Melanoma

Indoor tanning is associated with a fourfold increased risk of melanoma, according to findings published online May 27 in Cancer Epidemiology, Biomarkers & Prevention.

The findings were based on data from the Skin Health Study, a population-based, case-control study of 1,167 cases and 1,101 controls.

Photo copyright: Bora Ucak/iStockphoto.com

Melanoma was 2.9 times more likely to occur in users of high-speed/high-intensity (UVB-enhanced) tanning devices and 4.4 times more likely in users of high-pressure (primarily UVA-emitting) devices, compared with individuals who had never used the devices.

In addition, melanoma was 1.8 and 1.9 times more likely in users of conventional indoor tanning devices and sunlamps, respectively, compared with never users.

The study population included individuals aged 25-59 years who were diagnosed with invasive cutaneous melanoma between July 2004 and December 2007 in Minnesota and who were enrolled in a state cancer registry. Controls were selected at random from the Minnesota state driver’s license list. Study participants completed a self-administered questionnaire and a detailed 1-hour phone interview (Cancer Epidemiol. Biomarkers Prev. 2010 [doi: 10.1158/1055-9965.EPI-09-1249]).

DeAnn Lazovich, Ph.D., of the University of Minnesota, Minneapolis, and colleagues began the Skin Health Study in 2004 in Minnesota, a state with a documented high rate of indoor tanning. The data collected by the researchers included skin, hair, and eye color; presence of moles and freckles; lifetime routine sun exposure; age at which tanning beds were first used; duration and frequency of indoor tanning; and type of tanning device used.

Overall, 63% of individuals with melanoma and 51% of controls reported any indoor tanning. Melanoma risk increased significantly as the frequency of indoor tanning increased. Individuals with melanoma were more than twice as likely as controls to report painful burns resulting from indoor tanning, and they reported significantly more of these painful burns than controls.

The researchers also noted that a dose-response relationship between the number of tanning sessions and the number of melanoma lesions on the trunk was identified in both men and women.

“We did not find lifetime routine sun exposure or sun exposure via recreational outdoor activities or occupations to be associated with melanoma risk,” Dr. Lazovich and associates wrote. “To the extent that sunburns are a marker of intermittent sun exposure, then our results adequately represent the independent effect of indoor tanning use on the risk of melanoma.”

“As dermatologists, we see the horrible price paid for using these devices,” Dr. Allan C. Halpern, chief of dermatology at Memorial Sloan-Kettering Cancer Center, New York, said during a teleconference on May 27 to discuss the study findings. Dr. Halpern was not involved in the study.

“We now know that the total amount of UV exposure in tanning beds over time is important,” Dr. Halpern said. “I’m hopeful that this study is going to be very helpful in the hands of the FDA to further regulate the industry.” 

Dr. Halpern said that dermatologists have long understood the importance of educating patients about the dangers of indoor tanning devices, but that misinformation about the risks and benefits of indoor tanning persist.

 “I think this study very much strengthens our hand,” he said. Dr. Halpern added that he was encouraged to see the consumer video posted by the FDA earlier this week, which states than any UV indoor tanning device should be avoided.

In 2009, the International Agency for Research on Cancer classified tanning beds as carcinogenic to humans. In 2010, a Food and Drug Administration advisory panel recommended tighter restrictions on the use of indoor tanning devices, but the FDA has yet to issue any guidelines based on these recommendations.

The findings address several limitations of previous studies on this topic, including the ability to control for confounding variables such as sun exposure, the investigators noted.

None of the study authors stated that they had any conflicts of interest to disclose. The study was supported in part by a grant from the American Cancer Society and the National Cancer Institute.

Indoor tanning is associated with a fourfold increased risk of melanoma, according to findings published online May 27 in Cancer Epidemiology, Biomarkers & Prevention.

The findings were based on data from the Skin Health Study, a population-based, case-control study of 1,167 cases and 1,101 controls.

Photo copyright: Bora Ucak/iStockphoto.com

Melanoma was 2.9 times more likely to occur in users of high-speed/high-intensity (UVB-enhanced) tanning devices and 4.4 times more likely in users of high-pressure (primarily UVA-emitting) devices, compared with individuals who had never used the devices.

In addition, melanoma was 1.8 and 1.9 times more likely in users of conventional indoor tanning devices and sunlamps, respectively, compared with never users.

The study population included individuals aged 25-59 years who were diagnosed with invasive cutaneous melanoma between July 2004 and December 2007 in Minnesota and who were enrolled in a state cancer registry. Controls were selected at random from the Minnesota state driver’s license list. Study participants completed a self-administered questionnaire and a detailed 1-hour phone interview (Cancer Epidemiol. Biomarkers Prev. 2010 [doi: 10.1158/1055-9965.EPI-09-1249]).

DeAnn Lazovich, Ph.D., of the University of Minnesota, Minneapolis, and colleagues began the Skin Health Study in 2004 in Minnesota, a state with a documented high rate of indoor tanning. The data collected by the researchers included skin, hair, and eye color; presence of moles and freckles; lifetime routine sun exposure; age at which tanning beds were first used; duration and frequency of indoor tanning; and type of tanning device used.

Overall, 63% of individuals with melanoma and 51% of controls reported any indoor tanning. Melanoma risk increased significantly as the frequency of indoor tanning increased. Individuals with melanoma were more than twice as likely as controls to report painful burns resulting from indoor tanning, and they reported significantly more of these painful burns than controls.

The researchers also noted that a dose-response relationship between the number of tanning sessions and the number of melanoma lesions on the trunk was identified in both men and women.

“We did not find lifetime routine sun exposure or sun exposure via recreational outdoor activities or occupations to be associated with melanoma risk,” Dr. Lazovich and associates wrote. “To the extent that sunburns are a marker of intermittent sun exposure, then our results adequately represent the independent effect of indoor tanning use on the risk of melanoma.”

“As dermatologists, we see the horrible price paid for using these devices,” Dr. Allan C. Halpern, chief of dermatology at Memorial Sloan-Kettering Cancer Center, New York, said during a teleconference on May 27 to discuss the study findings. Dr. Halpern was not involved in the study.

“We now know that the total amount of UV exposure in tanning beds over time is important,” Dr. Halpern said. “I’m hopeful that this study is going to be very helpful in the hands of the FDA to further regulate the industry.” 

Dr. Halpern said that dermatologists have long understood the importance of educating patients about the dangers of indoor tanning devices, but that misinformation about the risks and benefits of indoor tanning persist.

 “I think this study very much strengthens our hand,” he said. Dr. Halpern added that he was encouraged to see the consumer video posted by the FDA earlier this week, which states than any UV indoor tanning device should be avoided.

In 2009, the International Agency for Research on Cancer classified tanning beds as carcinogenic to humans. In 2010, a Food and Drug Administration advisory panel recommended tighter restrictions on the use of indoor tanning devices, but the FDA has yet to issue any guidelines based on these recommendations.

The findings address several limitations of previous studies on this topic, including the ability to control for confounding variables such as sun exposure, the investigators noted.

None of the study authors stated that they had any conflicts of interest to disclose. The study was supported in part by a grant from the American Cancer Society and the National Cancer Institute.

Indoor tanning is associated with a fourfold increased risk of melanoma, according to findings published online May 27 in Cancer Epidemiology, Biomarkers & Prevention.

The findings were based on data from the Skin Health Study, a population-based, case-control study of 1,167 cases and 1,101 controls.

Photo copyright: Bora Ucak/iStockphoto.com

Melanoma was 2.9 times more likely to occur in users of high-speed/high-intensity (UVB-enhanced) tanning devices and 4.4 times more likely in users of high-pressure (primarily UVA-emitting) devices, compared with individuals who had never used the devices.

In addition, melanoma was 1.8 and 1.9 times more likely in users of conventional indoor tanning devices and sunlamps, respectively, compared with never users.

The study population included individuals aged 25-59 years who were diagnosed with invasive cutaneous melanoma between July 2004 and December 2007 in Minnesota and who were enrolled in a state cancer registry. Controls were selected at random from the Minnesota state driver’s license list. Study participants completed a self-administered questionnaire and a detailed 1-hour phone interview (Cancer Epidemiol. Biomarkers Prev. 2010 [doi: 10.1158/1055-9965.EPI-09-1249]).

DeAnn Lazovich, Ph.D., of the University of Minnesota, Minneapolis, and colleagues began the Skin Health Study in 2004 in Minnesota, a state with a documented high rate of indoor tanning. The data collected by the researchers included skin, hair, and eye color; presence of moles and freckles; lifetime routine sun exposure; age at which tanning beds were first used; duration and frequency of indoor tanning; and type of tanning device used.

Overall, 63% of individuals with melanoma and 51% of controls reported any indoor tanning. Melanoma risk increased significantly as the frequency of indoor tanning increased. Individuals with melanoma were more than twice as likely as controls to report painful burns resulting from indoor tanning, and they reported significantly more of these painful burns than controls.

The researchers also noted that a dose-response relationship between the number of tanning sessions and the number of melanoma lesions on the trunk was identified in both men and women.

“We did not find lifetime routine sun exposure or sun exposure via recreational outdoor activities or occupations to be associated with melanoma risk,” Dr. Lazovich and associates wrote. “To the extent that sunburns are a marker of intermittent sun exposure, then our results adequately represent the independent effect of indoor tanning use on the risk of melanoma.”

“As dermatologists, we see the horrible price paid for using these devices,” Dr. Allan C. Halpern, chief of dermatology at Memorial Sloan-Kettering Cancer Center, New York, said during a teleconference on May 27 to discuss the study findings. Dr. Halpern was not involved in the study.

“We now know that the total amount of UV exposure in tanning beds over time is important,” Dr. Halpern said. “I’m hopeful that this study is going to be very helpful in the hands of the FDA to further regulate the industry.” 

Dr. Halpern said that dermatologists have long understood the importance of educating patients about the dangers of indoor tanning devices, but that misinformation about the risks and benefits of indoor tanning persist.

 “I think this study very much strengthens our hand,” he said. Dr. Halpern added that he was encouraged to see the consumer video posted by the FDA earlier this week, which states than any UV indoor tanning device should be avoided.

In 2009, the International Agency for Research on Cancer classified tanning beds as carcinogenic to humans. In 2010, a Food and Drug Administration advisory panel recommended tighter restrictions on the use of indoor tanning devices, but the FDA has yet to issue any guidelines based on these recommendations.

The findings address several limitations of previous studies on this topic, including the ability to control for confounding variables such as sun exposure, the investigators noted.

None of the study authors stated that they had any conflicts of interest to disclose. The study was supported in part by a grant from the American Cancer Society and the National Cancer Institute.

MADRID — Regular use of a sunscreen prevented development of nonmelanoma skin cancer and reduced actinic keratosis counts in immunosuppressed organ transplant recipients in a 2-year, prospective, case-control study.

"I strongly believe, without being able to prove it, that sunscreen's protective mechanism involved blocking UV-induced impairment of cutaneous immunosurveillance. It's all about local immunity," Dr. Claas Ulrich said at the World Congress on Cancers of the Skin.

The single-center study involved 60 organ transplant recipients in the active treatment arm—20 each with a donor heart, liver, or kidney—and an equal number of organ transplant recipient control patients.

Both groups received the same instructions regarding the importance of following a comprehensive photoprotection program including the avoidance of sun exposure between 11 a.m. and 2 p.m.; a strict prohibition on tanning beds; and routinely wearing long-sleeved shirts, trousers, and broad-brimmed hats.

The active treatment group also received a steady supply of a broad-spectrum sunscreen, free of charge, throughout the 2-year study. They were instructed to apply 2 mg/cm² once daily to the head, neck, forearms, and hands, explained Dr. Ulrich, of the department of dermatology at Charité University Hospital, Berlin.

During the 2-year study, new invasive squamous cell carcinomas developed in 8 controls, but none of the sunscreen group. Nine controls developed new basal cell carcinomas, compared with two patients in the sunscreen group.

At baseline, patients in each group collectively had 191 actinic keratoses; after 24 months, the sunscreen group had 89 actinic keratoses, while the control group had 273.

Numerous studies have shown poor compliance with sunscreen use and other sun protection measures on the part of organ transplant recipients despite their markedly elevated rates of skin cancer.

In one study, for example, only 5% of 205 Canadian transplant recipients indicated they were committed to daily use of sunscreen. Thirty percent didn't use sunscreen at all. And 23% of the group continued to seek a tan (Am. J. Transplant. 2004;4:1852-8).

"When you ask patients why they don't use sunscreens, they say it takes too long to put on; they're messy, whitening, cosmetically unacceptable and very expensive if you buy high-quality sunscreens. We tried to optimize all those factors for the study," Dr. Ulrich said. "You need a good sunscreen. If we don't come close to their needs we've failed in our preventive strategies."

For the 2-year study, patients were supplied with Daylong Actinica, a broad-spectrum, once-daily, water-resistant lotion rated by the European Union as "very highly protective."

The study was sponsored by Spirig Pharma, which markets Daylong Actinica. Dr. Ulrich disclosed serving as a consultant to Spirig as well as Almirall, Novartis, and Wyeth (now part of Pfizer).

MADRID — Regular use of a sunscreen prevented development of nonmelanoma skin cancer and reduced actinic keratosis counts in immunosuppressed organ transplant recipients in a 2-year, prospective, case-control study.

"I strongly believe, without being able to prove it, that sunscreen's protective mechanism involved blocking UV-induced impairment of cutaneous immunosurveillance. It's all about local immunity," Dr. Claas Ulrich said at the World Congress on Cancers of the Skin.

The single-center study involved 60 organ transplant recipients in the active treatment arm—20 each with a donor heart, liver, or kidney—and an equal number of organ transplant recipient control patients.

Both groups received the same instructions regarding the importance of following a comprehensive photoprotection program including the avoidance of sun exposure between 11 a.m. and 2 p.m.; a strict prohibition on tanning beds; and routinely wearing long-sleeved shirts, trousers, and broad-brimmed hats.

The active treatment group also received a steady supply of a broad-spectrum sunscreen, free of charge, throughout the 2-year study. They were instructed to apply 2 mg/cm² once daily to the head, neck, forearms, and hands, explained Dr. Ulrich, of the department of dermatology at Charité University Hospital, Berlin.

During the 2-year study, new invasive squamous cell carcinomas developed in 8 controls, but none of the sunscreen group. Nine controls developed new basal cell carcinomas, compared with two patients in the sunscreen group.

At baseline, patients in each group collectively had 191 actinic keratoses; after 24 months, the sunscreen group had 89 actinic keratoses, while the control group had 273.

Numerous studies have shown poor compliance with sunscreen use and other sun protection measures on the part of organ transplant recipients despite their markedly elevated rates of skin cancer.

In one study, for example, only 5% of 205 Canadian transplant recipients indicated they were committed to daily use of sunscreen. Thirty percent didn't use sunscreen at all. And 23% of the group continued to seek a tan (Am. J. Transplant. 2004;4:1852-8).

"When you ask patients why they don't use sunscreens, they say it takes too long to put on; they're messy, whitening, cosmetically unacceptable and very expensive if you buy high-quality sunscreens. We tried to optimize all those factors for the study," Dr. Ulrich said. "You need a good sunscreen. If we don't come close to their needs we've failed in our preventive strategies."

For the 2-year study, patients were supplied with Daylong Actinica, a broad-spectrum, once-daily, water-resistant lotion rated by the European Union as "very highly protective."

The study was sponsored by Spirig Pharma, which markets Daylong Actinica. Dr. Ulrich disclosed serving as a consultant to Spirig as well as Almirall, Novartis, and Wyeth (now part of Pfizer).

MADRID — Regular use of a sunscreen prevented development of nonmelanoma skin cancer and reduced actinic keratosis counts in immunosuppressed organ transplant recipients in a 2-year, prospective, case-control study.

"I strongly believe, without being able to prove it, that sunscreen's protective mechanism involved blocking UV-induced impairment of cutaneous immunosurveillance. It's all about local immunity," Dr. Claas Ulrich said at the World Congress on Cancers of the Skin.

The single-center study involved 60 organ transplant recipients in the active treatment arm—20 each with a donor heart, liver, or kidney—and an equal number of organ transplant recipient control patients.

Both groups received the same instructions regarding the importance of following a comprehensive photoprotection program including the avoidance of sun exposure between 11 a.m. and 2 p.m.; a strict prohibition on tanning beds; and routinely wearing long-sleeved shirts, trousers, and broad-brimmed hats.

The active treatment group also received a steady supply of a broad-spectrum sunscreen, free of charge, throughout the 2-year study. They were instructed to apply 2 mg/cm² once daily to the head, neck, forearms, and hands, explained Dr. Ulrich, of the department of dermatology at Charité University Hospital, Berlin.

During the 2-year study, new invasive squamous cell carcinomas developed in 8 controls, but none of the sunscreen group. Nine controls developed new basal cell carcinomas, compared with two patients in the sunscreen group.

At baseline, patients in each group collectively had 191 actinic keratoses; after 24 months, the sunscreen group had 89 actinic keratoses, while the control group had 273.

Numerous studies have shown poor compliance with sunscreen use and other sun protection measures on the part of organ transplant recipients despite their markedly elevated rates of skin cancer.

In one study, for example, only 5% of 205 Canadian transplant recipients indicated they were committed to daily use of sunscreen. Thirty percent didn't use sunscreen at all. And 23% of the group continued to seek a tan (Am. J. Transplant. 2004;4:1852-8).

"When you ask patients why they don't use sunscreens, they say it takes too long to put on; they're messy, whitening, cosmetically unacceptable and very expensive if you buy high-quality sunscreens. We tried to optimize all those factors for the study," Dr. Ulrich said. "You need a good sunscreen. If we don't come close to their needs we've failed in our preventive strategies."

For the 2-year study, patients were supplied with Daylong Actinica, a broad-spectrum, once-daily, water-resistant lotion rated by the European Union as "very highly protective."

The study was sponsored by Spirig Pharma, which markets Daylong Actinica. Dr. Ulrich disclosed serving as a consultant to Spirig as well as Almirall, Novartis, and Wyeth (now part of Pfizer).

NEW YORK - Regular examination of the vulva for skin cancer may be indicated for women with at least one first- or second-degree relative with melanoma.

However, in a small pilot study, only one out of seven dermatologists surveyed reported always examining the vulvar on routine examinations.

In a poster presented at the annual meeting of the American College of Mohs Surgery, Dr. Michael Krathen and Dr. Daniel S. Loo of the dermatology department at Tufts Medical Center in Boston, surveyed 13 attending gynecologists and dermatologists recruited from both Tufts and the Boston Medical Center.

Among the gynecologists, 12 of 13 responded that they "agree or agree strongly that the diagnosis of vulvar melanoma is their responsibility," although 11 of 13 agreed that it is the coresponsibility of the dermatologist to diagnose vulvar melanoma.

Meanwhile, among the dermatologists, only one out of the seven agreed with the statement that they "always" examine the vulva on routine annular exams; four said they do "sometimes," and two stated that they do so "often."
Dr. Krathen and Dr. Loo also examined the charts of 10 patients with malignant melanoma (MM) diagnoses and 3 patients who had malignant melanoma in situ (MMIS).

"The medical charts reviewed were almost all from Tufts," said Dr. Krathen in an interview. "Only one case of vulvar melanoma was identified from Boston Medical Center, perhaps because of the greater diversity in racial groups served by this hospital."

For the MM patients, the average depth of invasion was 4.1 mm, the mean age was 69 years, and at least seven were white. Two of the patients had a brother with MM. Five cases presented as persistent bleeding, itching, or as a "nonhealing erosion."

Looking at the MMIS patients, the average age was 24 years. One case had a second-degree relative with a MM history. Only one of the three presented to the gynecologist specifically because of the melanoma (after becoming concerned about pigment change); the other two presented complaining of dysmenorrheal and abdominal pain, and the lesion was discovered incidentally.

"The standard of care should be to offer examination of the external genitalia in all patients, especially those with a family history of malignant melanoma," said Dr. Krathen.

"Furthermore, reminding female patients to self-examine this area with a hand-held mirror and to ensure that their gynecologist examines the external genitalia during regular examinations is recommended as well."

Dr. Loo and Dr. Krathen reported having no disclosures.

NEW YORK - Regular examination of the vulva for skin cancer may be indicated for women with at least one first- or second-degree relative with melanoma.

However, in a small pilot study, only one out of seven dermatologists surveyed reported always examining the vulvar on routine examinations.

In a poster presented at the annual meeting of the American College of Mohs Surgery, Dr. Michael Krathen and Dr. Daniel S. Loo of the dermatology department at Tufts Medical Center in Boston, surveyed 13 attending gynecologists and dermatologists recruited from both Tufts and the Boston Medical Center.

Among the gynecologists, 12 of 13 responded that they "agree or agree strongly that the diagnosis of vulvar melanoma is their responsibility," although 11 of 13 agreed that it is the coresponsibility of the dermatologist to diagnose vulvar melanoma.

Meanwhile, among the dermatologists, only one out of the seven agreed with the statement that they "always" examine the vulva on routine annular exams; four said they do "sometimes," and two stated that they do so "often."
Dr. Krathen and Dr. Loo also examined the charts of 10 patients with malignant melanoma (MM) diagnoses and 3 patients who had malignant melanoma in situ (MMIS).

"The medical charts reviewed were almost all from Tufts," said Dr. Krathen in an interview. "Only one case of vulvar melanoma was identified from Boston Medical Center, perhaps because of the greater diversity in racial groups served by this hospital."

For the MM patients, the average depth of invasion was 4.1 mm, the mean age was 69 years, and at least seven were white. Two of the patients had a brother with MM. Five cases presented as persistent bleeding, itching, or as a "nonhealing erosion."

Looking at the MMIS patients, the average age was 24 years. One case had a second-degree relative with a MM history. Only one of the three presented to the gynecologist specifically because of the melanoma (after becoming concerned about pigment change); the other two presented complaining of dysmenorrheal and abdominal pain, and the lesion was discovered incidentally.

"The standard of care should be to offer examination of the external genitalia in all patients, especially those with a family history of malignant melanoma," said Dr. Krathen.

"Furthermore, reminding female patients to self-examine this area with a hand-held mirror and to ensure that their gynecologist examines the external genitalia during regular examinations is recommended as well."

Dr. Loo and Dr. Krathen reported having no disclosures.

NEW YORK - Regular examination of the vulva for skin cancer may be indicated for women with at least one first- or second-degree relative with melanoma.

However, in a small pilot study, only one out of seven dermatologists surveyed reported always examining the vulvar on routine examinations.

In a poster presented at the annual meeting of the American College of Mohs Surgery, Dr. Michael Krathen and Dr. Daniel S. Loo of the dermatology department at Tufts Medical Center in Boston, surveyed 13 attending gynecologists and dermatologists recruited from both Tufts and the Boston Medical Center.

Among the gynecologists, 12 of 13 responded that they "agree or agree strongly that the diagnosis of vulvar melanoma is their responsibility," although 11 of 13 agreed that it is the coresponsibility of the dermatologist to diagnose vulvar melanoma.

Meanwhile, among the dermatologists, only one out of the seven agreed with the statement that they "always" examine the vulva on routine annular exams; four said they do "sometimes," and two stated that they do so "often."
Dr. Krathen and Dr. Loo also examined the charts of 10 patients with malignant melanoma (MM) diagnoses and 3 patients who had malignant melanoma in situ (MMIS).

"The medical charts reviewed were almost all from Tufts," said Dr. Krathen in an interview. "Only one case of vulvar melanoma was identified from Boston Medical Center, perhaps because of the greater diversity in racial groups served by this hospital."

For the MM patients, the average depth of invasion was 4.1 mm, the mean age was 69 years, and at least seven were white. Two of the patients had a brother with MM. Five cases presented as persistent bleeding, itching, or as a "nonhealing erosion."

Looking at the MMIS patients, the average age was 24 years. One case had a second-degree relative with a MM history. Only one of the three presented to the gynecologist specifically because of the melanoma (after becoming concerned about pigment change); the other two presented complaining of dysmenorrheal and abdominal pain, and the lesion was discovered incidentally.

"The standard of care should be to offer examination of the external genitalia in all patients, especially those with a family history of malignant melanoma," said Dr. Krathen.

"Furthermore, reminding female patients to self-examine this area with a hand-held mirror and to ensure that their gynecologist examines the external genitalia during regular examinations is recommended as well."

Dr. Loo and Dr. Krathen reported having no disclosures.

MADRID - Targeted therapy - the glamour area of cancer research in recent years - has arrived at the doorstep of nonmelanoma skin cancer in a big way.

"There are at least 24 open trials of targeted therapies for nonmelanoma skin cancer listed now at www.clinicaltrials.gov," Dr. Gunther Hofbauer noted at the 13th World Congress on Cancers of the Skin, sponsored by the Skin Cancer Foundation.

The mainstays of targeted cancer therapy are monoclonal antibodies and oral small molecules directed at specific enzyme pathways and receptors identified as important in carcinogenesis or tumor growth. These agents are designed to be considerably less toxic than standard chemotherapy.

Dr. Hofbauer, a dermatologist at the University of Zurich, highlighted a handful of the most promising investigational targeted agents for treatment and chemoprevention of nonmelanoma skin cancer. These include hedgehog inhibitors, cyclooxygenase inhibitors, and alpha-difluoromethylornithine for basal cell carcinoma (BCC), and epidermal growth factor receptor inhibitors for squamous cell carcinoma (SCC).

Furthest along in the developmental pipeline are the hedgehog inhibitors.

Most BCCs have mutations in the hedgehog signaling pathway, leading to activation of the smoothened homologue, with resultant promotion of tumor growth. The oral smoothened homologue inhibitor GDC-0449 being developed by Genentech selectively inhibits the hedgehog pathway, making it of particular interest as a potential targeted therapy for BCC and a number of other malignancies, including medulloblastoma, colon cancer, and pancreatic cancer, he explained.

Last year, American investigators reported a phase I study in which 33 patients with unresectable metastastic or locally advanced BCC were treated with GDC-0449. Sixteen had partial and 2 had complete responses by the standardized Response Evaluation Criteria in Solid Tumors (RECIST). Eleven others had stable disease during the 10-month study, while 4 had progressive disease (N. Engl. J. Med. 2009;361:1,164-72).

"In general, it looks like the longer people are on this drug, the more profit they have--and the profit seems to be sustained," Dr. Hofbauer observed.

BCCs are known to secrete prostaglandin E2, which acts upon stromal cells in the cancer's vicinity to promote tumor growth. Reasoning that this process might be amenable to pharmacologic inhibition of cyclooxygenase enzymes in the skin, investigators at the Children's Hospital of Oakland (Calif.) Research Institute conducted a 3-year, double-blind, randomized clinical trial of oral celecoxib versus placebo in 60 patients with the basal cell nevus syndrome.

Celecoxib showed considerable promise in the patients with less severe disease. That is, among the 36 patients with less than 15 BCCs at baseline, those randomized to celecoxib had a 20% increase per year in BCC burden or extent, significantly less than the 50% annual increase in burden in controls. In the 24 patients with 15 or more BCCs at baseline, however, celecoxib wasn't significantly better than placebo (Cancer Prev. Res. 2010;3:25-34).

This is an exciting development involving a low-risk chemopreventive agent for use in patients genetically predisposed to multiple BCCs, in Dr. Hofbauer's view.

Animal studies have shown that inhibition of ornithine decarboxylase by alpha-difluoromethylornithine (DFMO) diminishes tissue concentrations of the neoplasia-promoting polyamines spermidine and putrescine. These observations led to a phase III randomized, double-blind, placebo-controlled study of NMSC prevention via DFMO at 500 mg/m2 per day for 4-5 years.

The trial, led by investigators at the University of Wisconsin Cancer Center, Madison, involved 291 subjects with a mean age of 61 years and an average of 4.5 previous NMSCs.

After 1,200 patient-years of follow-up, there were 260 new nonmelanoma skin cancers in the DFMO group and 363 in controls, a nonsignificant difference (P = .069). Upon closer examination, however, the investigators noted that while DFMO had no impact on the incidence of new SCCs, it did have a significant inhibitory effect on new BCCs. There were 163 in the DFMO group, compared with 243 in controls. This translated into an event rate of 0.28 new BCCs per patient per year in the DFMO group, compared with 0.40 per patient per year with placebo (P =.03).

Compliance with DFMO was deemed excellent, at greater than 90%. The chief side effect was mild ototoxicity identified in serial audiometric examinations (Cancer Prev. Res. 2010;3:35-47).

Mutations or amplification of the epidermal growth factor receptor (EGFR) have been linked to cancers of the breast, colon, lung, and cervix, as well as to melanoma and SCC. Most keratinocytes express EGFR, and this expression is greatest in the keratinocytes located in hair follicle epithelium and the basal and suprabasal portions of the epidermis, which is where the action is in SCC.

For this reason, agents that specifically target the EGFR/mitogen-activated protein kinase signaling pathway are under scrutiny as potential treatments for SCC. A fair number of such agents are already approved for the treatment of other malignancies, including the monoclonal antibodies panitumumab (Vectibix) and cetuximab (Erbitux) and the small molecules gefitinib (Iressa) and erlotinib (Tarceva). Many more are in the pipeline.

 

Leading the way for SCC is cetuximab, which has been approved by the Food and Drug Administration as single-agent therapy for recurrent or metastatic disease and in combination with radiation therapy for locally advanced SCC of the head and neck.

But targeted therapy has its shortcomings, Dr. Hofbauer stressed. "These molecules are not as specific or targeted as we'd like them to be. That can lead to untoward outcomes," he noted.

Dr. Hofbauer cited as an example sorafenib (Nexavar), an oral inhibitor of multiple tyrosine protein kinases. Sorafenib is approved for the treatment of advanced renal cell carcinoma and advanced hepatocellular carcinoma. But in addition to its better-known dermatologic side effects, such as hand-foot syndrome, sorafenib also apparently induces SCC or inflammation of actinic keratosis in about 7% of treated patients (Clin. Genitourin. Cancer 2009;7:20-3). The likely mechanism involves impairment of skin immunosurveillance due to reduced dendritic cell function and a diminished primary immune response, he said.

Dr. Hofbauer reported having no conflicts of interest.

MADRID - Targeted therapy - the glamour area of cancer research in recent years - has arrived at the doorstep of nonmelanoma skin cancer in a big way.

"There are at least 24 open trials of targeted therapies for nonmelanoma skin cancer listed now at www.clinicaltrials.gov," Dr. Gunther Hofbauer noted at the 13th World Congress on Cancers of the Skin, sponsored by the Skin Cancer Foundation.

The mainstays of targeted cancer therapy are monoclonal antibodies and oral small molecules directed at specific enzyme pathways and receptors identified as important in carcinogenesis or tumor growth. These agents are designed to be considerably less toxic than standard chemotherapy.

Dr. Hofbauer, a dermatologist at the University of Zurich, highlighted a handful of the most promising investigational targeted agents for treatment and chemoprevention of nonmelanoma skin cancer. These include hedgehog inhibitors, cyclooxygenase inhibitors, and alpha-difluoromethylornithine for basal cell carcinoma (BCC), and epidermal growth factor receptor inhibitors for squamous cell carcinoma (SCC).

Furthest along in the developmental pipeline are the hedgehog inhibitors.

Most BCCs have mutations in the hedgehog signaling pathway, leading to activation of the smoothened homologue, with resultant promotion of tumor growth. The oral smoothened homologue inhibitor GDC-0449 being developed by Genentech selectively inhibits the hedgehog pathway, making it of particular interest as a potential targeted therapy for BCC and a number of other malignancies, including medulloblastoma, colon cancer, and pancreatic cancer, he explained.

Last year, American investigators reported a phase I study in which 33 patients with unresectable metastastic or locally advanced BCC were treated with GDC-0449. Sixteen had partial and 2 had complete responses by the standardized Response Evaluation Criteria in Solid Tumors (RECIST). Eleven others had stable disease during the 10-month study, while 4 had progressive disease (N. Engl. J. Med. 2009;361:1,164-72).

"In general, it looks like the longer people are on this drug, the more profit they have--and the profit seems to be sustained," Dr. Hofbauer observed.

BCCs are known to secrete prostaglandin E2, which acts upon stromal cells in the cancer's vicinity to promote tumor growth. Reasoning that this process might be amenable to pharmacologic inhibition of cyclooxygenase enzymes in the skin, investigators at the Children's Hospital of Oakland (Calif.) Research Institute conducted a 3-year, double-blind, randomized clinical trial of oral celecoxib versus placebo in 60 patients with the basal cell nevus syndrome.

Celecoxib showed considerable promise in the patients with less severe disease. That is, among the 36 patients with less than 15 BCCs at baseline, those randomized to celecoxib had a 20% increase per year in BCC burden or extent, significantly less than the 50% annual increase in burden in controls. In the 24 patients with 15 or more BCCs at baseline, however, celecoxib wasn't significantly better than placebo (Cancer Prev. Res. 2010;3:25-34).

This is an exciting development involving a low-risk chemopreventive agent for use in patients genetically predisposed to multiple BCCs, in Dr. Hofbauer's view.

Animal studies have shown that inhibition of ornithine decarboxylase by alpha-difluoromethylornithine (DFMO) diminishes tissue concentrations of the neoplasia-promoting polyamines spermidine and putrescine. These observations led to a phase III randomized, double-blind, placebo-controlled study of NMSC prevention via DFMO at 500 mg/m2 per day for 4-5 years.

The trial, led by investigators at the University of Wisconsin Cancer Center, Madison, involved 291 subjects with a mean age of 61 years and an average of 4.5 previous NMSCs.

After 1,200 patient-years of follow-up, there were 260 new nonmelanoma skin cancers in the DFMO group and 363 in controls, a nonsignificant difference (P = .069). Upon closer examination, however, the investigators noted that while DFMO had no impact on the incidence of new SCCs, it did have a significant inhibitory effect on new BCCs. There were 163 in the DFMO group, compared with 243 in controls. This translated into an event rate of 0.28 new BCCs per patient per year in the DFMO group, compared with 0.40 per patient per year with placebo (P =.03).

Compliance with DFMO was deemed excellent, at greater than 90%. The chief side effect was mild ototoxicity identified in serial audiometric examinations (Cancer Prev. Res. 2010;3:35-47).

Mutations or amplification of the epidermal growth factor receptor (EGFR) have been linked to cancers of the breast, colon, lung, and cervix, as well as to melanoma and SCC. Most keratinocytes express EGFR, and this expression is greatest in the keratinocytes located in hair follicle epithelium and the basal and suprabasal portions of the epidermis, which is where the action is in SCC.

For this reason, agents that specifically target the EGFR/mitogen-activated protein kinase signaling pathway are under scrutiny as potential treatments for SCC. A fair number of such agents are already approved for the treatment of other malignancies, including the monoclonal antibodies panitumumab (Vectibix) and cetuximab (Erbitux) and the small molecules gefitinib (Iressa) and erlotinib (Tarceva). Many more are in the pipeline.

 

Leading the way for SCC is cetuximab, which has been approved by the Food and Drug Administration as single-agent therapy for recurrent or metastatic disease and in combination with radiation therapy for locally advanced SCC of the head and neck.

But targeted therapy has its shortcomings, Dr. Hofbauer stressed. "These molecules are not as specific or targeted as we'd like them to be. That can lead to untoward outcomes," he noted.

Dr. Hofbauer cited as an example sorafenib (Nexavar), an oral inhibitor of multiple tyrosine protein kinases. Sorafenib is approved for the treatment of advanced renal cell carcinoma and advanced hepatocellular carcinoma. But in addition to its better-known dermatologic side effects, such as hand-foot syndrome, sorafenib also apparently induces SCC or inflammation of actinic keratosis in about 7% of treated patients (Clin. Genitourin. Cancer 2009;7:20-3). The likely mechanism involves impairment of skin immunosurveillance due to reduced dendritic cell function and a diminished primary immune response, he said.

Dr. Hofbauer reported having no conflicts of interest.

MADRID - Targeted therapy - the glamour area of cancer research in recent years - has arrived at the doorstep of nonmelanoma skin cancer in a big way.

"There are at least 24 open trials of targeted therapies for nonmelanoma skin cancer listed now at www.clinicaltrials.gov," Dr. Gunther Hofbauer noted at the 13th World Congress on Cancers of the Skin, sponsored by the Skin Cancer Foundation.

The mainstays of targeted cancer therapy are monoclonal antibodies and oral small molecules directed at specific enzyme pathways and receptors identified as important in carcinogenesis or tumor growth. These agents are designed to be considerably less toxic than standard chemotherapy.

Dr. Hofbauer, a dermatologist at the University of Zurich, highlighted a handful of the most promising investigational targeted agents for treatment and chemoprevention of nonmelanoma skin cancer. These include hedgehog inhibitors, cyclooxygenase inhibitors, and alpha-difluoromethylornithine for basal cell carcinoma (BCC), and epidermal growth factor receptor inhibitors for squamous cell carcinoma (SCC).

Furthest along in the developmental pipeline are the hedgehog inhibitors.

Most BCCs have mutations in the hedgehog signaling pathway, leading to activation of the smoothened homologue, with resultant promotion of tumor growth. The oral smoothened homologue inhibitor GDC-0449 being developed by Genentech selectively inhibits the hedgehog pathway, making it of particular interest as a potential targeted therapy for BCC and a number of other malignancies, including medulloblastoma, colon cancer, and pancreatic cancer, he explained.

Last year, American investigators reported a phase I study in which 33 patients with unresectable metastastic or locally advanced BCC were treated with GDC-0449. Sixteen had partial and 2 had complete responses by the standardized Response Evaluation Criteria in Solid Tumors (RECIST). Eleven others had stable disease during the 10-month study, while 4 had progressive disease (N. Engl. J. Med. 2009;361:1,164-72).

"In general, it looks like the longer people are on this drug, the more profit they have--and the profit seems to be sustained," Dr. Hofbauer observed.

BCCs are known to secrete prostaglandin E2, which acts upon stromal cells in the cancer's vicinity to promote tumor growth. Reasoning that this process might be amenable to pharmacologic inhibition of cyclooxygenase enzymes in the skin, investigators at the Children's Hospital of Oakland (Calif.) Research Institute conducted a 3-year, double-blind, randomized clinical trial of oral celecoxib versus placebo in 60 patients with the basal cell nevus syndrome.

Celecoxib showed considerable promise in the patients with less severe disease. That is, among the 36 patients with less than 15 BCCs at baseline, those randomized to celecoxib had a 20% increase per year in BCC burden or extent, significantly less than the 50% annual increase in burden in controls. In the 24 patients with 15 or more BCCs at baseline, however, celecoxib wasn't significantly better than placebo (Cancer Prev. Res. 2010;3:25-34).

This is an exciting development involving a low-risk chemopreventive agent for use in patients genetically predisposed to multiple BCCs, in Dr. Hofbauer's view.

Animal studies have shown that inhibition of ornithine decarboxylase by alpha-difluoromethylornithine (DFMO) diminishes tissue concentrations of the neoplasia-promoting polyamines spermidine and putrescine. These observations led to a phase III randomized, double-blind, placebo-controlled study of NMSC prevention via DFMO at 500 mg/m2 per day for 4-5 years.

The trial, led by investigators at the University of Wisconsin Cancer Center, Madison, involved 291 subjects with a mean age of 61 years and an average of 4.5 previous NMSCs.

After 1,200 patient-years of follow-up, there were 260 new nonmelanoma skin cancers in the DFMO group and 363 in controls, a nonsignificant difference (P = .069). Upon closer examination, however, the investigators noted that while DFMO had no impact on the incidence of new SCCs, it did have a significant inhibitory effect on new BCCs. There were 163 in the DFMO group, compared with 243 in controls. This translated into an event rate of 0.28 new BCCs per patient per year in the DFMO group, compared with 0.40 per patient per year with placebo (P =.03).

Compliance with DFMO was deemed excellent, at greater than 90%. The chief side effect was mild ototoxicity identified in serial audiometric examinations (Cancer Prev. Res. 2010;3:35-47).

Mutations or amplification of the epidermal growth factor receptor (EGFR) have been linked to cancers of the breast, colon, lung, and cervix, as well as to melanoma and SCC. Most keratinocytes express EGFR, and this expression is greatest in the keratinocytes located in hair follicle epithelium and the basal and suprabasal portions of the epidermis, which is where the action is in SCC.

For this reason, agents that specifically target the EGFR/mitogen-activated protein kinase signaling pathway are under scrutiny as potential treatments for SCC. A fair number of such agents are already approved for the treatment of other malignancies, including the monoclonal antibodies panitumumab (Vectibix) and cetuximab (Erbitux) and the small molecules gefitinib (Iressa) and erlotinib (Tarceva). Many more are in the pipeline.

 

Leading the way for SCC is cetuximab, which has been approved by the Food and Drug Administration as single-agent therapy for recurrent or metastatic disease and in combination with radiation therapy for locally advanced SCC of the head and neck.

But targeted therapy has its shortcomings, Dr. Hofbauer stressed. "These molecules are not as specific or targeted as we'd like them to be. That can lead to untoward outcomes," he noted.

Dr. Hofbauer cited as an example sorafenib (Nexavar), an oral inhibitor of multiple tyrosine protein kinases. Sorafenib is approved for the treatment of advanced renal cell carcinoma and advanced hepatocellular carcinoma. But in addition to its better-known dermatologic side effects, such as hand-foot syndrome, sorafenib also apparently induces SCC or inflammation of actinic keratosis in about 7% of treated patients (Clin. Genitourin. Cancer 2009;7:20-3). The likely mechanism involves impairment of skin immunosurveillance due to reduced dendritic cell function and a diminished primary immune response, he said.

Dr. Hofbauer reported having no conflicts of interest.

MADRID - Solar UV radiation may protect against melanoma of the vulva, a new international study suggests.

This and other recent studies have demonstrated that UV radiation is a double-edged sword in melanoma, acting predictably as a well-established risk factor for cutaneous melanoma in susceptible individuals, while paradoxically decreasing the incidence of melanoma at non-sun-exposed sites, Dr. Isabel Longo reported at the 13th World Congress on Cancers of the Skin.

©Sly/Fotolia.com

Sunshine's most likely protective mechanism against vulvar melanoma involves UV's stimulation of vitamin D synthesis, said Dr. Longo, a dermatologist at Gregorio Marañón University Hospital, Madrid.

The vulvar melanoma study, "Where the Sun Does Not Shine: Is Sunshine Protective Against Melanoma of the Vulva?'" was led by Johan Moan, Ph.D., of the Institute for Cancer Research at the Norwegian Radium Hospital, Oslo.

He and his coworkers analyzed melanoma trends over time and geography in the United States, Sweden, Germany, and Australia. They concluded that while the incidence of cutaneous melanoma on sun-exposed skin sites increased with decreasing latitude - moving north to south in the Northern Hemisphere and oppositely in the Southern Hemisphere - the incidence of vulvar melanoma followed the opposite latitudinal trend.

The most likely explanation, according to the investigators, is that solar UV-stimulated vitamin D synthesis in sun-exposed skin - greatest at latitudes closest to the equator - boosts serum levels of the vitamin, providing protection against melanoma at non-sun-exposed sites such as the vulva. However, these higher serum vitamin D levels are insufficient to protect against solar UV's cutaneous melanoma-promoting effect (J. Photochem. Photobiol. B. March 12, 2010; Epub ahead of print PMID: 20359907).

When the investigators analyzed melanoma incidence trends in the four countries over time, they observed that whenever cutaneous melanoma rates flattened or decreased - presumably in response to public health campaigns regarding sun protection - vulvar melanoma rates increased.

Dr. Moan and colleagues also recently demonstrated in an analysis of Norwegian Cancer Registry data for 1966-2007 that cutaneous melanoma rates for all body sites exhibited a strong latitude gradient, with a 2- to 2.5-fold greater incidence in the south of the Scandinavian nation as compared to the north (J. Photochem. Photobiol. B. April 6, 2010; Epub ahead of print PMID: 20430639).

Dr. Longo cited evidence suggesting that higher serum vitamin D levels may improve melanoma survival. For example, in a prospective cohort study involving 872 melanoma patients in the United Kingdom., investigators found that higher serum vitamin D levels at diagnosis were associated with a thinner tumor Breslow thickness and also - independent of Breslow thickness - with better survival (J. Clin. Oncol. 2009;27:5439-44).

This work followed an earlier study that found sun exposure to be inversely associated with death from melanoma in 528 patients followed for 5 years. Patients with evidence of solar elastosis had a 50% relative risk reduction, while those with a history of intermittent sun exposure or ever having been severely burned were 40% less likely to die from their skin cancer. Proposed mechanisms involve vitamin D's antiproliferative and proapoptotic effects. Alternatively, sun exposure may trigger less aggressive melanomas by enhancing DNA repair capability (J. Natl. Cancer Inst. 2005;97:195-9).

As to how to advise patients to increase their serum vitamin D levels, Dr. Longo was emphatic: no tanning beds."The high UVA levels and risk of sunburn overwhelms any possible benefit regarding vitamin D metabolism," she said.

Dr. Longo stressed that "not much" sun exposure is needed to achieve optimal serum vitamin D levels. UV-induced vitamin D synthesis is maximal at less than 1 minimal erythema dose - that is, a 5-minute exposure in the summer for fair-skinned individuals (10-30 minutes if sunscreen is used).

Patients can be reassured that regular use of high SPF sunscreens will not lower their serum vitamin D level. A review of the published evidence by investigators at the University of Edinburgh reached this conclusion based upon two findings: people generally apply sunscreen inadequately, and they tend to spend more time in the sun than nonusers of sunscreens (Br. J. Dermatol. 2009;161:732-6).

More research is clearly needed on the risks and benefits of enhancing vitamin D through sun exposure. Dr. Longo said expectations are high in Europe that important insights will come from the large, ongoing, European Union-funded ICEPURE study (Impact of Climatic and Environmental factors on Personal Ultraviolet Radiation Exposure and human health).

Dr. Longo reported no conflicts of interest.

MADRID - Solar UV radiation may protect against melanoma of the vulva, a new international study suggests.

This and other recent studies have demonstrated that UV radiation is a double-edged sword in melanoma, acting predictably as a well-established risk factor for cutaneous melanoma in susceptible individuals, while paradoxically decreasing the incidence of melanoma at non-sun-exposed sites, Dr. Isabel Longo reported at the 13th World Congress on Cancers of the Skin.

©Sly/Fotolia.com

Sunshine's most likely protective mechanism against vulvar melanoma involves UV's stimulation of vitamin D synthesis, said Dr. Longo, a dermatologist at Gregorio Marañón University Hospital, Madrid.

The vulvar melanoma study, "Where the Sun Does Not Shine: Is Sunshine Protective Against Melanoma of the Vulva?'" was led by Johan Moan, Ph.D., of the Institute for Cancer Research at the Norwegian Radium Hospital, Oslo.

He and his coworkers analyzed melanoma trends over time and geography in the United States, Sweden, Germany, and Australia. They concluded that while the incidence of cutaneous melanoma on sun-exposed skin sites increased with decreasing latitude - moving north to south in the Northern Hemisphere and oppositely in the Southern Hemisphere - the incidence of vulvar melanoma followed the opposite latitudinal trend.

The most likely explanation, according to the investigators, is that solar UV-stimulated vitamin D synthesis in sun-exposed skin - greatest at latitudes closest to the equator - boosts serum levels of the vitamin, providing protection against melanoma at non-sun-exposed sites such as the vulva. However, these higher serum vitamin D levels are insufficient to protect against solar UV's cutaneous melanoma-promoting effect (J. Photochem. Photobiol. B. March 12, 2010; Epub ahead of print PMID: 20359907).

When the investigators analyzed melanoma incidence trends in the four countries over time, they observed that whenever cutaneous melanoma rates flattened or decreased - presumably in response to public health campaigns regarding sun protection - vulvar melanoma rates increased.

Dr. Moan and colleagues also recently demonstrated in an analysis of Norwegian Cancer Registry data for 1966-2007 that cutaneous melanoma rates for all body sites exhibited a strong latitude gradient, with a 2- to 2.5-fold greater incidence in the south of the Scandinavian nation as compared to the north (J. Photochem. Photobiol. B. April 6, 2010; Epub ahead of print PMID: 20430639).

Dr. Longo cited evidence suggesting that higher serum vitamin D levels may improve melanoma survival. For example, in a prospective cohort study involving 872 melanoma patients in the United Kingdom., investigators found that higher serum vitamin D levels at diagnosis were associated with a thinner tumor Breslow thickness and also - independent of Breslow thickness - with better survival (J. Clin. Oncol. 2009;27:5439-44).

This work followed an earlier study that found sun exposure to be inversely associated with death from melanoma in 528 patients followed for 5 years. Patients with evidence of solar elastosis had a 50% relative risk reduction, while those with a history of intermittent sun exposure or ever having been severely burned were 40% less likely to die from their skin cancer. Proposed mechanisms involve vitamin D's antiproliferative and proapoptotic effects. Alternatively, sun exposure may trigger less aggressive melanomas by enhancing DNA repair capability (J. Natl. Cancer Inst. 2005;97:195-9).

As to how to advise patients to increase their serum vitamin D levels, Dr. Longo was emphatic: no tanning beds."The high UVA levels and risk of sunburn overwhelms any possible benefit regarding vitamin D metabolism," she said.

Dr. Longo stressed that "not much" sun exposure is needed to achieve optimal serum vitamin D levels. UV-induced vitamin D synthesis is maximal at less than 1 minimal erythema dose - that is, a 5-minute exposure in the summer for fair-skinned individuals (10-30 minutes if sunscreen is used).

Patients can be reassured that regular use of high SPF sunscreens will not lower their serum vitamin D level. A review of the published evidence by investigators at the University of Edinburgh reached this conclusion based upon two findings: people generally apply sunscreen inadequately, and they tend to spend more time in the sun than nonusers of sunscreens (Br. J. Dermatol. 2009;161:732-6).

More research is clearly needed on the risks and benefits of enhancing vitamin D through sun exposure. Dr. Longo said expectations are high in Europe that important insights will come from the large, ongoing, European Union-funded ICEPURE study (Impact of Climatic and Environmental factors on Personal Ultraviolet Radiation Exposure and human health).

Dr. Longo reported no conflicts of interest.

MADRID - Solar UV radiation may protect against melanoma of the vulva, a new international study suggests.

This and other recent studies have demonstrated that UV radiation is a double-edged sword in melanoma, acting predictably as a well-established risk factor for cutaneous melanoma in susceptible individuals, while paradoxically decreasing the incidence of melanoma at non-sun-exposed sites, Dr. Isabel Longo reported at the 13th World Congress on Cancers of the Skin.

©Sly/Fotolia.com

Sunshine's most likely protective mechanism against vulvar melanoma involves UV's stimulation of vitamin D synthesis, said Dr. Longo, a dermatologist at Gregorio Marañón University Hospital, Madrid.

The vulvar melanoma study, "Where the Sun Does Not Shine: Is Sunshine Protective Against Melanoma of the Vulva?'" was led by Johan Moan, Ph.D., of the Institute for Cancer Research at the Norwegian Radium Hospital, Oslo.

He and his coworkers analyzed melanoma trends over time and geography in the United States, Sweden, Germany, and Australia. They concluded that while the incidence of cutaneous melanoma on sun-exposed skin sites increased with decreasing latitude - moving north to south in the Northern Hemisphere and oppositely in the Southern Hemisphere - the incidence of vulvar melanoma followed the opposite latitudinal trend.

The most likely explanation, according to the investigators, is that solar UV-stimulated vitamin D synthesis in sun-exposed skin - greatest at latitudes closest to the equator - boosts serum levels of the vitamin, providing protection against melanoma at non-sun-exposed sites such as the vulva. However, these higher serum vitamin D levels are insufficient to protect against solar UV's cutaneous melanoma-promoting effect (J. Photochem. Photobiol. B. March 12, 2010; Epub ahead of print PMID: 20359907).

When the investigators analyzed melanoma incidence trends in the four countries over time, they observed that whenever cutaneous melanoma rates flattened or decreased - presumably in response to public health campaigns regarding sun protection - vulvar melanoma rates increased.

Dr. Moan and colleagues also recently demonstrated in an analysis of Norwegian Cancer Registry data for 1966-2007 that cutaneous melanoma rates for all body sites exhibited a strong latitude gradient, with a 2- to 2.5-fold greater incidence in the south of the Scandinavian nation as compared to the north (J. Photochem. Photobiol. B. April 6, 2010; Epub ahead of print PMID: 20430639).

Dr. Longo cited evidence suggesting that higher serum vitamin D levels may improve melanoma survival. For example, in a prospective cohort study involving 872 melanoma patients in the United Kingdom., investigators found that higher serum vitamin D levels at diagnosis were associated with a thinner tumor Breslow thickness and also - independent of Breslow thickness - with better survival (J. Clin. Oncol. 2009;27:5439-44).

This work followed an earlier study that found sun exposure to be inversely associated with death from melanoma in 528 patients followed for 5 years. Patients with evidence of solar elastosis had a 50% relative risk reduction, while those with a history of intermittent sun exposure or ever having been severely burned were 40% less likely to die from their skin cancer. Proposed mechanisms involve vitamin D's antiproliferative and proapoptotic effects. Alternatively, sun exposure may trigger less aggressive melanomas by enhancing DNA repair capability (J. Natl. Cancer Inst. 2005;97:195-9).

As to how to advise patients to increase their serum vitamin D levels, Dr. Longo was emphatic: no tanning beds."The high UVA levels and risk of sunburn overwhelms any possible benefit regarding vitamin D metabolism," she said.

Dr. Longo stressed that "not much" sun exposure is needed to achieve optimal serum vitamin D levels. UV-induced vitamin D synthesis is maximal at less than 1 minimal erythema dose - that is, a 5-minute exposure in the summer for fair-skinned individuals (10-30 minutes if sunscreen is used).

Patients can be reassured that regular use of high SPF sunscreens will not lower their serum vitamin D level. A review of the published evidence by investigators at the University of Edinburgh reached this conclusion based upon two findings: people generally apply sunscreen inadequately, and they tend to spend more time in the sun than nonusers of sunscreens (Br. J. Dermatol. 2009;161:732-6).

More research is clearly needed on the risks and benefits of enhancing vitamin D through sun exposure. Dr. Longo said expectations are high in Europe that important insights will come from the large, ongoing, European Union-funded ICEPURE study (Impact of Climatic and Environmental factors on Personal Ultraviolet Radiation Exposure and human health).

Dr. Longo reported no conflicts of interest.

NEW YORK – Recipients of pancreas transplants had a 19.6% cumulative incidence of developing skin cancer 10 years after transplant.

Moreover, those patients who developed squamous cell carcinoma (SCC) following transplant were found to have a 56% likelihood of developing a second SCC within 2 years, while patients who developed basal cell carcinoma (BCC) had a 36% chance of recurrence at 2 years.

The data, presented in a poster at the annual meeting of the American College of Mohs Surgery, show that “intensive educational and preventative strategies should be targeted at the pancreas transplant population,” according to Dr. Joshua Spanogle, a resident in the department of dermatology at the Mayo Clinic in Rochester, Minnesota.

Dr. Spanogle and his colleagues looked at 216 pancreas transplant recipients seen at a tertiary care center between 1996 and 2007. About half of the subjects were male, and the average age was 43 years, with a range of 21-71 years.

Overall, 107 patients received their pancreas transplant following a prior kidney transplant and were referred to as the “pancreas after kidney” group. A total of 67 patients received a pancreas transplant and did not receive a new kidney, and were known as the “pancreas transplant alone” group. Forty-two patients were in the “simultaneous pancreas-kidney” transplant group.

For all transplant recipients, the cumulative incidence of developing any skin cancer was 4.7% by 2 years. The cumulative incidence rose to 12.7% by 5 years and 19.6% by 10 years post transplant, Dr. Spanogle reported.

Looking at SCC specifically, the cumulative incidence was 2.8% at 2 years, 10.3% at 5 years, and 16.7% at 10 years. For BCC, the cumulative incidence rates were 2.4%, 7.8%, and 17.4% at 2, 5, and 10 years, respectively, he wrote.

Once patients were found to have an SCC, however, the chance of developing a second SCC within 2 years rose: There was a 56% cumulative incidence of subsequent SCC in that population. The risk for a second BCC after an initial post-transplant BCC diagnosis was also high, though less dramatic: The cumulative incidence for BCCs in the post-transplant, post-BCC-diagnosis population was 36%.

“None of the following variables were associated with an increased risk of skin cancer: type of transplant, induction therapy, initial immunosuppressive regimen, rejection status, or sex,” he pointed out. Only age was a significant predictor of the development of skin cancer, with a hazard ratio of 1.05.

Dr. Spanogle stated that he had no conflicts of interest to disclose.

NEW YORK – Recipients of pancreas transplants had a 19.6% cumulative incidence of developing skin cancer 10 years after transplant.

Moreover, those patients who developed squamous cell carcinoma (SCC) following transplant were found to have a 56% likelihood of developing a second SCC within 2 years, while patients who developed basal cell carcinoma (BCC) had a 36% chance of recurrence at 2 years.

The data, presented in a poster at the annual meeting of the American College of Mohs Surgery, show that “intensive educational and preventative strategies should be targeted at the pancreas transplant population,” according to Dr. Joshua Spanogle, a resident in the department of dermatology at the Mayo Clinic in Rochester, Minnesota.

Dr. Spanogle and his colleagues looked at 216 pancreas transplant recipients seen at a tertiary care center between 1996 and 2007. About half of the subjects were male, and the average age was 43 years, with a range of 21-71 years.

Overall, 107 patients received their pancreas transplant following a prior kidney transplant and were referred to as the “pancreas after kidney” group. A total of 67 patients received a pancreas transplant and did not receive a new kidney, and were known as the “pancreas transplant alone” group. Forty-two patients were in the “simultaneous pancreas-kidney” transplant group.

For all transplant recipients, the cumulative incidence of developing any skin cancer was 4.7% by 2 years. The cumulative incidence rose to 12.7% by 5 years and 19.6% by 10 years post transplant, Dr. Spanogle reported.

Looking at SCC specifically, the cumulative incidence was 2.8% at 2 years, 10.3% at 5 years, and 16.7% at 10 years. For BCC, the cumulative incidence rates were 2.4%, 7.8%, and 17.4% at 2, 5, and 10 years, respectively, he wrote.

Once patients were found to have an SCC, however, the chance of developing a second SCC within 2 years rose: There was a 56% cumulative incidence of subsequent SCC in that population. The risk for a second BCC after an initial post-transplant BCC diagnosis was also high, though less dramatic: The cumulative incidence for BCCs in the post-transplant, post-BCC-diagnosis population was 36%.

“None of the following variables were associated with an increased risk of skin cancer: type of transplant, induction therapy, initial immunosuppressive regimen, rejection status, or sex,” he pointed out. Only age was a significant predictor of the development of skin cancer, with a hazard ratio of 1.05.

Dr. Spanogle stated that he had no conflicts of interest to disclose.

NEW YORK – Recipients of pancreas transplants had a 19.6% cumulative incidence of developing skin cancer 10 years after transplant.

Moreover, those patients who developed squamous cell carcinoma (SCC) following transplant were found to have a 56% likelihood of developing a second SCC within 2 years, while patients who developed basal cell carcinoma (BCC) had a 36% chance of recurrence at 2 years.

The data, presented in a poster at the annual meeting of the American College of Mohs Surgery, show that “intensive educational and preventative strategies should be targeted at the pancreas transplant population,” according to Dr. Joshua Spanogle, a resident in the department of dermatology at the Mayo Clinic in Rochester, Minnesota.

Dr. Spanogle and his colleagues looked at 216 pancreas transplant recipients seen at a tertiary care center between 1996 and 2007. About half of the subjects were male, and the average age was 43 years, with a range of 21-71 years.

Overall, 107 patients received their pancreas transplant following a prior kidney transplant and were referred to as the “pancreas after kidney” group. A total of 67 patients received a pancreas transplant and did not receive a new kidney, and were known as the “pancreas transplant alone” group. Forty-two patients were in the “simultaneous pancreas-kidney” transplant group.

For all transplant recipients, the cumulative incidence of developing any skin cancer was 4.7% by 2 years. The cumulative incidence rose to 12.7% by 5 years and 19.6% by 10 years post transplant, Dr. Spanogle reported.

Looking at SCC specifically, the cumulative incidence was 2.8% at 2 years, 10.3% at 5 years, and 16.7% at 10 years. For BCC, the cumulative incidence rates were 2.4%, 7.8%, and 17.4% at 2, 5, and 10 years, respectively, he wrote.

Once patients were found to have an SCC, however, the chance of developing a second SCC within 2 years rose: There was a 56% cumulative incidence of subsequent SCC in that population. The risk for a second BCC after an initial post-transplant BCC diagnosis was also high, though less dramatic: The cumulative incidence for BCCs in the post-transplant, post-BCC-diagnosis population was 36%.

“None of the following variables were associated with an increased risk of skin cancer: type of transplant, induction therapy, initial immunosuppressive regimen, rejection status, or sex,” he pointed out. Only age was a significant predictor of the development of skin cancer, with a hazard ratio of 1.05.

Dr. Spanogle stated that he had no conflicts of interest to disclose.

MADRID - Sunscreens alone are not sufficient to prevent the development of melanocytic nevi in children, with consequent increased risk for melanoma later in life, results of numerous studies indicate.

"Sun avoidance and clothing are required for primary prevention in children," Dr. Claus Garbe stressed at the 13th World Congress on Cancers of the Skin. This concept is not yet understood by the public at large.

"The public supposes that by using sunscreens regularly they protect themselves from cancer, but it's a very poor quality protection," said Dr. Garbe, professor of dermatology and head of the division of dermato-oncology at Eberhard Karls University, Tübingen, Germany.

At least half a dozen studies dating back to the early 1990s have established that the most important risk factor for melanoma is a person's total number of melanocytic nevi. With growing numbers of melanocytic nevi the melanoma risk increases almost linearly. Another independent risk factor is the presence of atypical nevi. These risk factors are multiplicative, such that individuals with more than 100 melanocytic nevi and at least 5 atypical nevi are at close to 50-fold increased risk for melanoma.

"The message of these investigations is we are able to identify easily patients who are at elevated risk for melanoma development. That's the case for about 5% of the Caucasian population. These are the persons we should have in a serial examination program for early melanoma detection," he said at the meeting sponsored by the Skin Cancer Foundation.

In a cross-sectional study of 1,812 German children aged 2-7 years and their parents, Dr. Garbe and coworkers found that the melanocytic nevi counts increased from a median of 2 at age 2 years to 20 at age 7.

Nevi counts were strongly related to the number of weeks spent on holidays in sunny climes, the amount of time spent in summer outdoor activities without sunburns, facial freckling, skin type, parental ethnicity, and the number of parental moles - but not to previous sunburns (Cancer 2003;97:628-38).

In a subsequent analysis, the investigators found no significant protective effect for sunscreen use on melanocytic nevi counts, whereas a regular practice of wearing clothing at the beach or pool was inversely associated with the number of melanocytic nevi (Am. J. Epidemiol. 2005;161:620-7).

Next came a longitudinal interventional study in which Dr. Garbe and coinvestigators randomized 1,232 young German children in two cities to one of three study arms, each lasting 3 years: parental educational sessions three times per year on the importance of sun protection; parental education plus free broad-spectrum SPF 25 sunscreen; or a control group in which parents were informed of the importance of sun protection measures for their children only at an initial meeting. Sunscreen use proved to have no impact on the increase in melanocytic nevi counts over time, which was similar in all three groups (Int. J. Cancer 2005;116:755-61).

Australian investigators have also found that regular use of sunscreen was not associated with the number of melanocytic nevi in an observational study involving 1,623 children (Cancer Epidemiol. Biomarkers Prev. 2005;14:2873-6).

The key factor related to the number of melanocytic nevi was the amount of time spent outdoors between 11 a.m. and 2 p.m. Children whose backs were covered by clothing less than 70% of the time they were outdoors had 53% more nevi than those whose backs were always covered.

This finding, coupled with the German studies, led to the ongoing North Queensland Sun-Safe Clothing Study, in which 652 Caucasian Aussie children up to age 3 years were randomized to parental education plus free UV-protective beach suits for the children or to usual care.

At baseline the investigators didn't find a significant relationship between reported use of sunscreen and melanocytic nevi counts (Am. J. Epidemiol. 2005;161:536-45). Long-term follow-up results with the number of new melanocytic nevi as primary endpoint are due soon, and Dr. Garbe anticipates a positive result.

Asked why sunscreen usage doesn't prevent melanocytic nevi, he replied the main reason is that sunscreens are far less efficient than their measured SPF rating would suggest.

"The SPF is measured using 2 mg of sunscreen per square centimeter of body surface," he explained. "That would mean that with a roughly 1.5m2 body surface, after subtracting the hairy parts, we would need 30 g for a one-time use of sunscreen, which is one tube. Nobody does this. And the SPF decreases in logarithmic fashion, so if you use 7.5g of a sunscreen with an SPF of 30-50, you only have an SPF of 3-4."

 

Dr. Garbe reported having no financial conflicts in connection with these studies.

MADRID - Sunscreens alone are not sufficient to prevent the development of melanocytic nevi in children, with consequent increased risk for melanoma later in life, results of numerous studies indicate.

"Sun avoidance and clothing are required for primary prevention in children," Dr. Claus Garbe stressed at the 13th World Congress on Cancers of the Skin. This concept is not yet understood by the public at large.

"The public supposes that by using sunscreens regularly they protect themselves from cancer, but it's a very poor quality protection," said Dr. Garbe, professor of dermatology and head of the division of dermato-oncology at Eberhard Karls University, Tübingen, Germany.

At least half a dozen studies dating back to the early 1990s have established that the most important risk factor for melanoma is a person's total number of melanocytic nevi. With growing numbers of melanocytic nevi the melanoma risk increases almost linearly. Another independent risk factor is the presence of atypical nevi. These risk factors are multiplicative, such that individuals with more than 100 melanocytic nevi and at least 5 atypical nevi are at close to 50-fold increased risk for melanoma.

"The message of these investigations is we are able to identify easily patients who are at elevated risk for melanoma development. That's the case for about 5% of the Caucasian population. These are the persons we should have in a serial examination program for early melanoma detection," he said at the meeting sponsored by the Skin Cancer Foundation.

In a cross-sectional study of 1,812 German children aged 2-7 years and their parents, Dr. Garbe and coworkers found that the melanocytic nevi counts increased from a median of 2 at age 2 years to 20 at age 7.

Nevi counts were strongly related to the number of weeks spent on holidays in sunny climes, the amount of time spent in summer outdoor activities without sunburns, facial freckling, skin type, parental ethnicity, and the number of parental moles - but not to previous sunburns (Cancer 2003;97:628-38).

In a subsequent analysis, the investigators found no significant protective effect for sunscreen use on melanocytic nevi counts, whereas a regular practice of wearing clothing at the beach or pool was inversely associated with the number of melanocytic nevi (Am. J. Epidemiol. 2005;161:620-7).

Next came a longitudinal interventional study in which Dr. Garbe and coinvestigators randomized 1,232 young German children in two cities to one of three study arms, each lasting 3 years: parental educational sessions three times per year on the importance of sun protection; parental education plus free broad-spectrum SPF 25 sunscreen; or a control group in which parents were informed of the importance of sun protection measures for their children only at an initial meeting. Sunscreen use proved to have no impact on the increase in melanocytic nevi counts over time, which was similar in all three groups (Int. J. Cancer 2005;116:755-61).

Australian investigators have also found that regular use of sunscreen was not associated with the number of melanocytic nevi in an observational study involving 1,623 children (Cancer Epidemiol. Biomarkers Prev. 2005;14:2873-6).

The key factor related to the number of melanocytic nevi was the amount of time spent outdoors between 11 a.m. and 2 p.m. Children whose backs were covered by clothing less than 70% of the time they were outdoors had 53% more nevi than those whose backs were always covered.

This finding, coupled with the German studies, led to the ongoing North Queensland Sun-Safe Clothing Study, in which 652 Caucasian Aussie children up to age 3 years were randomized to parental education plus free UV-protective beach suits for the children or to usual care.

At baseline the investigators didn't find a significant relationship between reported use of sunscreen and melanocytic nevi counts (Am. J. Epidemiol. 2005;161:536-45). Long-term follow-up results with the number of new melanocytic nevi as primary endpoint are due soon, and Dr. Garbe anticipates a positive result.

Asked why sunscreen usage doesn't prevent melanocytic nevi, he replied the main reason is that sunscreens are far less efficient than their measured SPF rating would suggest.

"The SPF is measured using 2 mg of sunscreen per square centimeter of body surface," he explained. "That would mean that with a roughly 1.5m2 body surface, after subtracting the hairy parts, we would need 30 g for a one-time use of sunscreen, which is one tube. Nobody does this. And the SPF decreases in logarithmic fashion, so if you use 7.5g of a sunscreen with an SPF of 30-50, you only have an SPF of 3-4."

 

Dr. Garbe reported having no financial conflicts in connection with these studies.

MADRID - Sunscreens alone are not sufficient to prevent the development of melanocytic nevi in children, with consequent increased risk for melanoma later in life, results of numerous studies indicate.

"Sun avoidance and clothing are required for primary prevention in children," Dr. Claus Garbe stressed at the 13th World Congress on Cancers of the Skin. This concept is not yet understood by the public at large.

"The public supposes that by using sunscreens regularly they protect themselves from cancer, but it's a very poor quality protection," said Dr. Garbe, professor of dermatology and head of the division of dermato-oncology at Eberhard Karls University, Tübingen, Germany.

At least half a dozen studies dating back to the early 1990s have established that the most important risk factor for melanoma is a person's total number of melanocytic nevi. With growing numbers of melanocytic nevi the melanoma risk increases almost linearly. Another independent risk factor is the presence of atypical nevi. These risk factors are multiplicative, such that individuals with more than 100 melanocytic nevi and at least 5 atypical nevi are at close to 50-fold increased risk for melanoma.

"The message of these investigations is we are able to identify easily patients who are at elevated risk for melanoma development. That's the case for about 5% of the Caucasian population. These are the persons we should have in a serial examination program for early melanoma detection," he said at the meeting sponsored by the Skin Cancer Foundation.

In a cross-sectional study of 1,812 German children aged 2-7 years and their parents, Dr. Garbe and coworkers found that the melanocytic nevi counts increased from a median of 2 at age 2 years to 20 at age 7.

Nevi counts were strongly related to the number of weeks spent on holidays in sunny climes, the amount of time spent in summer outdoor activities without sunburns, facial freckling, skin type, parental ethnicity, and the number of parental moles - but not to previous sunburns (Cancer 2003;97:628-38).

In a subsequent analysis, the investigators found no significant protective effect for sunscreen use on melanocytic nevi counts, whereas a regular practice of wearing clothing at the beach or pool was inversely associated with the number of melanocytic nevi (Am. J. Epidemiol. 2005;161:620-7).

Next came a longitudinal interventional study in which Dr. Garbe and coinvestigators randomized 1,232 young German children in two cities to one of three study arms, each lasting 3 years: parental educational sessions three times per year on the importance of sun protection; parental education plus free broad-spectrum SPF 25 sunscreen; or a control group in which parents were informed of the importance of sun protection measures for their children only at an initial meeting. Sunscreen use proved to have no impact on the increase in melanocytic nevi counts over time, which was similar in all three groups (Int. J. Cancer 2005;116:755-61).

Australian investigators have also found that regular use of sunscreen was not associated with the number of melanocytic nevi in an observational study involving 1,623 children (Cancer Epidemiol. Biomarkers Prev. 2005;14:2873-6).

The key factor related to the number of melanocytic nevi was the amount of time spent outdoors between 11 a.m. and 2 p.m. Children whose backs were covered by clothing less than 70% of the time they were outdoors had 53% more nevi than those whose backs were always covered.

This finding, coupled with the German studies, led to the ongoing North Queensland Sun-Safe Clothing Study, in which 652 Caucasian Aussie children up to age 3 years were randomized to parental education plus free UV-protective beach suits for the children or to usual care.

At baseline the investigators didn't find a significant relationship between reported use of sunscreen and melanocytic nevi counts (Am. J. Epidemiol. 2005;161:536-45). Long-term follow-up results with the number of new melanocytic nevi as primary endpoint are due soon, and Dr. Garbe anticipates a positive result.

Asked why sunscreen usage doesn't prevent melanocytic nevi, he replied the main reason is that sunscreens are far less efficient than their measured SPF rating would suggest.

"The SPF is measured using 2 mg of sunscreen per square centimeter of body surface," he explained. "That would mean that with a roughly 1.5m2 body surface, after subtracting the hairy parts, we would need 30 g for a one-time use of sunscreen, which is one tube. Nobody does this. And the SPF decreases in logarithmic fashion, so if you use 7.5g of a sunscreen with an SPF of 30-50, you only have an SPF of 3-4."

 

Dr. Garbe reported having no financial conflicts in connection with these studies.

NEW YORK - The risk of developing a primary malignancy of the salivary gland, bone, prostate, and other areas is significantly--and in some cases dramatically--increased following a cutaneous melanoma diagnosis.

That's according to research by Dr. Joshua Spanogle, a resident in the department of dermatology at the Mayo Clinic in Rochester, Minn., presented during an abstract session at the American College of Mohs Surgery annual meeting.

Dr. Spanogle looked at data from the Surveillance, Epidemiology and End Results database (SEER) from 1973 to 2003, which included "over 1.3 million person years of observation," he said.

A total of 151,996 patients were found to have a cutaneous melanoma diagnosis during that period; 16,591 (11%) of these patients had a second documented primary malignancy sometime in the next 120 months. That observed rate was 32% higher than what would be expected among a healthy population in that time period, he said.

Further analysis of the results revealed that particular cancers carried a significantly higher risk than others.

The most striking, perhaps not surprisingly, is for a second primary cutaneous melanoma: there were 3,923 through 120 months of follow-up, for a standardized incidence ratio of 8.99. "This is the 600-pound elephant in the room," said Dr. Spanogle.

But other cancers have high standardized incidence ratios (SIRs) as well. Salivary gland malignancies following carcinoma had a SIR of 2.18 overall. Prostate cancer had a SIR of 1.13 following melanoma. Breast cancer showed a SIR of 1.07. And soft tissue cancers, including malignancies of the heart, had a SIR of 2.80.

On the other hand, "Quite a few cancers had a decreased incidence following melanoma," said Dr. Spanogle, including cancer of the liver (SIR 0.77), lungs (0.83), cervix (0.57), and pharynx (0.61).

That could be because risk factors for melanoma are associated with higher socioeconomic status, like fair skin and intermittent high intensity UV exposure (tanning), said Dr. Spanogle. In contrast, risk factors for lung cancer and liver cancer are associated with comorbidities commonly found in lower socioeconomic patients, like smoking and hepatitis.

Moreover, according to Dr. Spanogle, the risks of secondary cancers of the prostate gland, bone, soft tissue, and salivary gland remained elevated throughout the study period, "implying no surveillance bias."
Instead, he speculated that the link could be genetic, and said that future research into the possibility is warranted.

Dr. Spanogle reported having no disclosures relevant to his presentation. He added that this study has been accepted for publication in the Journal of the American Academy of Dermatology.

NEW YORK - The risk of developing a primary malignancy of the salivary gland, bone, prostate, and other areas is significantly--and in some cases dramatically--increased following a cutaneous melanoma diagnosis.

That's according to research by Dr. Joshua Spanogle, a resident in the department of dermatology at the Mayo Clinic in Rochester, Minn., presented during an abstract session at the American College of Mohs Surgery annual meeting.

Dr. Spanogle looked at data from the Surveillance, Epidemiology and End Results database (SEER) from 1973 to 2003, which included "over 1.3 million person years of observation," he said.

A total of 151,996 patients were found to have a cutaneous melanoma diagnosis during that period; 16,591 (11%) of these patients had a second documented primary malignancy sometime in the next 120 months. That observed rate was 32% higher than what would be expected among a healthy population in that time period, he said.

Further analysis of the results revealed that particular cancers carried a significantly higher risk than others.

The most striking, perhaps not surprisingly, is for a second primary cutaneous melanoma: there were 3,923 through 120 months of follow-up, for a standardized incidence ratio of 8.99. "This is the 600-pound elephant in the room," said Dr. Spanogle.

But other cancers have high standardized incidence ratios (SIRs) as well. Salivary gland malignancies following carcinoma had a SIR of 2.18 overall. Prostate cancer had a SIR of 1.13 following melanoma. Breast cancer showed a SIR of 1.07. And soft tissue cancers, including malignancies of the heart, had a SIR of 2.80.

On the other hand, "Quite a few cancers had a decreased incidence following melanoma," said Dr. Spanogle, including cancer of the liver (SIR 0.77), lungs (0.83), cervix (0.57), and pharynx (0.61).

That could be because risk factors for melanoma are associated with higher socioeconomic status, like fair skin and intermittent high intensity UV exposure (tanning), said Dr. Spanogle. In contrast, risk factors for lung cancer and liver cancer are associated with comorbidities commonly found in lower socioeconomic patients, like smoking and hepatitis.

Moreover, according to Dr. Spanogle, the risks of secondary cancers of the prostate gland, bone, soft tissue, and salivary gland remained elevated throughout the study period, "implying no surveillance bias."
Instead, he speculated that the link could be genetic, and said that future research into the possibility is warranted.

Dr. Spanogle reported having no disclosures relevant to his presentation. He added that this study has been accepted for publication in the Journal of the American Academy of Dermatology.

NEW YORK - The risk of developing a primary malignancy of the salivary gland, bone, prostate, and other areas is significantly--and in some cases dramatically--increased following a cutaneous melanoma diagnosis.

That's according to research by Dr. Joshua Spanogle, a resident in the department of dermatology at the Mayo Clinic in Rochester, Minn., presented during an abstract session at the American College of Mohs Surgery annual meeting.

Dr. Spanogle looked at data from the Surveillance, Epidemiology and End Results database (SEER) from 1973 to 2003, which included "over 1.3 million person years of observation," he said.

A total of 151,996 patients were found to have a cutaneous melanoma diagnosis during that period; 16,591 (11%) of these patients had a second documented primary malignancy sometime in the next 120 months. That observed rate was 32% higher than what would be expected among a healthy population in that time period, he said.

Further analysis of the results revealed that particular cancers carried a significantly higher risk than others.

The most striking, perhaps not surprisingly, is for a second primary cutaneous melanoma: there were 3,923 through 120 months of follow-up, for a standardized incidence ratio of 8.99. "This is the 600-pound elephant in the room," said Dr. Spanogle.

But other cancers have high standardized incidence ratios (SIRs) as well. Salivary gland malignancies following carcinoma had a SIR of 2.18 overall. Prostate cancer had a SIR of 1.13 following melanoma. Breast cancer showed a SIR of 1.07. And soft tissue cancers, including malignancies of the heart, had a SIR of 2.80.

On the other hand, "Quite a few cancers had a decreased incidence following melanoma," said Dr. Spanogle, including cancer of the liver (SIR 0.77), lungs (0.83), cervix (0.57), and pharynx (0.61).

That could be because risk factors for melanoma are associated with higher socioeconomic status, like fair skin and intermittent high intensity UV exposure (tanning), said Dr. Spanogle. In contrast, risk factors for lung cancer and liver cancer are associated with comorbidities commonly found in lower socioeconomic patients, like smoking and hepatitis.

Moreover, according to Dr. Spanogle, the risks of secondary cancers of the prostate gland, bone, soft tissue, and salivary gland remained elevated throughout the study period, "implying no surveillance bias."
Instead, he speculated that the link could be genetic, and said that future research into the possibility is warranted.

Dr. Spanogle reported having no disclosures relevant to his presentation. He added that this study has been accepted for publication in the Journal of the American Academy of Dermatology.

MIAMI -- A computer-automated device detected melanoma and high-grade dysplastic nevi lesions with 98% sensitivity in a large, prospective, multicenter study.

The digital dermoscopy device "sees" at different skin depths using 10 spectral bands ranging from 430 nm to 950 nm. The technology, which was more than a decade in development, objectively assesses up to 75 factors to differentiate melanoma from low-grade and high-grade dysplastic nevi, Dr. Gary D. Monheit said.

"This is an adjunct [that] I think will be helpful in the dermatologist's office, both because of the manpower issue and the difficult lesions we see," Dr. Monheit (photographed on the left) said at the annual meeting of the American Academy of Dermatology.

Dr. Monheit was an investigator at one of seven sites that used the MelaFind (Electro-Optical Sciences) to assess a total of 1,632 evaluable lesions. Lesions included 70 invasive melanomas and 57 melanoma in situ. "This is the largest prospective, blinded study ever conducted in melanoma detection," he noted.

The noninvasive device has a handheld wand for image capture at the point of care. Because of these features and a proprietary algorithm that analyzes multiple spectrums, it is "totally objective with a yes or no algorithm for excision," said Dr. Monheit, a private practice dermatologist in Birmingham, Ala., and an associate clinical professor in the departments of dermatology and ophthalmology at the University of Alabama at Birmingham. Detection is automatic with immediate feedback, Dr. Monheit said. "If we don't get a clear image, the machine tells us the image is not possible." The technology was developed after assessment of more than 10,000 pigmented lesions from more than 7,000 patients.

The aim of this "pivotal study" was to establish safety of the device and sensitivity for melanoma detection. No adverse events were reported, Dr. Monheit said. Lesions had to be pigmented with melanin, keratin, and/or blood. Clinical management was biopsy, he added.

For melanoma and high-grade dysplastic nevi, the device had a 98% sensitivity. "These are the [lesions] you will want to take out," Dr. Monheit said.

"At same time we should look at specificity--we do not want to biopsy every lesion that comes into our office," Dr. Monheit said. The specificity of the device was 9.4%, statistically superior to the dermatologist evaluations at 3.7%.

The results with the device were compared with prebiopsy investigator diagnoses and with an objective pathologic review of lesions by a panel of three dermatopathologists. If two of the three dermatopathologists concurred on the diagnosis, their consensus was final. The device had a 98% sensitivity for biopsy detection.

Dr. Monheit and the other study investigators also collected patient data, including age, gender, ethnicity, patient in-house or referred, and any risk factors for melanoma. Anatomic locations of the lesions were also noted.
This study provides "evidence for safety and efficacy for aid in evaluating pigmented lesions," Dr. Monheit said.

Disclosures: Dr. Monheit is a consultant and researcher for Electro-Optical Sciences.

MIAMI -- A computer-automated device detected melanoma and high-grade dysplastic nevi lesions with 98% sensitivity in a large, prospective, multicenter study.

The digital dermoscopy device "sees" at different skin depths using 10 spectral bands ranging from 430 nm to 950 nm. The technology, which was more than a decade in development, objectively assesses up to 75 factors to differentiate melanoma from low-grade and high-grade dysplastic nevi, Dr. Gary D. Monheit said.

"This is an adjunct [that] I think will be helpful in the dermatologist's office, both because of the manpower issue and the difficult lesions we see," Dr. Monheit (photographed on the left) said at the annual meeting of the American Academy of Dermatology.

Dr. Monheit was an investigator at one of seven sites that used the MelaFind (Electro-Optical Sciences) to assess a total of 1,632 evaluable lesions. Lesions included 70 invasive melanomas and 57 melanoma in situ. "This is the largest prospective, blinded study ever conducted in melanoma detection," he noted.

The noninvasive device has a handheld wand for image capture at the point of care. Because of these features and a proprietary algorithm that analyzes multiple spectrums, it is "totally objective with a yes or no algorithm for excision," said Dr. Monheit, a private practice dermatologist in Birmingham, Ala., and an associate clinical professor in the departments of dermatology and ophthalmology at the University of Alabama at Birmingham. Detection is automatic with immediate feedback, Dr. Monheit said. "If we don't get a clear image, the machine tells us the image is not possible." The technology was developed after assessment of more than 10,000 pigmented lesions from more than 7,000 patients.

The aim of this "pivotal study" was to establish safety of the device and sensitivity for melanoma detection. No adverse events were reported, Dr. Monheit said. Lesions had to be pigmented with melanin, keratin, and/or blood. Clinical management was biopsy, he added.

For melanoma and high-grade dysplastic nevi, the device had a 98% sensitivity. "These are the [lesions] you will want to take out," Dr. Monheit said.

"At same time we should look at specificity--we do not want to biopsy every lesion that comes into our office," Dr. Monheit said. The specificity of the device was 9.4%, statistically superior to the dermatologist evaluations at 3.7%.

The results with the device were compared with prebiopsy investigator diagnoses and with an objective pathologic review of lesions by a panel of three dermatopathologists. If two of the three dermatopathologists concurred on the diagnosis, their consensus was final. The device had a 98% sensitivity for biopsy detection.

Dr. Monheit and the other study investigators also collected patient data, including age, gender, ethnicity, patient in-house or referred, and any risk factors for melanoma. Anatomic locations of the lesions were also noted.
This study provides "evidence for safety and efficacy for aid in evaluating pigmented lesions," Dr. Monheit said.

Disclosures: Dr. Monheit is a consultant and researcher for Electro-Optical Sciences.

MIAMI -- A computer-automated device detected melanoma and high-grade dysplastic nevi lesions with 98% sensitivity in a large, prospective, multicenter study.

The digital dermoscopy device "sees" at different skin depths using 10 spectral bands ranging from 430 nm to 950 nm. The technology, which was more than a decade in development, objectively assesses up to 75 factors to differentiate melanoma from low-grade and high-grade dysplastic nevi, Dr. Gary D. Monheit said.

"This is an adjunct [that] I think will be helpful in the dermatologist's office, both because of the manpower issue and the difficult lesions we see," Dr. Monheit (photographed on the left) said at the annual meeting of the American Academy of Dermatology.

Dr. Monheit was an investigator at one of seven sites that used the MelaFind (Electro-Optical Sciences) to assess a total of 1,632 evaluable lesions. Lesions included 70 invasive melanomas and 57 melanoma in situ. "This is the largest prospective, blinded study ever conducted in melanoma detection," he noted.

The noninvasive device has a handheld wand for image capture at the point of care. Because of these features and a proprietary algorithm that analyzes multiple spectrums, it is "totally objective with a yes or no algorithm for excision," said Dr. Monheit, a private practice dermatologist in Birmingham, Ala., and an associate clinical professor in the departments of dermatology and ophthalmology at the University of Alabama at Birmingham. Detection is automatic with immediate feedback, Dr. Monheit said. "If we don't get a clear image, the machine tells us the image is not possible." The technology was developed after assessment of more than 10,000 pigmented lesions from more than 7,000 patients.

The aim of this "pivotal study" was to establish safety of the device and sensitivity for melanoma detection. No adverse events were reported, Dr. Monheit said. Lesions had to be pigmented with melanin, keratin, and/or blood. Clinical management was biopsy, he added.

For melanoma and high-grade dysplastic nevi, the device had a 98% sensitivity. "These are the [lesions] you will want to take out," Dr. Monheit said.

"At same time we should look at specificity--we do not want to biopsy every lesion that comes into our office," Dr. Monheit said. The specificity of the device was 9.4%, statistically superior to the dermatologist evaluations at 3.7%.

The results with the device were compared with prebiopsy investigator diagnoses and with an objective pathologic review of lesions by a panel of three dermatopathologists. If two of the three dermatopathologists concurred on the diagnosis, their consensus was final. The device had a 98% sensitivity for biopsy detection.

Dr. Monheit and the other study investigators also collected patient data, including age, gender, ethnicity, patient in-house or referred, and any risk factors for melanoma. Anatomic locations of the lesions were also noted.
This study provides "evidence for safety and efficacy for aid in evaluating pigmented lesions," Dr. Monheit said.

Disclosures: Dr. Monheit is a consultant and researcher for Electro-Optical Sciences.

SAN DIEGO - Reliably tracking and storing pathology slides is key to avoiding the possibility of major liability, Robert A. Cosgrove said at a melanoma conference sponsored by the Scripps Clinic.

To illustrate his point, Dr. Cosgrove presented the personal injury case of a woman with advanced melanoma. About 1 year after she presented to the physician-defendant for evaluation of a lesion on her toe, she required lymph node resection and amputation of the toe.

The plaintiff claimed that the physician had negligently lost biopsy results, resulting in a delay in proper treatment.

The defendant claimed that the plaintiff's lesion had disintegrated at the time it was originally removed and left nothing for further testing.

The jury awarded the plaintiff a settlement in excess of $8 million.

"I've had this come up in a number of cases," said Mr. Cosgrove, a health care attorney based in Encinitas, Calif. "The problem with losing or misplacing pathology slides [is that] it raises questions about whether that was done intentionally or not. Plus, it puts you in a difficult position of being able to prove or disprove what your diagnosis is or your interpretation of the slides."

Another case he discussed underscored the importance of solid chart documentation. The case was brought to trial by the heirs of a 36-year-old woman who died of melanoma while under the defendant dermatologist's care. The heirs contended that the defendant failed to diagnose the decedent's shoulder mole, which was cancerous, in a timely manner.

The defendant denied liability and contended that the decedent was comparatively negligent and failed to make her appointments for yearly full skin exams.

"It is imperative to have documentation in your charts - photo documentation, and in this situation, documentation of yearly examinations. … You can rely on custom and practice, but it's better evidence for the jury when you present the case at trial to have documentation in the chart to that effect," Mr. Cosgrove said.

The defendant also contended that the cancerous mole was not the same as the one that she complained about, and that the decedent would have survived at the time of diagnosis because the lesion was thin.

"Many of these cases are presented at time of trial 2 and 3 years downstream," Mr. Cosgrove noted. "So it comes down to chart documentation. Was it adequately documented in terms of the location of where the lesion was when you evaluated the patient?"

In this case the jury ruled in favor of the defense.

During a question and answer session, a meeting attendee asked Mr. Cosgrove how long physicians should keep medical records on file. "I would find out what the legal policy is in your state on this and follow it accordingly," he advised. "It's important to keep good records and to not do anything after the fact to change your records. By changing the record, by altering the records, by falsifying information, or by destroying records you expose yourself to tremendous personal liability."

Mr. Cosgrove said he had no relevant financial conflicts to disclose.

SAN DIEGO - Reliably tracking and storing pathology slides is key to avoiding the possibility of major liability, Robert A. Cosgrove said at a melanoma conference sponsored by the Scripps Clinic.

To illustrate his point, Dr. Cosgrove presented the personal injury case of a woman with advanced melanoma. About 1 year after she presented to the physician-defendant for evaluation of a lesion on her toe, she required lymph node resection and amputation of the toe.

The plaintiff claimed that the physician had negligently lost biopsy results, resulting in a delay in proper treatment.

The defendant claimed that the plaintiff's lesion had disintegrated at the time it was originally removed and left nothing for further testing.

The jury awarded the plaintiff a settlement in excess of $8 million.

"I've had this come up in a number of cases," said Mr. Cosgrove, a health care attorney based in Encinitas, Calif. "The problem with losing or misplacing pathology slides [is that] it raises questions about whether that was done intentionally or not. Plus, it puts you in a difficult position of being able to prove or disprove what your diagnosis is or your interpretation of the slides."

Another case he discussed underscored the importance of solid chart documentation. The case was brought to trial by the heirs of a 36-year-old woman who died of melanoma while under the defendant dermatologist's care. The heirs contended that the defendant failed to diagnose the decedent's shoulder mole, which was cancerous, in a timely manner.

The defendant denied liability and contended that the decedent was comparatively negligent and failed to make her appointments for yearly full skin exams.

"It is imperative to have documentation in your charts - photo documentation, and in this situation, documentation of yearly examinations. … You can rely on custom and practice, but it's better evidence for the jury when you present the case at trial to have documentation in the chart to that effect," Mr. Cosgrove said.

The defendant also contended that the cancerous mole was not the same as the one that she complained about, and that the decedent would have survived at the time of diagnosis because the lesion was thin.

"Many of these cases are presented at time of trial 2 and 3 years downstream," Mr. Cosgrove noted. "So it comes down to chart documentation. Was it adequately documented in terms of the location of where the lesion was when you evaluated the patient?"

In this case the jury ruled in favor of the defense.

During a question and answer session, a meeting attendee asked Mr. Cosgrove how long physicians should keep medical records on file. "I would find out what the legal policy is in your state on this and follow it accordingly," he advised. "It's important to keep good records and to not do anything after the fact to change your records. By changing the record, by altering the records, by falsifying information, or by destroying records you expose yourself to tremendous personal liability."

Mr. Cosgrove said he had no relevant financial conflicts to disclose.

SAN DIEGO - Reliably tracking and storing pathology slides is key to avoiding the possibility of major liability, Robert A. Cosgrove said at a melanoma conference sponsored by the Scripps Clinic.

To illustrate his point, Dr. Cosgrove presented the personal injury case of a woman with advanced melanoma. About 1 year after she presented to the physician-defendant for evaluation of a lesion on her toe, she required lymph node resection and amputation of the toe.

The plaintiff claimed that the physician had negligently lost biopsy results, resulting in a delay in proper treatment.

The defendant claimed that the plaintiff's lesion had disintegrated at the time it was originally removed and left nothing for further testing.

The jury awarded the plaintiff a settlement in excess of $8 million.

"I've had this come up in a number of cases," said Mr. Cosgrove, a health care attorney based in Encinitas, Calif. "The problem with losing or misplacing pathology slides [is that] it raises questions about whether that was done intentionally or not. Plus, it puts you in a difficult position of being able to prove or disprove what your diagnosis is or your interpretation of the slides."

Another case he discussed underscored the importance of solid chart documentation. The case was brought to trial by the heirs of a 36-year-old woman who died of melanoma while under the defendant dermatologist's care. The heirs contended that the defendant failed to diagnose the decedent's shoulder mole, which was cancerous, in a timely manner.

The defendant denied liability and contended that the decedent was comparatively negligent and failed to make her appointments for yearly full skin exams.

"It is imperative to have documentation in your charts - photo documentation, and in this situation, documentation of yearly examinations. … You can rely on custom and practice, but it's better evidence for the jury when you present the case at trial to have documentation in the chart to that effect," Mr. Cosgrove said.

The defendant also contended that the cancerous mole was not the same as the one that she complained about, and that the decedent would have survived at the time of diagnosis because the lesion was thin.

"Many of these cases are presented at time of trial 2 and 3 years downstream," Mr. Cosgrove noted. "So it comes down to chart documentation. Was it adequately documented in terms of the location of where the lesion was when you evaluated the patient?"

In this case the jury ruled in favor of the defense.

During a question and answer session, a meeting attendee asked Mr. Cosgrove how long physicians should keep medical records on file. "I would find out what the legal policy is in your state on this and follow it accordingly," he advised. "It's important to keep good records and to not do anything after the fact to change your records. By changing the record, by altering the records, by falsifying information, or by destroying records you expose yourself to tremendous personal liability."

Mr. Cosgrove said he had no relevant financial conflicts to disclose.