Melanoma

Twelve to 15 million white patients living in the United States have had at least one nonmelanoma skin cancer in their lifetimes, according to estimates based on a new mathematical model reported in the March issue of the Archives of Dermatology.

This figure is approximately twice that of previous estimates based on patient surveys, such as the estimate calculated in the U.S. National Health Interview Study, according to Dr. Robert S. Stern of Beth Israel Deaconess Medical Center and Harvard Medical School, Boston.

This difference can be attributed in part to people often incorrectly reporting their skin cancer histories when surveyed, falsely believing that basal cell and squamous cell lesions are not cancerous or that all skin cancers can be considered melanoma.

Dr. Stern devised his mathematical model using the same basic data available from national samples, such as the Surveillance, Epidemiology, and End Results (SEER) studies and information from the National Cancer Institute. His model, however, took into consideration several factors that had not been accounted for in previous estimates, such as the likelihood that patients develop numerous nonmelanoma skin cancers over the course of several years and that “a substantial proportion” of patients with melanoma also have nonmalignant skin cancers.

According to his model, “about 13 million white non-Hispanic U.S. residents (6%) have had more than 22 million nonmelanoma skin cancers” (Arch. Dermatol. 2010;146:279-82).

This puts the prevalence of a skin cancer history at a level far higher than that of any other cancer – prevalence that “exceeds that of all other cancers diagnosed since 1975,” he added. “Recent population-based data concerning skin cancer incidence, morbidity, and cost of care are lacking for the most common types of skin cancer, [basal cell carcinoma] and [squamous cell carcinoma].”

Regarding patients’ inaccurate reporting of skin cancer histories in surveys and interviews, Dr. Stern noted that many patients equate skin cancer with melanoma. “Hundreds of thousands of patients may be unnecessarily burdened with the belief that they have had a potentially lethal cancer (melanoma) when in fact they have had a skin tumor that is very unlikely to be lethal,he wrote.

In contrast, patients with breast or prostate cancer are much more likely to accurately report their cancer histories, so incidence and prevalence estimates for these tumors are much more accurate than those for skin cancer, Dr. Stern noted.

This study was funded in part by the National Institutes of Health. Dr. Stern reported being a consultant for Johnson & Johnson, Vertex, and Takeda and an expert witness for Alphapharm, Mutual Pharm, and Johnson & Johnson.

Twelve to 15 million white patients living in the United States have had at least one nonmelanoma skin cancer in their lifetimes, according to estimates based on a new mathematical model reported in the March issue of the Archives of Dermatology.

This figure is approximately twice that of previous estimates based on patient surveys, such as the estimate calculated in the U.S. National Health Interview Study, according to Dr. Robert S. Stern of Beth Israel Deaconess Medical Center and Harvard Medical School, Boston.

This difference can be attributed in part to people often incorrectly reporting their skin cancer histories when surveyed, falsely believing that basal cell and squamous cell lesions are not cancerous or that all skin cancers can be considered melanoma.

Dr. Stern devised his mathematical model using the same basic data available from national samples, such as the Surveillance, Epidemiology, and End Results (SEER) studies and information from the National Cancer Institute. His model, however, took into consideration several factors that had not been accounted for in previous estimates, such as the likelihood that patients develop numerous nonmelanoma skin cancers over the course of several years and that “a substantial proportion” of patients with melanoma also have nonmalignant skin cancers.

According to his model, “about 13 million white non-Hispanic U.S. residents (6%) have had more than 22 million nonmelanoma skin cancers” (Arch. Dermatol. 2010;146:279-82).

This puts the prevalence of a skin cancer history at a level far higher than that of any other cancer – prevalence that “exceeds that of all other cancers diagnosed since 1975,” he added. “Recent population-based data concerning skin cancer incidence, morbidity, and cost of care are lacking for the most common types of skin cancer, [basal cell carcinoma] and [squamous cell carcinoma].”

Regarding patients’ inaccurate reporting of skin cancer histories in surveys and interviews, Dr. Stern noted that many patients equate skin cancer with melanoma. “Hundreds of thousands of patients may be unnecessarily burdened with the belief that they have had a potentially lethal cancer (melanoma) when in fact they have had a skin tumor that is very unlikely to be lethal,he wrote.

In contrast, patients with breast or prostate cancer are much more likely to accurately report their cancer histories, so incidence and prevalence estimates for these tumors are much more accurate than those for skin cancer, Dr. Stern noted.

This study was funded in part by the National Institutes of Health. Dr. Stern reported being a consultant for Johnson & Johnson, Vertex, and Takeda and an expert witness for Alphapharm, Mutual Pharm, and Johnson & Johnson.

Twelve to 15 million white patients living in the United States have had at least one nonmelanoma skin cancer in their lifetimes, according to estimates based on a new mathematical model reported in the March issue of the Archives of Dermatology.

This figure is approximately twice that of previous estimates based on patient surveys, such as the estimate calculated in the U.S. National Health Interview Study, according to Dr. Robert S. Stern of Beth Israel Deaconess Medical Center and Harvard Medical School, Boston.

This difference can be attributed in part to people often incorrectly reporting their skin cancer histories when surveyed, falsely believing that basal cell and squamous cell lesions are not cancerous or that all skin cancers can be considered melanoma.

Dr. Stern devised his mathematical model using the same basic data available from national samples, such as the Surveillance, Epidemiology, and End Results (SEER) studies and information from the National Cancer Institute. His model, however, took into consideration several factors that had not been accounted for in previous estimates, such as the likelihood that patients develop numerous nonmelanoma skin cancers over the course of several years and that “a substantial proportion” of patients with melanoma also have nonmalignant skin cancers.

According to his model, “about 13 million white non-Hispanic U.S. residents (6%) have had more than 22 million nonmelanoma skin cancers” (Arch. Dermatol. 2010;146:279-82).

This puts the prevalence of a skin cancer history at a level far higher than that of any other cancer – prevalence that “exceeds that of all other cancers diagnosed since 1975,” he added. “Recent population-based data concerning skin cancer incidence, morbidity, and cost of care are lacking for the most common types of skin cancer, [basal cell carcinoma] and [squamous cell carcinoma].”

Regarding patients’ inaccurate reporting of skin cancer histories in surveys and interviews, Dr. Stern noted that many patients equate skin cancer with melanoma. “Hundreds of thousands of patients may be unnecessarily burdened with the belief that they have had a potentially lethal cancer (melanoma) when in fact they have had a skin tumor that is very unlikely to be lethal,he wrote.

In contrast, patients with breast or prostate cancer are much more likely to accurately report their cancer histories, so incidence and prevalence estimates for these tumors are much more accurate than those for skin cancer, Dr. Stern noted.

This study was funded in part by the National Institutes of Health. Dr. Stern reported being a consultant for Johnson & Johnson, Vertex, and Takeda and an expert witness for Alphapharm, Mutual Pharm, and Johnson & Johnson.

Treatment for melanoma costs the U.S. Medicare program about $249 million annually, but effective prevention and early detection could reduce expenses by up to 60%, according to a new study reported in the March issue of the Archives of Dermatology.

Treatment expenses for each patient who died from melanoma totaled more than $28,000 on average from the time of diagnosis until death, according to Dr. Anne M. Seidler and her colleagues. Policymakers should consider crafting guidelines for melanoma screening that reflect increased risks for patients older than age 65 years.

Although relatively few elderly patients die of melanoma, per-patient expenses are particularly high in cases of advanced disease, noted Dr. Seidler of the department of dermatology at Emory University in Atlanta and her associates.

“The majority of consumption is attributable to advanced-stage disease and the terminal phase of treatment,” they wrote. “If all patients were diagnosed and effectively treated in stage 0 or I, we estimate that the annual direct costs for the population 65 years or older would be between $99 million and $161 million, or 40% to 65% of their current value of $249 million.”

The researchers used Surveillance, Epidemiology, and End Results (SEER) data from 1,858 Medicare beneficiaries with a confirmed melanoma diagnosis and calculated cost by stage and treatment phase (Arch. Dermatol. 2010;146:249-56).

Average monthly per-patient melanoma charges were $2,194 during the initial 4 months of treatment. After this initial treatment phase, monthly costs fell to $902, but then increased to $3,933 if the cancer spread and became terminal, according to the investigators. Total costs may be higher than found based on how much patients spent on copayments and deductibles.

A total of 263 patients died of melanoma during the 6 years studied. These patients lived an average of 26 months after diagnosis, and their care cost an average of $13,020 per year, the study reported.

Early-stage melanoma costs appeared similar to those of prostate cancer, while late-stage melanoma costs resembled those of colon cancer, which generally is more expensive to treat. “The lack of definitive, effective therapy for melanoma, which may result in utilization of multiple chemotherapeutic agents in these later stages, likely drives up the costs,” the investigators noted.

The authors reported no financial conflicts of interest.

Treatment for melanoma costs the U.S. Medicare program about $249 million annually, but effective prevention and early detection could reduce expenses by up to 60%, according to a new study reported in the March issue of the Archives of Dermatology.

Treatment expenses for each patient who died from melanoma totaled more than $28,000 on average from the time of diagnosis until death, according to Dr. Anne M. Seidler and her colleagues. Policymakers should consider crafting guidelines for melanoma screening that reflect increased risks for patients older than age 65 years.

Although relatively few elderly patients die of melanoma, per-patient expenses are particularly high in cases of advanced disease, noted Dr. Seidler of the department of dermatology at Emory University in Atlanta and her associates.

“The majority of consumption is attributable to advanced-stage disease and the terminal phase of treatment,” they wrote. “If all patients were diagnosed and effectively treated in stage 0 or I, we estimate that the annual direct costs for the population 65 years or older would be between $99 million and $161 million, or 40% to 65% of their current value of $249 million.”

The researchers used Surveillance, Epidemiology, and End Results (SEER) data from 1,858 Medicare beneficiaries with a confirmed melanoma diagnosis and calculated cost by stage and treatment phase (Arch. Dermatol. 2010;146:249-56).

Average monthly per-patient melanoma charges were $2,194 during the initial 4 months of treatment. After this initial treatment phase, monthly costs fell to $902, but then increased to $3,933 if the cancer spread and became terminal, according to the investigators. Total costs may be higher than found based on how much patients spent on copayments and deductibles.

A total of 263 patients died of melanoma during the 6 years studied. These patients lived an average of 26 months after diagnosis, and their care cost an average of $13,020 per year, the study reported.

Early-stage melanoma costs appeared similar to those of prostate cancer, while late-stage melanoma costs resembled those of colon cancer, which generally is more expensive to treat. “The lack of definitive, effective therapy for melanoma, which may result in utilization of multiple chemotherapeutic agents in these later stages, likely drives up the costs,” the investigators noted.

The authors reported no financial conflicts of interest.

Treatment for melanoma costs the U.S. Medicare program about $249 million annually, but effective prevention and early detection could reduce expenses by up to 60%, according to a new study reported in the March issue of the Archives of Dermatology.

Treatment expenses for each patient who died from melanoma totaled more than $28,000 on average from the time of diagnosis until death, according to Dr. Anne M. Seidler and her colleagues. Policymakers should consider crafting guidelines for melanoma screening that reflect increased risks for patients older than age 65 years.

Although relatively few elderly patients die of melanoma, per-patient expenses are particularly high in cases of advanced disease, noted Dr. Seidler of the department of dermatology at Emory University in Atlanta and her associates.

“The majority of consumption is attributable to advanced-stage disease and the terminal phase of treatment,” they wrote. “If all patients were diagnosed and effectively treated in stage 0 or I, we estimate that the annual direct costs for the population 65 years or older would be between $99 million and $161 million, or 40% to 65% of their current value of $249 million.”

The researchers used Surveillance, Epidemiology, and End Results (SEER) data from 1,858 Medicare beneficiaries with a confirmed melanoma diagnosis and calculated cost by stage and treatment phase (Arch. Dermatol. 2010;146:249-56).

Average monthly per-patient melanoma charges were $2,194 during the initial 4 months of treatment. After this initial treatment phase, monthly costs fell to $902, but then increased to $3,933 if the cancer spread and became terminal, according to the investigators. Total costs may be higher than found based on how much patients spent on copayments and deductibles.

A total of 263 patients died of melanoma during the 6 years studied. These patients lived an average of 26 months after diagnosis, and their care cost an average of $13,020 per year, the study reported.

Early-stage melanoma costs appeared similar to those of prostate cancer, while late-stage melanoma costs resembled those of colon cancer, which generally is more expensive to treat. “The lack of definitive, effective therapy for melanoma, which may result in utilization of multiple chemotherapeutic agents in these later stages, likely drives up the costs,” the investigators noted.

The authors reported no financial conflicts of interest.

The American College of Graduate Medical Education recently approved revised program requirements for procedural dermatology, they announced in a March 1 e-communication. The revised requirements are available at http://www.acgme.org/acWebsite/RRC_080/080_prIndex.asp.

Story to follow.

The American College of Graduate Medical Education recently approved revised program requirements for procedural dermatology, they announced in a March 1 e-communication. The revised requirements are available at http://www.acgme.org/acWebsite/RRC_080/080_prIndex.asp.

Story to follow.

The American College of Graduate Medical Education recently approved revised program requirements for procedural dermatology, they announced in a March 1 e-communication. The revised requirements are available at http://www.acgme.org/acWebsite/RRC_080/080_prIndex.asp.

Story to follow.

"The benefits of sun protection clearly outweigh the risks," said Dr. Sheila Fallon Friedlander, but the debate continues over how to balance the benefits of outdoor activities for children with protection against skin cancer.

Some studies suggest outdoor activity is protective against melanoma, Dr. Friedlander said  She cited a case-control study of 583 cases of cutaneous malignant melanoma and 608 controls (Int. J. Epidemiol. 1999;28:418-27). Intermittent sun exposure, such as beach vacations during adolescence and the use of tanning beds and sunlamps, was associated with a significantly greater risk for melanoma, whereas chronic exposure, indicated by days of outdoor activity during adolescence and by outdoor jobs in adulthood, was associated with a significantly reduced risk for melanoma.

But sun protection and patient education does appear to play a role in reducing the number of nevi in children. Dr. Friedlander, clinical professor of pediatrics and medicine at the University of California, San Diego, cited another study in which 458 children in first to fourth grade in Canada were randomized to receive sunscreen and counseling about sun protection. Three years later, the sunscreen group had significantly fewer new nevi compared with the control group (JAMA 2000;283:2955-60).

What's a dermatologist to do? "Common sense prevails," Dr. Friedlander said. She advised dermatologists to counsel children and their parents to protect against sunburns by using sunscreens and sun-protective clothing. Also, "identify high-risk patients and follow them" so that any problems can be spotted early, she said.

But once parents and children are on board with sun protection, what should they use? The Environmental Working Group (EWG), a nonprofit organization that reviews and disseminates information about contaminants in consumer products and the environment, has come down in favor of physical sunscreens, based on a review of 400 studies and 2,000 sunscreens, Dr. Friedlander said.

Some parents and children prefer organic sunscreens, which contain oxybenzones, but the EWG rates these products as more dangerous than physical sunscreens. Some research suggests that oxybenzones can be absorbed into the skin in a way that the nano-particles of zinc oxide and titanium dioxide in physical sunscreens cannot, Dr. Friedlander said.

Be aware of what sunscreen characteristics raise concerns in your patients and their parents, Dr. Friedlander said. Share information with them, refer them to the EWG Web (www.ewg.org) and come up with a reasonable plan for sun protection.

Dr. Friedlander has served as a clinical investigator for Johnson & Johnson, which manufactures sunscreen products. SDEF and this news organization are owned by Elsevier.

"The benefits of sun protection clearly outweigh the risks," said Dr. Sheila Fallon Friedlander, but the debate continues over how to balance the benefits of outdoor activities for children with protection against skin cancer.

Some studies suggest outdoor activity is protective against melanoma, Dr. Friedlander said  She cited a case-control study of 583 cases of cutaneous malignant melanoma and 608 controls (Int. J. Epidemiol. 1999;28:418-27). Intermittent sun exposure, such as beach vacations during adolescence and the use of tanning beds and sunlamps, was associated with a significantly greater risk for melanoma, whereas chronic exposure, indicated by days of outdoor activity during adolescence and by outdoor jobs in adulthood, was associated with a significantly reduced risk for melanoma.

But sun protection and patient education does appear to play a role in reducing the number of nevi in children. Dr. Friedlander, clinical professor of pediatrics and medicine at the University of California, San Diego, cited another study in which 458 children in first to fourth grade in Canada were randomized to receive sunscreen and counseling about sun protection. Three years later, the sunscreen group had significantly fewer new nevi compared with the control group (JAMA 2000;283:2955-60).

What's a dermatologist to do? "Common sense prevails," Dr. Friedlander said. She advised dermatologists to counsel children and their parents to protect against sunburns by using sunscreens and sun-protective clothing. Also, "identify high-risk patients and follow them" so that any problems can be spotted early, she said.

But once parents and children are on board with sun protection, what should they use? The Environmental Working Group (EWG), a nonprofit organization that reviews and disseminates information about contaminants in consumer products and the environment, has come down in favor of physical sunscreens, based on a review of 400 studies and 2,000 sunscreens, Dr. Friedlander said.

Some parents and children prefer organic sunscreens, which contain oxybenzones, but the EWG rates these products as more dangerous than physical sunscreens. Some research suggests that oxybenzones can be absorbed into the skin in a way that the nano-particles of zinc oxide and titanium dioxide in physical sunscreens cannot, Dr. Friedlander said.

Be aware of what sunscreen characteristics raise concerns in your patients and their parents, Dr. Friedlander said. Share information with them, refer them to the EWG Web (www.ewg.org) and come up with a reasonable plan for sun protection.

Dr. Friedlander has served as a clinical investigator for Johnson & Johnson, which manufactures sunscreen products. SDEF and this news organization are owned by Elsevier.

"The benefits of sun protection clearly outweigh the risks," said Dr. Sheila Fallon Friedlander, but the debate continues over how to balance the benefits of outdoor activities for children with protection against skin cancer.

Some studies suggest outdoor activity is protective against melanoma, Dr. Friedlander said  She cited a case-control study of 583 cases of cutaneous malignant melanoma and 608 controls (Int. J. Epidemiol. 1999;28:418-27). Intermittent sun exposure, such as beach vacations during adolescence and the use of tanning beds and sunlamps, was associated with a significantly greater risk for melanoma, whereas chronic exposure, indicated by days of outdoor activity during adolescence and by outdoor jobs in adulthood, was associated with a significantly reduced risk for melanoma.

But sun protection and patient education does appear to play a role in reducing the number of nevi in children. Dr. Friedlander, clinical professor of pediatrics and medicine at the University of California, San Diego, cited another study in which 458 children in first to fourth grade in Canada were randomized to receive sunscreen and counseling about sun protection. Three years later, the sunscreen group had significantly fewer new nevi compared with the control group (JAMA 2000;283:2955-60).

What's a dermatologist to do? "Common sense prevails," Dr. Friedlander said. She advised dermatologists to counsel children and their parents to protect against sunburns by using sunscreens and sun-protective clothing. Also, "identify high-risk patients and follow them" so that any problems can be spotted early, she said.

But once parents and children are on board with sun protection, what should they use? The Environmental Working Group (EWG), a nonprofit organization that reviews and disseminates information about contaminants in consumer products and the environment, has come down in favor of physical sunscreens, based on a review of 400 studies and 2,000 sunscreens, Dr. Friedlander said.

Some parents and children prefer organic sunscreens, which contain oxybenzones, but the EWG rates these products as more dangerous than physical sunscreens. Some research suggests that oxybenzones can be absorbed into the skin in a way that the nano-particles of zinc oxide and titanium dioxide in physical sunscreens cannot, Dr. Friedlander said.

Be aware of what sunscreen characteristics raise concerns in your patients and their parents, Dr. Friedlander said. Share information with them, refer them to the EWG Web (www.ewg.org) and come up with a reasonable plan for sun protection.

Dr. Friedlander has served as a clinical investigator for Johnson & Johnson, which manufactures sunscreen products. SDEF and this news organization are owned by Elsevier.

Three clinical factors help estimate which thin melanomas are likely to harbor occult nodal metastases, and thus aid in selecting which patients would benefit most from sentinel node biopsy, according to a report in the February issue of the Archives of Surgery.

The three factors--patient sex, patient age at diagnosis, and lesion Breslow thickness--were used to develop a scoring system for estimating the risk of nodal recurrence. "This risk assessment is not intended to mandate what risk level is appropriate for sentinel node evaluation, but it allows for a better informed discussion with the patient newly diagnosed as having melanoma.

"Such information could be used to reassure extremely low-risk patients who may be anxious about the possibility of metastases or convince patients at higher risk of the need to consider biopsy," said Dr. Mark B. Faries of the John Wayne Cancer Institute, Santa Monica, Calif., and his associates (Arch. Surg. 2010;145:137-42) .

The use of sentinel node biopsy in patients with thin melanoma is controversial, since most such cases are at low risk for metastasis but the disease is usually fatal for the few patients who do develop recurrence. Doing the procedure in every case "would be prohibitively expensive and would expose a large number of patients with an extremely low risk of nodal disease to the real, albeit low, risk of toxic effects related to the procedure," they noted.

Dr. Faries and his colleagues reviewed the records in a prospective database of over 13,000 cases of thin (<1 mm) melanoma treated in 1971-2005 with wide excision but no nodal staging or lymphadenectomy. A total of 1,732 subjects were enrolled in the study. They were followed every 3 months for 2 years, every 4-6 months for the next 3 years, and annually thereafter.

During a median follow-up of 13 years, 51 patients (3%) developed nodal metastases. The median time to such recurrence was 38 months.

A variety of clinical factors were assessed to identify which ones were the strongest predictors of metastasis. Male sex, younger age at diagnosis, and greater tumor Breslow thickness were strongly predictive of metastasis, while factors such as tumor site and Clark level were not.

The investigators developed a scoring system using these 3 factors. Applying it to the study subjects, they found that the system predicted a 0.1% risk of metastasis in the lowest-risk subjects, compared with predicting a 17% risk of metastasis in the highest-risk subjects.

Tumor ulceration was predictive of nodal recurrence, with an 8% rate of metastasis in cases of ulcerated lesions compared to a 3% rate in cases without ulceration. However, ulceration was not included in the scoring system because information on ulceration often was not included in patient records, and a small proportion (approximately 2%) of this subset of patients showed lesion ulceration.

"Although such ulcerated lesions clearly deserve greater concern and evaluation, the rarity of this finding decreases the utility of including it in a prediction scheme," Dr. Faries and his associates said.

This study was funded in part by the National Cancer Institute and the Amyx Foundation. No financial conflicts of interest were reported.

Three clinical factors help estimate which thin melanomas are likely to harbor occult nodal metastases, and thus aid in selecting which patients would benefit most from sentinel node biopsy, according to a report in the February issue of the Archives of Surgery.

The three factors--patient sex, patient age at diagnosis, and lesion Breslow thickness--were used to develop a scoring system for estimating the risk of nodal recurrence. "This risk assessment is not intended to mandate what risk level is appropriate for sentinel node evaluation, but it allows for a better informed discussion with the patient newly diagnosed as having melanoma.

"Such information could be used to reassure extremely low-risk patients who may be anxious about the possibility of metastases or convince patients at higher risk of the need to consider biopsy," said Dr. Mark B. Faries of the John Wayne Cancer Institute, Santa Monica, Calif., and his associates (Arch. Surg. 2010;145:137-42) .

The use of sentinel node biopsy in patients with thin melanoma is controversial, since most such cases are at low risk for metastasis but the disease is usually fatal for the few patients who do develop recurrence. Doing the procedure in every case "would be prohibitively expensive and would expose a large number of patients with an extremely low risk of nodal disease to the real, albeit low, risk of toxic effects related to the procedure," they noted.

Dr. Faries and his colleagues reviewed the records in a prospective database of over 13,000 cases of thin (<1 mm) melanoma treated in 1971-2005 with wide excision but no nodal staging or lymphadenectomy. A total of 1,732 subjects were enrolled in the study. They were followed every 3 months for 2 years, every 4-6 months for the next 3 years, and annually thereafter.

During a median follow-up of 13 years, 51 patients (3%) developed nodal metastases. The median time to such recurrence was 38 months.

A variety of clinical factors were assessed to identify which ones were the strongest predictors of metastasis. Male sex, younger age at diagnosis, and greater tumor Breslow thickness were strongly predictive of metastasis, while factors such as tumor site and Clark level were not.

The investigators developed a scoring system using these 3 factors. Applying it to the study subjects, they found that the system predicted a 0.1% risk of metastasis in the lowest-risk subjects, compared with predicting a 17% risk of metastasis in the highest-risk subjects.

Tumor ulceration was predictive of nodal recurrence, with an 8% rate of metastasis in cases of ulcerated lesions compared to a 3% rate in cases without ulceration. However, ulceration was not included in the scoring system because information on ulceration often was not included in patient records, and a small proportion (approximately 2%) of this subset of patients showed lesion ulceration.

"Although such ulcerated lesions clearly deserve greater concern and evaluation, the rarity of this finding decreases the utility of including it in a prediction scheme," Dr. Faries and his associates said.

This study was funded in part by the National Cancer Institute and the Amyx Foundation. No financial conflicts of interest were reported.

Three clinical factors help estimate which thin melanomas are likely to harbor occult nodal metastases, and thus aid in selecting which patients would benefit most from sentinel node biopsy, according to a report in the February issue of the Archives of Surgery.

The three factors--patient sex, patient age at diagnosis, and lesion Breslow thickness--were used to develop a scoring system for estimating the risk of nodal recurrence. "This risk assessment is not intended to mandate what risk level is appropriate for sentinel node evaluation, but it allows for a better informed discussion with the patient newly diagnosed as having melanoma.

"Such information could be used to reassure extremely low-risk patients who may be anxious about the possibility of metastases or convince patients at higher risk of the need to consider biopsy," said Dr. Mark B. Faries of the John Wayne Cancer Institute, Santa Monica, Calif., and his associates (Arch. Surg. 2010;145:137-42) .

The use of sentinel node biopsy in patients with thin melanoma is controversial, since most such cases are at low risk for metastasis but the disease is usually fatal for the few patients who do develop recurrence. Doing the procedure in every case "would be prohibitively expensive and would expose a large number of patients with an extremely low risk of nodal disease to the real, albeit low, risk of toxic effects related to the procedure," they noted.

Dr. Faries and his colleagues reviewed the records in a prospective database of over 13,000 cases of thin (<1 mm) melanoma treated in 1971-2005 with wide excision but no nodal staging or lymphadenectomy. A total of 1,732 subjects were enrolled in the study. They were followed every 3 months for 2 years, every 4-6 months for the next 3 years, and annually thereafter.

During a median follow-up of 13 years, 51 patients (3%) developed nodal metastases. The median time to such recurrence was 38 months.

A variety of clinical factors were assessed to identify which ones were the strongest predictors of metastasis. Male sex, younger age at diagnosis, and greater tumor Breslow thickness were strongly predictive of metastasis, while factors such as tumor site and Clark level were not.

The investigators developed a scoring system using these 3 factors. Applying it to the study subjects, they found that the system predicted a 0.1% risk of metastasis in the lowest-risk subjects, compared with predicting a 17% risk of metastasis in the highest-risk subjects.

Tumor ulceration was predictive of nodal recurrence, with an 8% rate of metastasis in cases of ulcerated lesions compared to a 3% rate in cases without ulceration. However, ulceration was not included in the scoring system because information on ulceration often was not included in patient records, and a small proportion (approximately 2%) of this subset of patients showed lesion ulceration.

"Although such ulcerated lesions clearly deserve greater concern and evaluation, the rarity of this finding decreases the utility of including it in a prediction scheme," Dr. Faries and his associates said.

This study was funded in part by the National Cancer Institute and the Amyx Foundation. No financial conflicts of interest were reported.

The use of nonsteroidal anti-inflammatory drugs does not reduce the risk of cutaneous squamous cell carcinoma, according to a study published online Feb. 15 in the Archives of Dermatology.

In a retrospective case-control study involving more than 800 subjects, the dose, duration, and type of NSAID exposure exerted "no clear effect" on the risk of developing squamous cell carcinoma (SCC), said Dr. Maryam M. Asgari of Kaiser Permanente of Northern California, Oakland, and associates.

NSAIDs block the synthesis of proinflammatory prostaglandins and "inhibit neoplastic proliferation by inducing apoptosis and inhibiting angiogenesis," the authors wrote. They have been reported to protect against colorectal, breast, prostate, and lung cancer, and have shown activity against SCCs both in animal and in vitro studies. However, human studies have produced conflicting results.

Dr. Asgari and her colleagues assessed NSAID use during the preceding decade in 415 patients with pathologically confirmed SCC who were diagnosed in 2004 and 415 control subjects matched for age, sex, and race. Only cases of extragenital and nonmucosal SCC were included.

The subjects (aged 43-85 years) completed 3-page questionnaires detailing medication use, health history, skin cancer history, and risk factors. NSAID use was analyzed by four categories: any NSAIDs, aspirin, ibuprofen, and nonaspirin NSAIDs. Regular use was defined as taking the medication at least once per week for at least 1 year.

Most of the subjects (61%) reported regular use of NSAIDs at some time during the preceding 10 years, most commonly aspirin (48%), followed by ibuprofen (18%), naproxen (5%), and nabumetone (4%).

There was no association between self-reported NSAID use and SCC risk.

This finding was validated in a separate analysis of pharmacy records of NSAIDs dispensed to the same group of subjects, the investigators said (Arch. Dermatol. 2010 Feb. 15 [doi:10.1001/archdermatol.2009.374]).

Dose and duration of exposure had no effect on the results.

"Our results are largely consistent with" three of the four published articles examining the association of NSAIDs with SCC risk, they added.

Disclosures: This study was funded by the National Institute of Arthritis, Musculoskeletal, and Skin Diseases and the National Cancer Institute. One of Dr. Asgari's associates reported serving on an advisory committee for Roche Laboratories and consulting for law firms serving both plaintiffs and Ortho-McNeil-Janssen Pharmaceuticals in legal cases. No other potential conflicts of interest were reported.

The use of nonsteroidal anti-inflammatory drugs does not reduce the risk of cutaneous squamous cell carcinoma, according to a study published online Feb. 15 in the Archives of Dermatology.

In a retrospective case-control study involving more than 800 subjects, the dose, duration, and type of NSAID exposure exerted "no clear effect" on the risk of developing squamous cell carcinoma (SCC), said Dr. Maryam M. Asgari of Kaiser Permanente of Northern California, Oakland, and associates.

NSAIDs block the synthesis of proinflammatory prostaglandins and "inhibit neoplastic proliferation by inducing apoptosis and inhibiting angiogenesis," the authors wrote. They have been reported to protect against colorectal, breast, prostate, and lung cancer, and have shown activity against SCCs both in animal and in vitro studies. However, human studies have produced conflicting results.

Dr. Asgari and her colleagues assessed NSAID use during the preceding decade in 415 patients with pathologically confirmed SCC who were diagnosed in 2004 and 415 control subjects matched for age, sex, and race. Only cases of extragenital and nonmucosal SCC were included.

The subjects (aged 43-85 years) completed 3-page questionnaires detailing medication use, health history, skin cancer history, and risk factors. NSAID use was analyzed by four categories: any NSAIDs, aspirin, ibuprofen, and nonaspirin NSAIDs. Regular use was defined as taking the medication at least once per week for at least 1 year.

Most of the subjects (61%) reported regular use of NSAIDs at some time during the preceding 10 years, most commonly aspirin (48%), followed by ibuprofen (18%), naproxen (5%), and nabumetone (4%).

There was no association between self-reported NSAID use and SCC risk.

This finding was validated in a separate analysis of pharmacy records of NSAIDs dispensed to the same group of subjects, the investigators said (Arch. Dermatol. 2010 Feb. 15 [doi:10.1001/archdermatol.2009.374]).

Dose and duration of exposure had no effect on the results.

"Our results are largely consistent with" three of the four published articles examining the association of NSAIDs with SCC risk, they added.

Disclosures: This study was funded by the National Institute of Arthritis, Musculoskeletal, and Skin Diseases and the National Cancer Institute. One of Dr. Asgari's associates reported serving on an advisory committee for Roche Laboratories and consulting for law firms serving both plaintiffs and Ortho-McNeil-Janssen Pharmaceuticals in legal cases. No other potential conflicts of interest were reported.

The use of nonsteroidal anti-inflammatory drugs does not reduce the risk of cutaneous squamous cell carcinoma, according to a study published online Feb. 15 in the Archives of Dermatology.

In a retrospective case-control study involving more than 800 subjects, the dose, duration, and type of NSAID exposure exerted "no clear effect" on the risk of developing squamous cell carcinoma (SCC), said Dr. Maryam M. Asgari of Kaiser Permanente of Northern California, Oakland, and associates.

NSAIDs block the synthesis of proinflammatory prostaglandins and "inhibit neoplastic proliferation by inducing apoptosis and inhibiting angiogenesis," the authors wrote. They have been reported to protect against colorectal, breast, prostate, and lung cancer, and have shown activity against SCCs both in animal and in vitro studies. However, human studies have produced conflicting results.

Dr. Asgari and her colleagues assessed NSAID use during the preceding decade in 415 patients with pathologically confirmed SCC who were diagnosed in 2004 and 415 control subjects matched for age, sex, and race. Only cases of extragenital and nonmucosal SCC were included.

The subjects (aged 43-85 years) completed 3-page questionnaires detailing medication use, health history, skin cancer history, and risk factors. NSAID use was analyzed by four categories: any NSAIDs, aspirin, ibuprofen, and nonaspirin NSAIDs. Regular use was defined as taking the medication at least once per week for at least 1 year.

Most of the subjects (61%) reported regular use of NSAIDs at some time during the preceding 10 years, most commonly aspirin (48%), followed by ibuprofen (18%), naproxen (5%), and nabumetone (4%).

There was no association between self-reported NSAID use and SCC risk.

This finding was validated in a separate analysis of pharmacy records of NSAIDs dispensed to the same group of subjects, the investigators said (Arch. Dermatol. 2010 Feb. 15 [doi:10.1001/archdermatol.2009.374]).

Dose and duration of exposure had no effect on the results.

"Our results are largely consistent with" three of the four published articles examining the association of NSAIDs with SCC risk, they added.

Disclosures: This study was funded by the National Institute of Arthritis, Musculoskeletal, and Skin Diseases and the National Cancer Institute. One of Dr. Asgari's associates reported serving on an advisory committee for Roche Laboratories and consulting for law firms serving both plaintiffs and Ortho-McNeil-Janssen Pharmaceuticals in legal cases. No other potential conflicts of interest were reported.

A number of new therapies for cutaneous diseases are helping dermatologists improve patient care.

One such agent, ingenol mebutate, is a plant extract being used to treat actinic keratoses, Dr. J. Mark Jackson explained at the annual Hawaii Dermatology Seminar sponsored by Skin Disease Education Foundation.

An active component of radium weed, the extract is believed to induce primary necrosis by a neutrophil-mediated, antibody-dependent cellular toxicity. Ingenol mebutate is widely used in Australia to treat actinic keratoses, said Dr. Jackson, a clinical professor of medicine and dermatology at the University of Louisville in Kentucky.

Phase III trial results were released at press time by LEO Pharma, the manufacturer of ingenol mebutate. A 0.05% concentration of ingenol mebutate was used for 2 consecutive days in 250 patients with actinic keratoses on non-head locations. According to the company's press release, the gel met its primary clinical endpoint of complete lesion clearance. The study's full findings are expected to be presented at the upcoming meeting of the American Academy of Dermatology.

In the phase II, randomized, double-blind, placebo-controlled trial, 58 patients with 5 biopsy-proven actinic keratoses were treated with ingenol mebutate gel or placebo on days 1 and 2 or days 1 and 8 (Australasian J. Dermatol. 2009;50:16-22). 

Complete clearance was achieved in 71% of actinic keratoses treated with the 0.05% formulation of ingenol mebutate, compared with 25% of those treated with the 0.01% formulation, 40% of those treated with the 0.0025% formulation, and 32% of those treated with the placebo gel.

Side effects were mild to moderate, including four cases of hypopigmentation at the treatment sites and one case of persistent scabbing and pain that extended beyond the study period in three of five actinic keratoses.

The use of itraconazole for treating palmoplantar pustulosis is another advance, he said. In a recent open-label study, six patients with palmoplantar pustulosis and no other evidence of psoriasis received 100 mg itraconazole daily for 1 month, followed by every other day for 1 month (Dermatol. Ther. 2009;22:85-9).

Three patients achieved complete response, with improvement after 2 weeks of treatment. The remaining three patients developed no new pustules but continued to have some disease activity. All patients experienced relapse, but retreatment controlled disease in two patients.

During a discussion of retapamulin, which is approved for the topical treatment of impetigo due to Staphylococcus aureus (methicillin-susceptible S. aureus only) and S. pyogenes in patients older than 9 months of age, Dr. Jackson noted that the agent can cause irritation to the nasal mucosa "and is, therefore, not a good treatment for many patients with nasal carriage of MRSA. If nasal carriage is resistant to mupirocin, you may try retapamulin, but you should warn the patient in advance to try a test area first."

Cutaneous reactions can occur in response to epidermal growth factor receptors (EGFRs), Dr. Jackson warned. A prospective study of 30 patients taking either cetuximab or erlotinib for cancer noted acneiform pustule and follicular eruptions in a seborrheic distribution 7-10 days after therapy (J. Am. Acad. Dermatol. 2006;55:429-37).

"Palmoplantar eruptions have also been reported," he said. "So have xerosis, pyogenic granulomas, and paronychia." Cutaneous reactions to EGFRs are dose dependent and recur with subsequent treatment.

Be aware of the procoagulant effects of thalidomide, which is approved for the treatment of chronic recurrent and severe erythema nodosum leprosum and is used for many other inflammatory dermatologic conditions, he said. A study of 25 patients found that deep vein thrombosis occurred in 20% of patients taking thalidomide for various inflammatory conditions (J. Dermatolog. Treat. 2007;18:335-40).

Patients at particular risk include those with systemic lupus erythematosus, a malignancy, antiphospholipid syndrome, smokers, women on oral contraceptives, patients with hyperhomocysteinemia, and patients withdrawing from antimalarials, he added.

Dr. Jackson advised that dermatologists should have a basic understanding of interstitial granulomatous dermatitis, first described in 1993. Also known as granulomatous dermatitis with associated arthritis, the condition "generally presents as erythematous, violaceous, hyperpigmented, annular plaques on the trunk and thighs," he said. "Sometimes there is an acral distribution."

Histopathology reveals dense inflammatory mixed cell infiltrate, necrobiosis, sparse mucin deposition, and no vasculitis.

Associated diseases include rheumatoid arthritis, systemic lupus erythematosus, and other autoimmune conditions. The disease can also be triggered by infections and certain medications, including ACE inhibitors, calcium channel blockers, beta blockers, and lipid lowering agents.

Treatment options include glucocorticoids, NSAIDs, and TNF-alpha inhibitors.

^{Several new therapies are under study to help physicians treat cutaneous diseases such as actinic keratoses (shown here on an elbow). Photo courtesy Dr. Roger I. Ceilley.}

Dr. Jackson disclosed that he has received research, honoraria, consulting or other support from Abbott, Amgen, Biogen Idec, Centocor Ortho Biotech, Ferndale Laboratories, Galderma, Genentech, Medicis, Novartis, Promius Pharma, Quinnova Pharmaceuticals, Roche, and Stiefel.

SDEF and this news organization are owned by Elsevier.

A number of new therapies for cutaneous diseases are helping dermatologists improve patient care.

One such agent, ingenol mebutate, is a plant extract being used to treat actinic keratoses, Dr. J. Mark Jackson explained at the annual Hawaii Dermatology Seminar sponsored by Skin Disease Education Foundation.

An active component of radium weed, the extract is believed to induce primary necrosis by a neutrophil-mediated, antibody-dependent cellular toxicity. Ingenol mebutate is widely used in Australia to treat actinic keratoses, said Dr. Jackson, a clinical professor of medicine and dermatology at the University of Louisville in Kentucky.

Phase III trial results were released at press time by LEO Pharma, the manufacturer of ingenol mebutate. A 0.05% concentration of ingenol mebutate was used for 2 consecutive days in 250 patients with actinic keratoses on non-head locations. According to the company's press release, the gel met its primary clinical endpoint of complete lesion clearance. The study's full findings are expected to be presented at the upcoming meeting of the American Academy of Dermatology.

In the phase II, randomized, double-blind, placebo-controlled trial, 58 patients with 5 biopsy-proven actinic keratoses were treated with ingenol mebutate gel or placebo on days 1 and 2 or days 1 and 8 (Australasian J. Dermatol. 2009;50:16-22). 

Complete clearance was achieved in 71% of actinic keratoses treated with the 0.05% formulation of ingenol mebutate, compared with 25% of those treated with the 0.01% formulation, 40% of those treated with the 0.0025% formulation, and 32% of those treated with the placebo gel.

Side effects were mild to moderate, including four cases of hypopigmentation at the treatment sites and one case of persistent scabbing and pain that extended beyond the study period in three of five actinic keratoses.

The use of itraconazole for treating palmoplantar pustulosis is another advance, he said. In a recent open-label study, six patients with palmoplantar pustulosis and no other evidence of psoriasis received 100 mg itraconazole daily for 1 month, followed by every other day for 1 month (Dermatol. Ther. 2009;22:85-9).

Three patients achieved complete response, with improvement after 2 weeks of treatment. The remaining three patients developed no new pustules but continued to have some disease activity. All patients experienced relapse, but retreatment controlled disease in two patients.

During a discussion of retapamulin, which is approved for the topical treatment of impetigo due to Staphylococcus aureus (methicillin-susceptible S. aureus only) and S. pyogenes in patients older than 9 months of age, Dr. Jackson noted that the agent can cause irritation to the nasal mucosa "and is, therefore, not a good treatment for many patients with nasal carriage of MRSA. If nasal carriage is resistant to mupirocin, you may try retapamulin, but you should warn the patient in advance to try a test area first."

Cutaneous reactions can occur in response to epidermal growth factor receptors (EGFRs), Dr. Jackson warned. A prospective study of 30 patients taking either cetuximab or erlotinib for cancer noted acneiform pustule and follicular eruptions in a seborrheic distribution 7-10 days after therapy (J. Am. Acad. Dermatol. 2006;55:429-37).

"Palmoplantar eruptions have also been reported," he said. "So have xerosis, pyogenic granulomas, and paronychia." Cutaneous reactions to EGFRs are dose dependent and recur with subsequent treatment.

Be aware of the procoagulant effects of thalidomide, which is approved for the treatment of chronic recurrent and severe erythema nodosum leprosum and is used for many other inflammatory dermatologic conditions, he said. A study of 25 patients found that deep vein thrombosis occurred in 20% of patients taking thalidomide for various inflammatory conditions (J. Dermatolog. Treat. 2007;18:335-40).

Patients at particular risk include those with systemic lupus erythematosus, a malignancy, antiphospholipid syndrome, smokers, women on oral contraceptives, patients with hyperhomocysteinemia, and patients withdrawing from antimalarials, he added.

Dr. Jackson advised that dermatologists should have a basic understanding of interstitial granulomatous dermatitis, first described in 1993. Also known as granulomatous dermatitis with associated arthritis, the condition "generally presents as erythematous, violaceous, hyperpigmented, annular plaques on the trunk and thighs," he said. "Sometimes there is an acral distribution."

Histopathology reveals dense inflammatory mixed cell infiltrate, necrobiosis, sparse mucin deposition, and no vasculitis.

Associated diseases include rheumatoid arthritis, systemic lupus erythematosus, and other autoimmune conditions. The disease can also be triggered by infections and certain medications, including ACE inhibitors, calcium channel blockers, beta blockers, and lipid lowering agents.

Treatment options include glucocorticoids, NSAIDs, and TNF-alpha inhibitors.

^{Several new therapies are under study to help physicians treat cutaneous diseases such as actinic keratoses (shown here on an elbow). Photo courtesy Dr. Roger I. Ceilley.}

Dr. Jackson disclosed that he has received research, honoraria, consulting or other support from Abbott, Amgen, Biogen Idec, Centocor Ortho Biotech, Ferndale Laboratories, Galderma, Genentech, Medicis, Novartis, Promius Pharma, Quinnova Pharmaceuticals, Roche, and Stiefel.

SDEF and this news organization are owned by Elsevier.

A number of new therapies for cutaneous diseases are helping dermatologists improve patient care.

One such agent, ingenol mebutate, is a plant extract being used to treat actinic keratoses, Dr. J. Mark Jackson explained at the annual Hawaii Dermatology Seminar sponsored by Skin Disease Education Foundation.

An active component of radium weed, the extract is believed to induce primary necrosis by a neutrophil-mediated, antibody-dependent cellular toxicity. Ingenol mebutate is widely used in Australia to treat actinic keratoses, said Dr. Jackson, a clinical professor of medicine and dermatology at the University of Louisville in Kentucky.

Phase III trial results were released at press time by LEO Pharma, the manufacturer of ingenol mebutate. A 0.05% concentration of ingenol mebutate was used for 2 consecutive days in 250 patients with actinic keratoses on non-head locations. According to the company's press release, the gel met its primary clinical endpoint of complete lesion clearance. The study's full findings are expected to be presented at the upcoming meeting of the American Academy of Dermatology.

In the phase II, randomized, double-blind, placebo-controlled trial, 58 patients with 5 biopsy-proven actinic keratoses were treated with ingenol mebutate gel or placebo on days 1 and 2 or days 1 and 8 (Australasian J. Dermatol. 2009;50:16-22). 

Complete clearance was achieved in 71% of actinic keratoses treated with the 0.05% formulation of ingenol mebutate, compared with 25% of those treated with the 0.01% formulation, 40% of those treated with the 0.0025% formulation, and 32% of those treated with the placebo gel.

Side effects were mild to moderate, including four cases of hypopigmentation at the treatment sites and one case of persistent scabbing and pain that extended beyond the study period in three of five actinic keratoses.

The use of itraconazole for treating palmoplantar pustulosis is another advance, he said. In a recent open-label study, six patients with palmoplantar pustulosis and no other evidence of psoriasis received 100 mg itraconazole daily for 1 month, followed by every other day for 1 month (Dermatol. Ther. 2009;22:85-9).

Three patients achieved complete response, with improvement after 2 weeks of treatment. The remaining three patients developed no new pustules but continued to have some disease activity. All patients experienced relapse, but retreatment controlled disease in two patients.

During a discussion of retapamulin, which is approved for the topical treatment of impetigo due to Staphylococcus aureus (methicillin-susceptible S. aureus only) and S. pyogenes in patients older than 9 months of age, Dr. Jackson noted that the agent can cause irritation to the nasal mucosa "and is, therefore, not a good treatment for many patients with nasal carriage of MRSA. If nasal carriage is resistant to mupirocin, you may try retapamulin, but you should warn the patient in advance to try a test area first."

Cutaneous reactions can occur in response to epidermal growth factor receptors (EGFRs), Dr. Jackson warned. A prospective study of 30 patients taking either cetuximab or erlotinib for cancer noted acneiform pustule and follicular eruptions in a seborrheic distribution 7-10 days after therapy (J. Am. Acad. Dermatol. 2006;55:429-37).

"Palmoplantar eruptions have also been reported," he said. "So have xerosis, pyogenic granulomas, and paronychia." Cutaneous reactions to EGFRs are dose dependent and recur with subsequent treatment.

Be aware of the procoagulant effects of thalidomide, which is approved for the treatment of chronic recurrent and severe erythema nodosum leprosum and is used for many other inflammatory dermatologic conditions, he said. A study of 25 patients found that deep vein thrombosis occurred in 20% of patients taking thalidomide for various inflammatory conditions (J. Dermatolog. Treat. 2007;18:335-40).

Patients at particular risk include those with systemic lupus erythematosus, a malignancy, antiphospholipid syndrome, smokers, women on oral contraceptives, patients with hyperhomocysteinemia, and patients withdrawing from antimalarials, he added.

Dr. Jackson advised that dermatologists should have a basic understanding of interstitial granulomatous dermatitis, first described in 1993. Also known as granulomatous dermatitis with associated arthritis, the condition "generally presents as erythematous, violaceous, hyperpigmented, annular plaques on the trunk and thighs," he said. "Sometimes there is an acral distribution."

Histopathology reveals dense inflammatory mixed cell infiltrate, necrobiosis, sparse mucin deposition, and no vasculitis.

Associated diseases include rheumatoid arthritis, systemic lupus erythematosus, and other autoimmune conditions. The disease can also be triggered by infections and certain medications, including ACE inhibitors, calcium channel blockers, beta blockers, and lipid lowering agents.

Treatment options include glucocorticoids, NSAIDs, and TNF-alpha inhibitors.

^{Several new therapies are under study to help physicians treat cutaneous diseases such as actinic keratoses (shown here on an elbow). Photo courtesy Dr. Roger I. Ceilley.}

Dr. Jackson disclosed that he has received research, honoraria, consulting or other support from Abbott, Amgen, Biogen Idec, Centocor Ortho Biotech, Ferndale Laboratories, Galderma, Genentech, Medicis, Novartis, Promius Pharma, Quinnova Pharmaceuticals, Roche, and Stiefel.

SDEF and this news organization are owned by Elsevier.

Misdiagnosis of melanoma is a major cause of litigation against both dermatologists and dermatopathologists.

The majority of claims filed between 1985 and 2001 involving the misdiagnosis of melanoma were because of a false negative diagnosis, which may translate to a reduced chance of survival for some patients, Dr. Ashfaq A. Marghoob reported at the seminar

Two important strategies can help minimize missing melanoma, he said. First, remain vigilant and remember that many melanomas lack the classic ABCD features.

"Questioning yourself and your pathologist regarding the diagnosis will help towards identifying many of these melanomas. In other words, remain skeptical of lesions lacking clinical-dermoscopy correlation or lesions lacking dermoscopy-histopathology correlation. Second, engage patients in their own care by having them share the responsibility of detecting early melanoma by encouraging them to examine their own skin on a regular basis," said Dr. Marghoob, who is a dermatologist at Memorial Sloan-Kettering Cancer Center in New York.

Some melanomas may not manifest concerning features, and can mimic benign lesions. To assure that a malignant melanoma will eventually be found, periodic total body examinations by a physician, and regular patient self-examinations, are key. He stressed that physician examinations and self-skin exams are complementary.

While it is widely accepted that early detection means better prognosis, modest delays of up to 6 months have not been shown to affect ultimate outcomes. However, there is one exception. Nodular melanoma can grow rapidly, and even small delays in diagnosis can have serious consequences.

The most common scenarios in melanoma litigation cases include nodular melanoma being misdiagnosed by a clinician or pathologist; a partial biopsy not capturing the most diagnostically relevant part of the lesion; malignant melanoma being misdiagnosed as a dysplastic or spitz nevus; unrecognized desmoplastic malignant melanoma; and metastatic malignant melanoma with an unknown primary or recurrence of melanoma (Am. J. Surg. Pathol. 2003;27:1278-83).

Dr. Marghoob discussed each of these cases in detail.

Misdiagnosis of nodular melanoma as nevus by a clinician or pathologist. Many nodular melanomas lack helpful diagnostic features, such as those in the ABCD criteria for malignant melanoma, which can lead to a misdiagnosis. However, the ABCDE criteria that take lesion evolution into account may be of some help, noted Dr. Marghoob.

In order to track lesion evolution, ask patients about the history of changes and symptoms. Total body photography may help on rare occasions to detect new lesions, some of which may be subtle. In addition, dermoscopy results may persuade the clinician to obtain a biopsy of a clinically banal appearing lesion that is in fact a nodular melanoma.

Partial biopsy issues. If a biopsy is performed of a lesion that clinically looks like melanoma and the pathology diagnosis is nevus, it is imperative that the clinician and pathologist reconcile the difference. In cases where there is discordance, consider asking for step-sectioning, special stains, or--in very rare instances--fluorescence in situ hybridization to look for signature chromosomal aberrations. In addition, a partial biopsy may not be representative of the rest of the lesion. If a partial biopsy was performed, re-excise the lesion, said Dr. Marghoob. Remember that a pathology report should never be read in a vacuum.

Excisional biopsy is the preferred method for melanocytic lesions, when possible, because partial biopsy may sample nondiagnostic areas or miss the prognostically-worse portion of the lesion.

"Partial biopsy assumes that a clinician can consistently predict the portion of a suspicious pigmented lesion that will have the worst representative histology," said Dr. Marghoob. In one study, 40% of excised melanomas had worse pathology, compared with initial punch biopsy, and 20% of melanomas revealed invasion, which was not seen in initial punch biopsy (Arch. Dermatol. 1996;132:1297-1302).

The ideal biopsy is excisional with a 2- to 3-mm margin, is oriented along the lines of lymphatic drainage, and is step sectioned. This limits sampling error, removes dysplastic nevus completely (preventing recurrence), and better predicts the Breslow depth if the lesion proves to be a melanoma, said Dr. Marghoob.

Even when step sectioned, less than 2% of the lesion is evaluated. In one study, thorough block sampling resulted in identification of increased tumor thickness in 43% of cases by a mean of 0.16 mm (Arch. Dermatol. 2005;141:734-6).

Misdiagnosis of a melanoma as dysplastic or spitz nevus. When a partial biopsy reveals dysplastic or spitz nevus, it is important to completely excise the lesion. Malignant melanoma can sometimes masquerade as a spitz nevus, and focus of malignant melanoma may have been missed on the biopsy. Many dermatologists are of the opinion that spitz nevi should be completely excised--at least in adults, said Dr. Marghoob.

Unrecognized desmoplastic malignant melanoma. Desmoplastic melanoma can be banal in appearance, with 70% appearing amelanotic, he said. These lesions may only present as firmness in the subcutaneous tissue. For "banal" appearing firm lesions on chronically sun-damaged skin, suspicion should be raised if the lesions are symptomatic, growing, are associated with a lentigo maligna, or reveal irregular vessels with dermoscopy, said Dr. Marghoob.

Metastatic melanoma with unknown primary or recurrence of melanoma. Whenever possible, do not remove seemingly benign lesions and discard them, he said. Also, be careful and selective about the use of liquid nitrogen or a laser on lesions that have not been confirmed to be benign through biopsy.

He noted that cases of assumed benign lesions that recur after ablation (via liquid nitrogen, curettage, or laser), may ultimately prove to be melanoma on histopathology. Furthermore, in the unlikely event that a patient develops metastatic melanoma with an unknown primary, it may be presumed that one of the ablated lesions may have been the primary.

Dr. Marghoob disclosed having no conflicts of interest. SDEF and this news organization are owned by Elsevier.

^{A partial biopsy was performed of this lesion which had clinical features of melanoma. The pathology analysis was reported as a Clark’s nevus (this area is the white scar on the left upper portion of the lesion). Due the clinical-pathology discordance the clinician decided to excise the lesion.  As can be seen from the histology, this lesion was a melanoma and depending on the location of a partial biopsy the results can range from a Clark’s nevus to melanoma in situ to microinvasive to deeply invasive melanoma. Photo courtesy Dr. Ashfaq Marghoob.}

Misdiagnosis of melanoma is a major cause of litigation against both dermatologists and dermatopathologists.

The majority of claims filed between 1985 and 2001 involving the misdiagnosis of melanoma were because of a false negative diagnosis, which may translate to a reduced chance of survival for some patients, Dr. Ashfaq A. Marghoob reported at the seminar

Two important strategies can help minimize missing melanoma, he said. First, remain vigilant and remember that many melanomas lack the classic ABCD features.

"Questioning yourself and your pathologist regarding the diagnosis will help towards identifying many of these melanomas. In other words, remain skeptical of lesions lacking clinical-dermoscopy correlation or lesions lacking dermoscopy-histopathology correlation. Second, engage patients in their own care by having them share the responsibility of detecting early melanoma by encouraging them to examine their own skin on a regular basis," said Dr. Marghoob, who is a dermatologist at Memorial Sloan-Kettering Cancer Center in New York.

Some melanomas may not manifest concerning features, and can mimic benign lesions. To assure that a malignant melanoma will eventually be found, periodic total body examinations by a physician, and regular patient self-examinations, are key. He stressed that physician examinations and self-skin exams are complementary.

While it is widely accepted that early detection means better prognosis, modest delays of up to 6 months have not been shown to affect ultimate outcomes. However, there is one exception. Nodular melanoma can grow rapidly, and even small delays in diagnosis can have serious consequences.

The most common scenarios in melanoma litigation cases include nodular melanoma being misdiagnosed by a clinician or pathologist; a partial biopsy not capturing the most diagnostically relevant part of the lesion; malignant melanoma being misdiagnosed as a dysplastic or spitz nevus; unrecognized desmoplastic malignant melanoma; and metastatic malignant melanoma with an unknown primary or recurrence of melanoma (Am. J. Surg. Pathol. 2003;27:1278-83).

Dr. Marghoob discussed each of these cases in detail.

Misdiagnosis of nodular melanoma as nevus by a clinician or pathologist. Many nodular melanomas lack helpful diagnostic features, such as those in the ABCD criteria for malignant melanoma, which can lead to a misdiagnosis. However, the ABCDE criteria that take lesion evolution into account may be of some help, noted Dr. Marghoob.

In order to track lesion evolution, ask patients about the history of changes and symptoms. Total body photography may help on rare occasions to detect new lesions, some of which may be subtle. In addition, dermoscopy results may persuade the clinician to obtain a biopsy of a clinically banal appearing lesion that is in fact a nodular melanoma.

Partial biopsy issues. If a biopsy is performed of a lesion that clinically looks like melanoma and the pathology diagnosis is nevus, it is imperative that the clinician and pathologist reconcile the difference. In cases where there is discordance, consider asking for step-sectioning, special stains, or--in very rare instances--fluorescence in situ hybridization to look for signature chromosomal aberrations. In addition, a partial biopsy may not be representative of the rest of the lesion. If a partial biopsy was performed, re-excise the lesion, said Dr. Marghoob. Remember that a pathology report should never be read in a vacuum.

Excisional biopsy is the preferred method for melanocytic lesions, when possible, because partial biopsy may sample nondiagnostic areas or miss the prognostically-worse portion of the lesion.

"Partial biopsy assumes that a clinician can consistently predict the portion of a suspicious pigmented lesion that will have the worst representative histology," said Dr. Marghoob. In one study, 40% of excised melanomas had worse pathology, compared with initial punch biopsy, and 20% of melanomas revealed invasion, which was not seen in initial punch biopsy (Arch. Dermatol. 1996;132:1297-1302).

The ideal biopsy is excisional with a 2- to 3-mm margin, is oriented along the lines of lymphatic drainage, and is step sectioned. This limits sampling error, removes dysplastic nevus completely (preventing recurrence), and better predicts the Breslow depth if the lesion proves to be a melanoma, said Dr. Marghoob.

Even when step sectioned, less than 2% of the lesion is evaluated. In one study, thorough block sampling resulted in identification of increased tumor thickness in 43% of cases by a mean of 0.16 mm (Arch. Dermatol. 2005;141:734-6).

Misdiagnosis of a melanoma as dysplastic or spitz nevus. When a partial biopsy reveals dysplastic or spitz nevus, it is important to completely excise the lesion. Malignant melanoma can sometimes masquerade as a spitz nevus, and focus of malignant melanoma may have been missed on the biopsy. Many dermatologists are of the opinion that spitz nevi should be completely excised--at least in adults, said Dr. Marghoob.

Unrecognized desmoplastic malignant melanoma. Desmoplastic melanoma can be banal in appearance, with 70% appearing amelanotic, he said. These lesions may only present as firmness in the subcutaneous tissue. For "banal" appearing firm lesions on chronically sun-damaged skin, suspicion should be raised if the lesions are symptomatic, growing, are associated with a lentigo maligna, or reveal irregular vessels with dermoscopy, said Dr. Marghoob.

Metastatic melanoma with unknown primary or recurrence of melanoma. Whenever possible, do not remove seemingly benign lesions and discard them, he said. Also, be careful and selective about the use of liquid nitrogen or a laser on lesions that have not been confirmed to be benign through biopsy.

He noted that cases of assumed benign lesions that recur after ablation (via liquid nitrogen, curettage, or laser), may ultimately prove to be melanoma on histopathology. Furthermore, in the unlikely event that a patient develops metastatic melanoma with an unknown primary, it may be presumed that one of the ablated lesions may have been the primary.

Dr. Marghoob disclosed having no conflicts of interest. SDEF and this news organization are owned by Elsevier.

^{A partial biopsy was performed of this lesion which had clinical features of melanoma. The pathology analysis was reported as a Clark’s nevus (this area is the white scar on the left upper portion of the lesion). Due the clinical-pathology discordance the clinician decided to excise the lesion.  As can be seen from the histology, this lesion was a melanoma and depending on the location of a partial biopsy the results can range from a Clark’s nevus to melanoma in situ to microinvasive to deeply invasive melanoma. Photo courtesy Dr. Ashfaq Marghoob.}

Misdiagnosis of melanoma is a major cause of litigation against both dermatologists and dermatopathologists.

The majority of claims filed between 1985 and 2001 involving the misdiagnosis of melanoma were because of a false negative diagnosis, which may translate to a reduced chance of survival for some patients, Dr. Ashfaq A. Marghoob reported at the seminar

Two important strategies can help minimize missing melanoma, he said. First, remain vigilant and remember that many melanomas lack the classic ABCD features.

"Questioning yourself and your pathologist regarding the diagnosis will help towards identifying many of these melanomas. In other words, remain skeptical of lesions lacking clinical-dermoscopy correlation or lesions lacking dermoscopy-histopathology correlation. Second, engage patients in their own care by having them share the responsibility of detecting early melanoma by encouraging them to examine their own skin on a regular basis," said Dr. Marghoob, who is a dermatologist at Memorial Sloan-Kettering Cancer Center in New York.

Some melanomas may not manifest concerning features, and can mimic benign lesions. To assure that a malignant melanoma will eventually be found, periodic total body examinations by a physician, and regular patient self-examinations, are key. He stressed that physician examinations and self-skin exams are complementary.

While it is widely accepted that early detection means better prognosis, modest delays of up to 6 months have not been shown to affect ultimate outcomes. However, there is one exception. Nodular melanoma can grow rapidly, and even small delays in diagnosis can have serious consequences.

The most common scenarios in melanoma litigation cases include nodular melanoma being misdiagnosed by a clinician or pathologist; a partial biopsy not capturing the most diagnostically relevant part of the lesion; malignant melanoma being misdiagnosed as a dysplastic or spitz nevus; unrecognized desmoplastic malignant melanoma; and metastatic malignant melanoma with an unknown primary or recurrence of melanoma (Am. J. Surg. Pathol. 2003;27:1278-83).

Dr. Marghoob discussed each of these cases in detail.

Misdiagnosis of nodular melanoma as nevus by a clinician or pathologist. Many nodular melanomas lack helpful diagnostic features, such as those in the ABCD criteria for malignant melanoma, which can lead to a misdiagnosis. However, the ABCDE criteria that take lesion evolution into account may be of some help, noted Dr. Marghoob.

In order to track lesion evolution, ask patients about the history of changes and symptoms. Total body photography may help on rare occasions to detect new lesions, some of which may be subtle. In addition, dermoscopy results may persuade the clinician to obtain a biopsy of a clinically banal appearing lesion that is in fact a nodular melanoma.

Partial biopsy issues. If a biopsy is performed of a lesion that clinically looks like melanoma and the pathology diagnosis is nevus, it is imperative that the clinician and pathologist reconcile the difference. In cases where there is discordance, consider asking for step-sectioning, special stains, or--in very rare instances--fluorescence in situ hybridization to look for signature chromosomal aberrations. In addition, a partial biopsy may not be representative of the rest of the lesion. If a partial biopsy was performed, re-excise the lesion, said Dr. Marghoob. Remember that a pathology report should never be read in a vacuum.

Excisional biopsy is the preferred method for melanocytic lesions, when possible, because partial biopsy may sample nondiagnostic areas or miss the prognostically-worse portion of the lesion.

"Partial biopsy assumes that a clinician can consistently predict the portion of a suspicious pigmented lesion that will have the worst representative histology," said Dr. Marghoob. In one study, 40% of excised melanomas had worse pathology, compared with initial punch biopsy, and 20% of melanomas revealed invasion, which was not seen in initial punch biopsy (Arch. Dermatol. 1996;132:1297-1302).

The ideal biopsy is excisional with a 2- to 3-mm margin, is oriented along the lines of lymphatic drainage, and is step sectioned. This limits sampling error, removes dysplastic nevus completely (preventing recurrence), and better predicts the Breslow depth if the lesion proves to be a melanoma, said Dr. Marghoob.

Even when step sectioned, less than 2% of the lesion is evaluated. In one study, thorough block sampling resulted in identification of increased tumor thickness in 43% of cases by a mean of 0.16 mm (Arch. Dermatol. 2005;141:734-6).

Misdiagnosis of a melanoma as dysplastic or spitz nevus. When a partial biopsy reveals dysplastic or spitz nevus, it is important to completely excise the lesion. Malignant melanoma can sometimes masquerade as a spitz nevus, and focus of malignant melanoma may have been missed on the biopsy. Many dermatologists are of the opinion that spitz nevi should be completely excised--at least in adults, said Dr. Marghoob.

Unrecognized desmoplastic malignant melanoma. Desmoplastic melanoma can be banal in appearance, with 70% appearing amelanotic, he said. These lesions may only present as firmness in the subcutaneous tissue. For "banal" appearing firm lesions on chronically sun-damaged skin, suspicion should be raised if the lesions are symptomatic, growing, are associated with a lentigo maligna, or reveal irregular vessels with dermoscopy, said Dr. Marghoob.

Metastatic melanoma with unknown primary or recurrence of melanoma. Whenever possible, do not remove seemingly benign lesions and discard them, he said. Also, be careful and selective about the use of liquid nitrogen or a laser on lesions that have not been confirmed to be benign through biopsy.

He noted that cases of assumed benign lesions that recur after ablation (via liquid nitrogen, curettage, or laser), may ultimately prove to be melanoma on histopathology. Furthermore, in the unlikely event that a patient develops metastatic melanoma with an unknown primary, it may be presumed that one of the ablated lesions may have been the primary.

Dr. Marghoob disclosed having no conflicts of interest. SDEF and this news organization are owned by Elsevier.

^{A partial biopsy was performed of this lesion which had clinical features of melanoma. The pathology analysis was reported as a Clark’s nevus (this area is the white scar on the left upper portion of the lesion). Due the clinical-pathology discordance the clinician decided to excise the lesion.  As can be seen from the histology, this lesion was a melanoma and depending on the location of a partial biopsy the results can range from a Clark’s nevus to melanoma in situ to microinvasive to deeply invasive melanoma. Photo courtesy Dr. Ashfaq Marghoob.}

Not all patients are equal when it comes to melanoma risk.

Knowing which patients may be more likely to develop melanoma can serve as a prompt to increase suspicion during examination, said Dr. James M. Grichnik. Be on the lookout for patients with the following features and characteristics, he suggested at the annual Hawaii Dermatology Seminar sponsored by Skin Disease Education Foundation.

Nevi
The presence of even one atypical (dysplastic) nevus independently predicts up to a 60% greater risk for melanoma, said Dr. Grichnik, director of the melanoma program and professor of dermatology at the University of Miami.

Higher numbers of common nevi also increase risk. Nevi counts are associated with UV exposure, and can be used as a surrogate marker for UV-induced cutaneous damage. Melanoma risk increases 47% with 16-40 common nevi on the whole body, he noted. Risk increases as mole count climbs, with nearly a seven-fold increased risk associated with nevi counts of 101 and higher (Euro. J. Ca. 2005;41:28-44).

Phenotype
Light-colored skin, hair, and eyes are associated with an increased melanoma risk. In 60 studies published before Sept. 2002, melanoma risk was twice as high with skin type I, compared with skin type IV; with fair skin color, compared with dark skin color; and with a high density rather than a low density of freckles. Compared with dark eyes, blue eyes were associated with a 47% higher risk. And melanoma risk was more than three times higher with red hair, compared with dark hair (Euro. J. Ca. 2005;41:28-44).

UV Exposure
Use of tanning beds increases melanoma risk 75% if the first exposure occurs before age 35 years, according to Dr. Grichnik. Multiple studies report that melanoma risk is higher in people who have experienced short, intense episodes of burning sun exposure (especially during childhood). The effects of chronic sun exposure are more difficult to determine, but may be associated with lentigo maligna-type melanoma.

Occupation
Airline crews, especially pilots, have a higher-than expected incidence of melanoma (BMJ 2002;325:567). This may be due to greater sun-exposed activities between flights in areas of the world with high sun exposure levels, he speculated.

Socioeconomics
Wealthier people are more likely to develop melanoma, compared with age-matched populations - the opposite of trends for squamous cell carcinoma, according to studies. Again, the higher risk for melanoma may be associated with sunny holidays in winter, and sun-exposed recreational activities enabled by affluence, Dr. Grichnik suggested.

History
Taking a good personal history can identify some of the risk factors listed above. Family history is important too - a significant proportion of patients with melanoma will have genetic risk factors for the disease, he said.

Thirteen percent of melanoma patients have at least one first-degree relative with melanoma (Hum. Genet. 2009;126:499-510). The disease appears to be twice as common in people who have a parent with a history of melanoma, three times as common if a sibling has had melanoma, and nine times as common if both a parent and a sibling have had melanoma, compared with people who have no family history of melanoma.

Once a melanoma is identifed, a variety of tools can help discern whether it is deadly, Dr. Grichnik added. These include the American Joint Committee on Cancer criteria for staging and classification of melanomas, the mitotic rate, nodal status, circulating tumor cell status, molecular marker status, and a history of prior nonmelanoma skin cancer or other cancers.

Dr. Grichnik is a founder and shareholder in DigitalDerm Inc. and has been a consultant and researcher for Electro-Optical Systems Inc. and Spectral Image Inc. SDEF and this news organization are owned by Elsevier.

^{Young girl having sun cream administered to her shoulder by her mother.
©Mark Swallow/iStockphoto.com}

Not all patients are equal when it comes to melanoma risk.

Knowing which patients may be more likely to develop melanoma can serve as a prompt to increase suspicion during examination, said Dr. James M. Grichnik. Be on the lookout for patients with the following features and characteristics, he suggested at the annual Hawaii Dermatology Seminar sponsored by Skin Disease Education Foundation.

Nevi
The presence of even one atypical (dysplastic) nevus independently predicts up to a 60% greater risk for melanoma, said Dr. Grichnik, director of the melanoma program and professor of dermatology at the University of Miami.

Higher numbers of common nevi also increase risk. Nevi counts are associated with UV exposure, and can be used as a surrogate marker for UV-induced cutaneous damage. Melanoma risk increases 47% with 16-40 common nevi on the whole body, he noted. Risk increases as mole count climbs, with nearly a seven-fold increased risk associated with nevi counts of 101 and higher (Euro. J. Ca. 2005;41:28-44).

Phenotype
Light-colored skin, hair, and eyes are associated with an increased melanoma risk. In 60 studies published before Sept. 2002, melanoma risk was twice as high with skin type I, compared with skin type IV; with fair skin color, compared with dark skin color; and with a high density rather than a low density of freckles. Compared with dark eyes, blue eyes were associated with a 47% higher risk. And melanoma risk was more than three times higher with red hair, compared with dark hair (Euro. J. Ca. 2005;41:28-44).

UV Exposure
Use of tanning beds increases melanoma risk 75% if the first exposure occurs before age 35 years, according to Dr. Grichnik. Multiple studies report that melanoma risk is higher in people who have experienced short, intense episodes of burning sun exposure (especially during childhood). The effects of chronic sun exposure are more difficult to determine, but may be associated with lentigo maligna-type melanoma.

Occupation
Airline crews, especially pilots, have a higher-than expected incidence of melanoma (BMJ 2002;325:567). This may be due to greater sun-exposed activities between flights in areas of the world with high sun exposure levels, he speculated.

Socioeconomics
Wealthier people are more likely to develop melanoma, compared with age-matched populations - the opposite of trends for squamous cell carcinoma, according to studies. Again, the higher risk for melanoma may be associated with sunny holidays in winter, and sun-exposed recreational activities enabled by affluence, Dr. Grichnik suggested.

History
Taking a good personal history can identify some of the risk factors listed above. Family history is important too - a significant proportion of patients with melanoma will have genetic risk factors for the disease, he said.

Thirteen percent of melanoma patients have at least one first-degree relative with melanoma (Hum. Genet. 2009;126:499-510). The disease appears to be twice as common in people who have a parent with a history of melanoma, three times as common if a sibling has had melanoma, and nine times as common if both a parent and a sibling have had melanoma, compared with people who have no family history of melanoma.

Once a melanoma is identifed, a variety of tools can help discern whether it is deadly, Dr. Grichnik added. These include the American Joint Committee on Cancer criteria for staging and classification of melanomas, the mitotic rate, nodal status, circulating tumor cell status, molecular marker status, and a history of prior nonmelanoma skin cancer or other cancers.

Dr. Grichnik is a founder and shareholder in DigitalDerm Inc. and has been a consultant and researcher for Electro-Optical Systems Inc. and Spectral Image Inc. SDEF and this news organization are owned by Elsevier.

^{Young girl having sun cream administered to her shoulder by her mother.
©Mark Swallow/iStockphoto.com}

Not all patients are equal when it comes to melanoma risk.

Knowing which patients may be more likely to develop melanoma can serve as a prompt to increase suspicion during examination, said Dr. James M. Grichnik. Be on the lookout for patients with the following features and characteristics, he suggested at the annual Hawaii Dermatology Seminar sponsored by Skin Disease Education Foundation.

Nevi
The presence of even one atypical (dysplastic) nevus independently predicts up to a 60% greater risk for melanoma, said Dr. Grichnik, director of the melanoma program and professor of dermatology at the University of Miami.

Higher numbers of common nevi also increase risk. Nevi counts are associated with UV exposure, and can be used as a surrogate marker for UV-induced cutaneous damage. Melanoma risk increases 47% with 16-40 common nevi on the whole body, he noted. Risk increases as mole count climbs, with nearly a seven-fold increased risk associated with nevi counts of 101 and higher (Euro. J. Ca. 2005;41:28-44).

Phenotype
Light-colored skin, hair, and eyes are associated with an increased melanoma risk. In 60 studies published before Sept. 2002, melanoma risk was twice as high with skin type I, compared with skin type IV; with fair skin color, compared with dark skin color; and with a high density rather than a low density of freckles. Compared with dark eyes, blue eyes were associated with a 47% higher risk. And melanoma risk was more than three times higher with red hair, compared with dark hair (Euro. J. Ca. 2005;41:28-44).

UV Exposure
Use of tanning beds increases melanoma risk 75% if the first exposure occurs before age 35 years, according to Dr. Grichnik. Multiple studies report that melanoma risk is higher in people who have experienced short, intense episodes of burning sun exposure (especially during childhood). The effects of chronic sun exposure are more difficult to determine, but may be associated with lentigo maligna-type melanoma.

Occupation
Airline crews, especially pilots, have a higher-than expected incidence of melanoma (BMJ 2002;325:567). This may be due to greater sun-exposed activities between flights in areas of the world with high sun exposure levels, he speculated.

Socioeconomics
Wealthier people are more likely to develop melanoma, compared with age-matched populations - the opposite of trends for squamous cell carcinoma, according to studies. Again, the higher risk for melanoma may be associated with sunny holidays in winter, and sun-exposed recreational activities enabled by affluence, Dr. Grichnik suggested.

History
Taking a good personal history can identify some of the risk factors listed above. Family history is important too - a significant proportion of patients with melanoma will have genetic risk factors for the disease, he said.

Thirteen percent of melanoma patients have at least one first-degree relative with melanoma (Hum. Genet. 2009;126:499-510). The disease appears to be twice as common in people who have a parent with a history of melanoma, three times as common if a sibling has had melanoma, and nine times as common if both a parent and a sibling have had melanoma, compared with people who have no family history of melanoma.

Once a melanoma is identifed, a variety of tools can help discern whether it is deadly, Dr. Grichnik added. These include the American Joint Committee on Cancer criteria for staging and classification of melanomas, the mitotic rate, nodal status, circulating tumor cell status, molecular marker status, and a history of prior nonmelanoma skin cancer or other cancers.

Dr. Grichnik is a founder and shareholder in DigitalDerm Inc. and has been a consultant and researcher for Electro-Optical Systems Inc. and Spectral Image Inc. SDEF and this news organization are owned by Elsevier.

^{Young girl having sun cream administered to her shoulder by her mother.
©Mark Swallow/iStockphoto.com}

The lifetime risk of white patients developing melanoma is currently estimated at 1 in 50, compared with 1 in 1,000 for black patients. Although darker-pigmented populations are consistently reported to have lower melanoma risk--possibly related to protection from ultraviolet radiation provided by melanin--darker skinned patients have been consistently shown to have worse outcomes than whites.

While less common in blacks, malignant melanoma is nonetheless an aggressive, deadly disease and presents at a more advanced stage at diagnosis and with a decreased chance of survival than in white patints. Underlying etiologies for the disparity in prognosis are still poorly understood.

Many of the public health interventions for melanoma prevention have focused predominantly on whites. However, recent studies in blacks and Hispanics that have elucidated advanced stage of melanoma at presentation and a higher mortality rate have led to increased efforts to characterize melanoma in ethnic minorities.

One such study found that ethnic disparities persist in the incidence of melanoma and its stage at diagnosis (Arch Dermatol. 2009;145:1369-74). Researchers analyzed information in the Florida Cancer Data System, a statewide, population-based cancer registry. They looked at three 5-year periods: 1990 to 1994, 1995 to 1999, and 2000 to 2004.

Of 41,072 cases of melanoma diagnosed from 1990 to 2004, 39,670 were in whites, 1,148 in Hispanics, and 254 in blacks. Advanced melanoma diagnosed at either regional or distant stages were seen in 26.4% of black patients, compared with 17.8% of Hispanics and 11.6% of whites. Blacks and Hispanic patients had advanced cancer odd ratios of 2.7 and 1.6, respectively, compared with whites.

The authors of the study concluded that public health efforts are one of the primary sources of ethnic disparities. However the question still remains: is race (and in essence a more aggressive tumor biology) an independent prognostic indicator? 

Multiple studies have elucidated worse prognosis in blacks even when controlling for socioeconomic status, stage, tumor thickness, ulceration, anatomic site, and histological type. This data has been refuted in other studies that show no survival advantage in whites; however, the controversy still remains.

This study is a much needed reminder that increased surveillance is needed, as well as more targeted public health efforts, prevention models, and educational programs specific to the culture and languages of ethnic groups. We also need to continue to investigate the unique genetic and biologic markers of melanoma in different ethnic populations to improve clinical detection and develop targeted therapies.

The lifetime risk of white patients developing melanoma is currently estimated at 1 in 50, compared with 1 in 1,000 for black patients. Although darker-pigmented populations are consistently reported to have lower melanoma risk--possibly related to protection from ultraviolet radiation provided by melanin--darker skinned patients have been consistently shown to have worse outcomes than whites.

While less common in blacks, malignant melanoma is nonetheless an aggressive, deadly disease and presents at a more advanced stage at diagnosis and with a decreased chance of survival than in white patints. Underlying etiologies for the disparity in prognosis are still poorly understood.

Many of the public health interventions for melanoma prevention have focused predominantly on whites. However, recent studies in blacks and Hispanics that have elucidated advanced stage of melanoma at presentation and a higher mortality rate have led to increased efforts to characterize melanoma in ethnic minorities.

One such study found that ethnic disparities persist in the incidence of melanoma and its stage at diagnosis (Arch Dermatol. 2009;145:1369-74). Researchers analyzed information in the Florida Cancer Data System, a statewide, population-based cancer registry. They looked at three 5-year periods: 1990 to 1994, 1995 to 1999, and 2000 to 2004.

Of 41,072 cases of melanoma diagnosed from 1990 to 2004, 39,670 were in whites, 1,148 in Hispanics, and 254 in blacks. Advanced melanoma diagnosed at either regional or distant stages were seen in 26.4% of black patients, compared with 17.8% of Hispanics and 11.6% of whites. Blacks and Hispanic patients had advanced cancer odd ratios of 2.7 and 1.6, respectively, compared with whites.

The authors of the study concluded that public health efforts are one of the primary sources of ethnic disparities. However the question still remains: is race (and in essence a more aggressive tumor biology) an independent prognostic indicator? 

Multiple studies have elucidated worse prognosis in blacks even when controlling for socioeconomic status, stage, tumor thickness, ulceration, anatomic site, and histological type. This data has been refuted in other studies that show no survival advantage in whites; however, the controversy still remains.

This study is a much needed reminder that increased surveillance is needed, as well as more targeted public health efforts, prevention models, and educational programs specific to the culture and languages of ethnic groups. We also need to continue to investigate the unique genetic and biologic markers of melanoma in different ethnic populations to improve clinical detection and develop targeted therapies.

The lifetime risk of white patients developing melanoma is currently estimated at 1 in 50, compared with 1 in 1,000 for black patients. Although darker-pigmented populations are consistently reported to have lower melanoma risk--possibly related to protection from ultraviolet radiation provided by melanin--darker skinned patients have been consistently shown to have worse outcomes than whites.

While less common in blacks, malignant melanoma is nonetheless an aggressive, deadly disease and presents at a more advanced stage at diagnosis and with a decreased chance of survival than in white patints. Underlying etiologies for the disparity in prognosis are still poorly understood.

Many of the public health interventions for melanoma prevention have focused predominantly on whites. However, recent studies in blacks and Hispanics that have elucidated advanced stage of melanoma at presentation and a higher mortality rate have led to increased efforts to characterize melanoma in ethnic minorities.

One such study found that ethnic disparities persist in the incidence of melanoma and its stage at diagnosis (Arch Dermatol. 2009;145:1369-74). Researchers analyzed information in the Florida Cancer Data System, a statewide, population-based cancer registry. They looked at three 5-year periods: 1990 to 1994, 1995 to 1999, and 2000 to 2004.

Of 41,072 cases of melanoma diagnosed from 1990 to 2004, 39,670 were in whites, 1,148 in Hispanics, and 254 in blacks. Advanced melanoma diagnosed at either regional or distant stages were seen in 26.4% of black patients, compared with 17.8% of Hispanics and 11.6% of whites. Blacks and Hispanic patients had advanced cancer odd ratios of 2.7 and 1.6, respectively, compared with whites.

The authors of the study concluded that public health efforts are one of the primary sources of ethnic disparities. However the question still remains: is race (and in essence a more aggressive tumor biology) an independent prognostic indicator? 

Multiple studies have elucidated worse prognosis in blacks even when controlling for socioeconomic status, stage, tumor thickness, ulceration, anatomic site, and histological type. This data has been refuted in other studies that show no survival advantage in whites; however, the controversy still remains.

This study is a much needed reminder that increased surveillance is needed, as well as more targeted public health efforts, prevention models, and educational programs specific to the culture and languages of ethnic groups. We also need to continue to investigate the unique genetic and biologic markers of melanoma in different ethnic populations to improve clinical detection and develop targeted therapies.