at the dermal epidermal junction, and are often seen clinically as a dark flat nevus.

A junctional nevus will typically evolve over time into a compound nevus, which is a nevus with both epidermal and dermal melanocytes. Compound nevi become elevated and usually are more pale. Junctional nevi will typically grow to be 3 or 4 mm across, stop growing sideways, and begin to evolve into a compound nevus. This evolution continues through the compound nevus stage to the dermal nevus stage. In the dermal nevus all of the melanocytes are in the dermis. Dermal nevi are clinically manifested as pale soft wrinkled polyps on the skin. This sequence is the normal life pattern of a nevus. Dermal nevi can eventually drop off the skin.

Dysplastic nevi do not follow this pattern of maturation and self-destruction. Dysplastic nevi do not age properly. The junctional phase can be prolonged, so that the lesion grows beyond 6 mm. Very often, with increasing size, the lesion shows increasing variation in colour and edge. Variable colour, irregularly irregular within a dysplastic nevus, is indicative of genetic instability for the production of melanin. An irregular edge suggests a genetic instability in terms of lateral growth rate. Either are indicative of a tendency to progress to invasive melanoma.

Dysplastic nevi can be identified clinically as mild, moderate, or severe.

Mildly dysplastic nevi are nevi that show this tendency to become very much larger than a normal nevus yet there is some central maturation. This can produce a "fried egg" appearance to the nevus. Mildly dysplastic nevi do not show asymmetrical colour variation or irregularity or edge.

Moderately atypical nevi do not show the central maturation of the fried egg nevus. They tend to be larger than normal junctional nevi with some variation of colour and edge. Colour is often regularly irregular.

A severely dysplastic nevus is indistinguishable from early melanoma. Very often these lesions show considerable irregularity of edge and irregularly irregular colour. The differentiation between a moderate and severely dysplastic nevus is one of degree.

Mildly dysplastic nevi can be observed. Severely dysplastic nevi should certainly be surgically removed. Depending upon the degree of clinical abnormality, moderately atypical nevi can be followed closely if there are many, or surgically removed if there are only a few.

Photos for Lentigo Maligna - click on tab labelled Lentigo.
Photos for Lentigo Malignant Melanoma - click on tab labelled Lentigo maligna melanoma.

Lentigo maligna is a brown patch, generally on the face of the elderly. This precursor lesion leads to lentigo maligna melanoma. Clinically it is a spreading brown patch, often with considerable variation in colour. It is absolutely flat. It can slowly expand for decades. Over time, a nodule can develop within it, lentigo maligna melanoma.

Lentigo maligna and lentigo maligna melanoma occur most often in areas of maximal sun exposure on the face. This is unlike other types of melanoma that tend to predominate in areas of intermittent severe sun exposure. The distribution of lentigo maligna lesions on the face closely parallels that of actinic keratoses, and squamous carcinoma.

Lentigo maligna can be confused with lentigo simplex. Elderly people frequently develop benign brown patches on the face secondary to actinic damage. Only in a few cases is this pre-malignant, lentigo maligna. An incisional shave biopsy, submitted to a dermatopathologist, with an appropriate history, will establish whether the brown patch is benign or premalignant.

The treatment of choice for most cases of lentigo maligna is surgical excision. Radiation therapy can be the treatment of choice in the elderly with an extensive lesion. These lesions should not be treated with liquid nitrogen cryotherapy, as a rule, because the dysplastic melanocytes go down hair follicles and deep recurrence post-cryotherapy is common.

Photos - click on tab labelled Subungual melanoma

Subungual melanoma frequently presents as a pigmented streak in the nail. Nevi can also be present in the nail producing parallel streaks. Dark streaks in the nail, benign, are very common in darker skinned Caucasians including those of Indo-Pakistani decent, as well as Chinese and Japanese. Multiple pigmented streaks are generally not worrisome.

A single pigmented streak, particularly in a fair skinned individual, is of concern. Atypical lesions grow more rapidly than benign nevi, and this is evidenced by non-parallel sides to the pigmented streaks. The most proximal area is wider than the most distal because the lesion has grown. In addition, in dysplastic or malignant lesions the pigment can extend onto the proximal nail fold, Hutchinson's sign. If these features are evident, the nail must be removed and the nail matrix biopsied.

Look for and initiate "teachable moments" for prevention.

• When the patient visit directly pertains to a related concern (sunburn, moles, etc.).
• During routine physical examinations.
• When the patient refers to related topics (desire to quit smoking, concerns about family history, etc.).
• Have prevention information materials available in waiting rooms.
• Consider having sun screen samples available.
• By observing risk factors (life style, number of existing nevi, multiple atypical nevi, etc.).

General Advice on Counselling Techniques

• Use open ended questions ("What" and "How" questions are effective). Avoid "Why" questions which provoke defensiveness.
• Use active listening skills to demonstrate your interest in the patient's response (eye contact, appropriate body language, not interrupting).
• Use empathetic responses to demonstrate you understand (this is different from agreeing).
• Roll with resistance.
• Acknowledge and support the patient's right to make autonomous choices.

Assess the patient's readiness for acting on prevention advice

• Determine the level of awareness of risk.
• Discover and discuss how important this is to the patient.
• Assess the patient's conviction to implement prevention suggestions.

Discussions with unaware or cynical patients

• Provide new information.
• Offer help when ready.
• Accept the situation and the patient.

When language or literacy may be an issue

• Limit your advice to a few key points.
• Use visual aids and demonstrations to support your words.
• Adjust the message to fit the patient's context (suitable examples, appropriate language level).

Stephen Hansen, M.A.(Ed.)
Provincial Education Leader
BC Cancer

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​​Summary 

The incidence of malignant melanoma has risen significantly over the last 30 to 40 years, and continues to increase in the United States, Canada, Australia and Europe, becoming a major public health concern nevi.pdf​. A number of studies have identified three categories of major risk factors:

• Environmental - Solar ultraviolet (UV) exposure is the major environmental risk.
• Constitutional - Light skin and hair colour and propensity to burn rather than tan in the sun are genetically based constitutional risk factors.
• Combination - Acquired melanocytic nevi and freckles combine the risks of constitutional susceptibility and environmental UV exposure.

The single greatest predictor of risk for developing melanoma is the total number of nevi. Studies over the last 15 years have revealed a great deal about the way nevi develop and the relationship between nevi and melanoma. The studies can be divided into adult and child investigations to determine the prevalence of nevi by sex and age, and to identify factors associated with a high number of nevi.

Studies of Nevi in Adults

The findings on adult nevi are somewhat contradictory, because many of the studies were conducted over broad age ranges and may have differences in UV exposure and the number of nevi. Highlights include:

• Sunburn frequency up to ten years old showed the strongest relationship with the number of nevi in one study, suggesting childhood sun exposure is connected to nevus prevalence in young adults.
• Sun exposed surfaces had higher counts than less exposed areas.

Different results may arise because people who are most likely to burn avoided the sun.

Studies of Nevi in Children

Recent research focuses on childhood and adolescence since most nevi develop by age 20. Results have shown:

• Boys developed more nevi than girls, and the number of nevi increased with age. Girls showed substantial gains between 13 and 18 in one study.
• Nevus density increased to about age 14.
• Nevi were more common in sun sensitive children, based on predisposition to burn or tan, light eye and hair colour, freckling, and a history of childhood sunburns.
• Higher counts were seen in children with a family history of skin cancer.
• The number of nevi increased among children who lived closer to the equator.

Results among children are clearer than for adults. Nevus density increases up to ages 9-14, and peaks in areas with higher sun exposure, which suggests exposure is involved in nevus development. It's also been suggested sunlight may be involved in the disappearance of nevi in older people. Nevus counts appear to be higher in children with light skin and a propensity to burn. Children with a history of sunburns, particularly with blisters, have higher counts than those who have not burned.

Pre-existing nevi are present in about 50% of adult melanomas, suggesting some nevi may be precursors of melanoma. As a result, reducing nevi in children may substantially lower melanoma rates as they move into adulthood. Regularly covering the skin with clothing, using a high SPF sunscreen containing Parsol 1789, and minimizing sun exposure between 11 am and 3 pm can prevent the development of some nevi.

Refer to the complete journal article for additional details on individual studies ​​nevi.pdf.

Good lighting is required to examine the skin for early skin cancers. Standard office ceiling lighting is rarely satisfactory. A wall or floor mounted gooseneck lamp added as a supplement is very helpful.

The areas of skin cancer involvement are usually areas of either maximum sun exposure (i.e. the face and dorsum of the hands) or areas of intermittent severe sun exposure: back and arms of men and women and the lower legs of women. It is important in female patients to examine the legs, particularly below the knees. Wearing dresses as a child is the probable reason for this increased of melanomas on the legs of women as compared to men.

Ideally, all patients should be examined clothing free. This is not practical in most practice settings. High risk patients should have such an examination, but for the average patient removing the shirt exposes 60% of the body surface area to scrutiny, and a larger percentage of sun-damaged skin. Examining the lower legs of women should be routine in this context.

It is important not to be distracted by one lesion. If one notices a basal cell carcinoma on the face one can stop an examination and miss a melanoma on the back. The risk factors are similar. It is important to do an examination as thorough on a patient with a known or suspect pathology as one would do for a patient that was simply at high risk. In addition, it has been noted that approximately 40% of patients with one melanoma have a dysplastic nevus that is obvious at that same examination. It is important to review melanoma patients for dysplastic nevi at that first examination, and annually thereafter.

Biopsies can be divided into two broad groups, incisional and excisional. Excisional biopsy of a suspect skin lesion is ideal if the lesion is less than 1 cm, and good cosmetic and functional closure can be obtained. Incisional biopsy is useful in some cases where an excisional biopsy is not practical.

Incisional biopsy is particularly useful in basal cell carcinoma, where the tumour is homogeneous and a small fragment is generally representative of the entire lesion's histology. It is also very useful in the separation of lentigo maligna from the much more common benign lentigo simplex. A small shave biopsy of this flat brown patch on the face of an elderly individual can clearly differentiate whether the melanocytes are dysplastic or completely benign

Excisional biopsy is the preferred biopsy for most squamous carcinomas, particularly nodular squamous carcinomas. A nodular squamous carcinoma must be distinguished from a keratoacanthoma. Keratoacanthoma has a histology similar to but architecturally different from a squamous carcinoma. These self-limited lesions grow quickly over 8 to 12 weeks and then self remit. An incisional fragment of a keratoacanthoma can be misinterpreted as a squamous carcinoma and vice versa. The entire lesion should be submitted for histological review. That said, a large plaque of squamous carcinoma on for instance the forehead of an individual can be biopsied to define the diagnosis, and aid in the decision on appropriate therapy, whether surgical excision with flap closure and graft or radiation therapy.

It is important when biopsying a lesion that could be suspect for melanoma that the thickest part be biopsied to the full depth of the lesion and beyond. Prognosis depends upon the measured depth of invasion. If the thickest part is incompletely biopsied, and the base cauterized, it may not be possible to plan appropriate therapy because the depth of invasion will not be known. This is particularly a problem with "saucerization" as a method of biopsy.

It is important that the lesion not be shaved off the surface with cautery of the base, but rather deeply saucerized, if this technique is to be used. If there is any pigment at the base of the biopsy after the main tissue has been removed, that pigmented area should be submitted separately, and not cauterized from hemostasis.

Biopsy of melanoma and other skin cancers does not worsen prognosis.

Many patients inquire about the risk to other family members given that they have had a skin cancer. There is a definite familial association with all types of skin cancer, but the genetics is complicated. Families with an outdoor lifestyle or who have been residents in a very sunny area will of course have an increased risk compared to the general population.

The skin colour is obviously familial in most cases. Fair skinned individuals are much more likely to develop all types of skin cancer than darkly skinned individuals. Appropriate family counselling must take these factors into account.

Nevoid basal cell carcinoma syndrome is a dominant condition where multiple basal cell carcinomas develop over a lifetime. Hundreds of basal cell carcinomas can develop before age 40. It is associated with hypertelorism and palmar pitting, as well as jaw cysts and other abnormalities. Xeroderma pigmentosum is another condition where there is incomplete DNA repair of UV damage, leading to the early development of all major types of skin cancer. This is evidenced by obviously accelerated photoaging of the skin in the teenage or early adult years, with the development of skin cancers shortly thereafter.

The most clinically significant genetic association is the dysplastic nevus syndrome. The tendency towards developing multiple dysplastic nevi can be inherited as an autosomal dominant trait. This is a common condition. A single dysplastic nevus does not imply the dysplastic nevus syndrome. A patient with an increased number of nevi, many of which are clinically atypical is at risk for this syndrome. In addition to their personal risk of developing multiple melanomas, there is an increase of melanoma in first-degree relatives. Patients with a melanoma and dysplastic nevi, or simply multiple dysplastic nevi, should be advised to have first degree relatives reviewed in the context of that diagnosis.

It is difficult to recommend a precise follow up for the early diagnosis of new lesions. Approximately 40% of patients with one basal cell carcinoma will develop a second basal cell carcinoma within 5 years. Six percent of patients with one melanoma will develop a second melanoma. Patients with dysplastic nevi and a family history of melanoma have, without regular review, an almost certainty of developing melanoma in their lifetime. Significantly freckled individuals are at high risk for melanoma, as are those with nevi numbering more than 50.

All of these must be taken into account when recommending appropriate follow-up examinations. In general, if a patient has had a skin cancer or a pre-skin cancer, review by a physician once a year would be appropriate. In some individuals a pace of new lesions would suggest that a more frequent follow-up would be appropriate. Patients with multiple actinic keratoses are frequently seen at 3 to 4 monthly intervals with new lesions being treated at each visit.

Avoiding sunshine can prevent most types of skin cancer. However one should be realistic about sun avoidance in older adults. The squamous carcinoma on the forehead of an elderly individual probably relates more to occupational and childhood exposure than to exposure in the past few years.

It would be unrealistic for the elderly to adopt a significant sun avoidance strategy as most of the damage has already been done. Also, vitamin D production may be impaired by excessive sun avoidance.

It is very different for young adults. Young adults with a pre-cancerous or cancerous lesion are telling us that they are at significant risk for new skin cancers. Avoiding sunshine is entirely reasonable in this case. Sun avoidance is best undertaken by the timing of outdoor activities so as to avoid the mid-day maximum, wearing appropriate clothing, and lastly, if one can not do the first two, using a sunscreen.

Sunscreens certainly prevent sunburns. It is proven that sunscreens can prevent actinic keratoses and there is good evidence that they will prevent some squamous carcinomas. There is no direct evidence that sunscreens prevent basal cell carcinoma or melanoma, although there is good evidence that sunscreens prevent the development of nevi, which is an important precursor of melanoma.

Photos - click on tab labelled Actinic keratosis.

Actinic keratoses are precancerous lesions that if untreated may progress to invasive squamous carcinoma. Clinically they are manifested by a hyperkeratotic (scaling) lesion often on a pink base. The scale is very adherent. When rubbed the lesion is often tender. Actinic keratoses are frequent in areas of maximum sun exposure. Whereas basal cell carcinomas and melanomas occur most frequently on skin areas receiving intermittent severe sun damage, squamous carcinomas occur in areas of the skin receiving maximum lifetime exposure. These areas include the face, scalp in balding individuals, dorsum of the hands, arms and legs, as well as elsewhere if there has been severe sun damage.

Progression to squamous carcinoma is usually slow, extending over many years. While some actinic keratoses can disappear spontaneously, it is generally a good practice to treat these lesions. The use of sunscreens can prevent the development of actinic keratoses, and by inference, squamous carcinomas.

Dysplastic leukoplakia is the equivalent of an actinic keratosis on non-moist skin. Hyperkeratotic skin, when wet, turns white. A patch of white skin on a moist area such as the mouth or vaginal mucosa is suggestive of thickened skin. Skin can become thickened from many causes. This spectrum of causation extends from a hypertrophic response to trauma, to benign human papilloma virus infection, through to dysplastic leukoplakia that is precancerous.

Dysplastic leukoplakia can be secondary to an oncogenic human papilloma virus, or can be secondary to other carcinogens such as, in the case of the oral mucosa, chronic exposure to chewing tobacco. A biopsy is necessary to diagnose dysplastic leukoplakia. If untreated, dysplastic leukoplakia can lead to squamous carcinoma.​

Photos

Squamous carcinoma is manifested on the skin as a hard keratotic nodule or plaque. There is often a very adherent scale centrally with a hard rolled edge. It does not have the telangiectatic vessels or translucency of a basal cell carcinoma. There may be some associated inflammation. Squamous carcinoma can be clinically and histologically confused with benign keratoacanthoma. 

Squamous carcinomas have a feeling of depth when palpated. While generally non-tender some can be painful to palpation.

Squamous carcinoma on areas of the skin that are moist, such as the lips, oral mucosa or vaginal mucosa, can be very white, secondary to the absorption of moisture.

Squamous carcinomas can develop from actinic keratoses or from dysplastic leukoplakia. They can also occur at the site of chronic irritation such as a chronic leg ulcer or old burn scar.

Photos 

Basal cell carcinoma has no precursor lesion. The earliest lesions of basal cell carcinoma are generally seen as a small pink papule sometimes only 1 to 3 mm across. This papule commonly bleeds on minor trauma such as dragging a fingernail across it. This can be a useful diagnostic sign in the identification of an early basal cell carcinoma, particularly if the small papule has been present for many months and is thus obviously not a simple folliculitis.

As basal cell carcinomas grow the most common types develop the more characteristic nodularity, translucency, and telangiectasia.

There are four main clinical variants of basal cell carcinoma. These are nodular, superficial spreading, sclerosing and pigmented basal cell carcinomas.

a) Nodular Basal Cell Carcinoma

Nodular basal cell carcinoma is clinically manifested as a translucent nodule, often with telangiectatic vessels being very evident. As the nodule expands beyond 1 cm the center can begin to break down causing an ulcer surrounded by a rolled edge. The alternative name for this is "rodent ulcer".

Nodular basal cell carcinomas are common on the face, particularly along embryonal fusion planes such as the inner canthus, perinasal skin and periauricular skin. They can occur anywhere on the body that has been subject to intermittent severe sun exposure.

Childhood exposure appears to be of considerable significance, as it is for melanoma, in the development of basal cell carcinoma.

b) Superficial Spreading Basal Cell Carcinoma

Superficial spreading basal cell carcinoma is most common on the upper back. It consists of shallow plaques, pink to almost skin coloured, that slowly expand over many years. The shallowness of the lesion prevents ulceration until quite late. Typically, these lesions are very friable, and minor trauma such as dragging a fingernail across the lesion while often result in multiple pinpoint bleeding areas.

Superficial spreading basal cell carcinomas are almost all secondary to sun damage.

c) Sclerosing Basal Cell Carcinoma

Sclerosing basal cell carcinoma is often a significant diagnostic problem. The early lesion can look like a small white scar on the skin. This scar-like area slowly expands. Nodules of basal cell carcinoma can be apparent in late lesions but the sclerotic scarred area can expand to a very large size before it is clinically obvious as a skin cancer. It is most common on the face, and can produce quite significant morbidity because of its size at the time of diagnosis.

Because the margins of sclerosing basal cell carcinoma are almost always very poorly defined, it is commonly recurrent after simple surgical excision. Micrographic surgery, if available, is the surgical treatment of choice or, in patients over 60, radiation therapy with generous margins. In all cases, the lesion must be examined carefully under very good light to ascertain the approximate margins.

d) Pigmented Basal Cell Carcinoma

Pigmented basal cell carcinoma occurs in dark skinned individuals, particularly Asians. Nodular basal cell carcinomas can be pigmented, as can superficial spreading basal cell carcinomas. Nodular basal cell carcinomas that are pigmented may be confused clinically with nodular melanoma. The differentiating feature, if completely pigmented, is that there are pigment flecks around the base of the nodule that are absent in melanoma. These flecks are the engorged melanocytes. In many cases the only way to clearly differentiate is a biopsy.

Photos - click on tab labelled Congenital nevus

Congenital nevi, compared to normal skin and compared to banal acquired nevi, are at increased risk for developing melanoma. As a congenital nevus is, essentially, a large accumulation of abnormal melanocytes, this is not unexpected. The risk of melanoma appears to be related to size ie: the number of melanocytes. Congenital nevi less than 1 cm diameter appear to have a melanoma risk of less than 1%, whereas nevi of twice the size of the palm probably have a lifetime risk in the order of 5%.

Changes in a congenital nevus that would indicate a potentially worrisome alteration include partial regression (depressed white areas) and inflammation, as well as a rapidly changing localized colour change or the development of a firm nodule.

Congenital nevi are often excised if small to medium in size. If very large, such as the entire bathing trunk area, excision is practically impossible. In that case yearly review may be indicated. A good close up photograph is often helpful to the patient when doing self examination.

A note on history taking: It is often more useful to ask the patient if they were told that the lesion was present at birth, rather than if the lesion was present at birth. Present since they can remember does not indicate that they have a congenital nevus.

Café au lait lesions (see benign lentigo, click on the tab labelled Lentigo), must be separated from a flat congenital lesion. 26% of children have one café au lait lentigo, whereas only 2% have a congenital nevus. Café au lait lesions have no malignant potential. If in doubt, a small biopsy will define the diagnosis.

Photos - click on tab labelled Dysplastic (Atypical)

Banal common nevi evolve through a process from a junctional nevus to a compound nevus to a dermal nevus. Junctional nevi are the result of a single abnormal melanocyte that begins to proliferate at the dermal epidermal junction, and is often seen clinically as a dark flat nevus. A junctional nevus will typically evolve over time into a compound nevus, which is a nevus with both epidermal and dermal melanocytes. Compound nevi become elevated and usually are more pale. Junctional nevi will typically grow to be 3 or 4 mm across, stop growing sideways, and begin to evolve into a compound nevus. This evolution continues through the compound nevus stage to the dermal nevus stage. In the dermal nevus all of the melanocytes are in the dermis. Dermal nevi are clinically manifested as pale soft wrinkled polyps on the skin. This sequence is the normal life pattern of a nevus. Dermal nevi can eventually drop off the skin.

Dysplastic nevi do not follow this pattern of maturation and self-destruction. Dysplastic nevi do not age properly. The junctional phase can be prolonged, so that the lesion grows beyond 6 mm. Very often, with increasing size, the lesion shows increasing variation in colour and edge. Variable colour, irregularly irregular within a dysplastic nevus, is indicative of genetic instability for the production of melanin. An irregular edge suggests a genetic instability in terms of lateral growth rate. Either are indicative of a tendency to progress to invasive melanoma.

Dysplastic nevi can be identified clinically as mild, moderate, or severe.

Mildly dysplastic nevi are nevi that show this tendency to become very much larger than a normal nevus yet there is some central maturation. This can produce a "fried egg" appearance to the nevus. Mildly dysplastic nevi do not show asymmetrical colour variation or irregularity of edge.

Moderately atypical nevi do not show the central maturation of the fried egg nevus. They tend to be larger than normal junctional nevi with some variation of colour and edge. Colour is often regularly irregular.

A severely dysplastic nevus is indistinguishable from early melanoma. Very often these lesions show considerable irregularity of edge and irregularly irregular colour. The differentiation between a moderate and severely dysplastic nevus is one of degree.

Mildly dysplastic nevi can be observed. Severely dysplastic nevi should certainly be surgically removed. Depending upon the degree of clinical abnormality, moderately atypical nevi can be followed closely if there are many, or surgically removed if there are only a few.

Photos - click on tab labelled Superficial spreading melanoma

Superficial spreading melanoma evolves fifty percent of the time from a dysplastic nevus. Melanoma can also arise directly as melanoma in the other 50% of cases. A 1 mm black dot, often with a fine scale on top, can be in-situ or minimally invasive melanoma. That said, fifty percent of superficial spreading melanoma have an identifiable nevus in them. That nevus is the presumed precursor lesion.

Superficial spreading melanoma can, in many cases, be recognised as an extension of the abnormalities noted in dysplastic nevi. Its features include Asymmetry, irregularity of Border, Colour variation, and large Diameter. These ABCD rules can be useful, but many melanomas are not identified using them. For instance, the D of ABCD includes a lesion diameter greater than 6 mm in diameter. Thanks to an educated physician and general public, melanomas in Australia are diagnosed smaller than 6 mm 60 percent of the time. Thus size alone is not a useful predictor, unless the lesion is large. Similarly, edge and colour variation are common in very tiny new nevi that are not dysplastic. As nevi evolve beyond 2 to 4 mm, the variation becomes less and less in the normal nevus. Conversely, the irregularity of edge and colour can be accentuated in the dysplastic nevus evolving into a melanoma.

Thus, while the ABCD rule is useful as a way of thinking about morphology, strict adherence to it may result in the missing of some melanomas.

Another rule that is sometimes useful is the "ugly duckling rule". If all of the patient's nevi are a pale to mid brown colour and one of them is very dark, that one is suspect. Similarly, if all the patient's nevi are very dark and one is showing evidence of pale brown, that one is suspect. In other words one looks for the nevus that does not fit in the general pattern. That general impression approach can be very useful.

Yet another rule is to rely on the experience that you the practitioner have gained over many years. If the average individual has 50 nevi, you will have seen, assuming that at least the shirt is removed from the patient, many hundreds of nevi a day for your practice life. When you see something that does not fit in to the pattern that you have been seeing for years, that lesion warrants a closer look, and possibly a biopsy. This later rule can be called the "experience" rule and is quite possibly the most useful rule of all.

Photos - click on tab labelled Nodular melanoma

Nodular melanoma has no known precursor. It is a small black, or if amelanotic, pink nodule that simply enlarges. The absence of a precursor lesion means that nodular melanomas tend to be diagnosed later than superficial spreading melanomas. This lateness means that they are thicker at the time of diagnosis, on average, and tend to have a worse prognosis because of that.

Amelanotic melanoma, a pink to purple-red nodule, is particularly likely to be diagnosed late because neither physicians nor the public expect a pink lesion to be a melanoma. A rapidly growing pink nodule can be amelanotic melanoma or squamous carcinoma, among a broad differential diagnosis.

Photos for Lentigo Maligna - click on tab labelled Lentigo.
Photos for Lentigo Malignant Melanoma - click on tab labelled Lentigo maligna melanoma.

Lentigo maligna is a brown patch, generally on the face of the elderly. This precursor lesion leads to lentigo maligna melanoma. Clinically it is a spreading brown patch, often with considerable variation in colour. It is absolutely flat. It can slowly expand for decades. Over time, a nodule can develop within it, lentigo maligna melanoma.

Lentigo maligna and lentigo maligna melanoma occur most often in areas of maximal sun exposure on the face. This is unlike other types of melanoma that tend to predominate in areas of intermittent severe sun exposure. The distribution of lentigo maligna lesions on the face closely parallels that of actinic keratoses, and squamous carcinoma.

Lentigo maligna can be confused with lentigo simplex. Elderly people frequently develop brown patches on the face secondary to actinic damage. Only in a few cases is this lentigo, lentigo maligna. An incisional shave biopsy, submitted to a dermatopathologist, with an appropriate history, will establish whether the brown patch is benign or premalignant.

The treatment of choice of lentigo maligna is surgical excision if the lesion is small. Radiation therapy is frequently the treatment of choice in the elderly with an extensive lesion. These lesions should not be treated with liquid nitrogen cryotherapy, as a rule, because the dysplastic melanocytes go down hair follicles and deep recurrence post-cryotherapy is common.

Photos - click on tab labelled Subungual melanoma

Subungual melanoma frequently presents as a pigmented streak in the nail. Nevi can also be present in the nail producing parallel streaks. Dark streaks in the nail, benign, are very common in darker skinned Caucasians including those of Indo-Pakistani decent, as well as Chinese and Japanese. Multiple pigmented streaks are generally not worrisome.

A single pigmented streak, particularly in a fair skinned individual, is of concern. Atypical lesions grow more rapidly than benign nevi, and this is evidenced by non-parallel sides to the pigmented streaks. The most proximal area is wider than the most distal because the lesion has grown. In addition, in dysplastic or malignant lesions the pigment can extend onto the proximal nail fold, Hutchinson's sign. If these features are evident, the nail must be removed and the nail matrix biopsied.

Photos - click on tab labelled Palmoplantar melanoma

Palmoplantar melanoma occurs in all races. The palms and soles of even the darkest skinned individuals are white. The white palms of a black person contain as many melanocytes as the black dorsum of the hand, but the melanocytes on the palm are not making pigment. Banal looking nevi on the palms and soles are not of particular concern as they are very common. Nevi that show features of a dysplastic nevus are different, and these nevi are at increased risk for becoming melanoma. The same features on the palms and soles that are seen in dysplastic nevi on the rest of the body should be noted.

Melanoma can occur on mucosal surfaces, and can be pigmented or non-pigmented. Clinically there is often an extensive in situ component surrounding a nodule or polyp. These melanomas are usually diagnosed late because they are not in a site that is clinically obvious. The etiology of mucosal melanoma is not known.

Photos - click on tab labelled Spitz nevus

Children and occasionally adults can develop a melanotic neoplasm called a Spitz nevus, named for Sophie Spitz, a pathologist. This lesion is typically a rapidly growing pink nodule, but the lesion can sometimes be pigmented. Histologically this benign lesion can be easily confused with melanoma . All biopsies in children with a suggested diagnosis should be examined by an experienced dermatologist.

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