Melanoma

Eli Lilly & Co. announced Dec. 13, 2010, the immediate suspension of their phase III trial of tasisulam for unresectable or metastatic melanoma.

The company said in a statement that its action was taken in consultation with an independent data monitoring committee that recommended a "full clinical hold" because of safety concerns. The statement did not specify the nature of those safety concerns.

Lilly is testing tasisulam in other cancers, including soft tissue sarcoma; breast, ovarian, and renal cancers; non-small cell lung cancer; and acute leukemia. The company is continuing those trials without modification because the dosing of tasisulam is different.

Eli Lilly & Co. announced Dec. 13, 2010, the immediate suspension of their phase III trial of tasisulam for unresectable or metastatic melanoma.

The company said in a statement that its action was taken in consultation with an independent data monitoring committee that recommended a "full clinical hold" because of safety concerns. The statement did not specify the nature of those safety concerns.

Lilly is testing tasisulam in other cancers, including soft tissue sarcoma; breast, ovarian, and renal cancers; non-small cell lung cancer; and acute leukemia. The company is continuing those trials without modification because the dosing of tasisulam is different.

Eli Lilly & Co. announced Dec. 13, 2010, the immediate suspension of their phase III trial of tasisulam for unresectable or metastatic melanoma.

The company said in a statement that its action was taken in consultation with an independent data monitoring committee that recommended a "full clinical hold" because of safety concerns. The statement did not specify the nature of those safety concerns.

Lilly is testing tasisulam in other cancers, including soft tissue sarcoma; breast, ovarian, and renal cancers; non-small cell lung cancer; and acute leukemia. The company is continuing those trials without modification because the dosing of tasisulam is different.

SAN DIEGO – To receive appropriate payment for Mohs surgery, using the correct codes is key.

While there are not many CPT codes for Mohs, it is crucial to use the right ones, and the right add-on codes, to get full payment for work and to avoid the headache of resubmission and third-payer arguments, Denise Harriman Koger said at a meeting sponsored by the American Society for Mohs Surgery.

One aspect of Mohs makes it unique among all other dermatologic surgeries, said Ms. Kroger, a billing specialist from San Diego. "You must act as both surgeon and pathologist for this, and if you don't, you are not doing Mohs, and you can’t use Mohs codes to bill. If either of these responsibilities is delegated to another physician who reports his services separately, these codes are not appropriate."

The money trail begins with clear documentation of why Mohs is the best treatment, she said. "You need to document this – whether it's an aggressive tumor, one with poorly defined margins – whatever it is. If you are subject to a post-review audit after submitting the claim, they will want to see your reasoning about why you chose Mohs rather than a simple excision."

CPT code 17311 is probably the "most-utilized code for stage I Mohs," she said. It covers procedures on the head, neck, hands, feet, genitals, or any other location that directly involves any of those areas – including muscle, cartilage, bone, tendon, major nerves, or blood vessels. "These are the areas where Mohs is most indicated, especially the face, because lesions on the face are where you want to preserve as much tissue as possible." This code covers up to five tissue blocks from stage I.

For every additional stage performed, use the 17312 code and bill it in units. "For example, if you do three more stages, you would bill 17312 times three," Ms. Koger said. Code 17312 is only used in conjunction with 17311. "That primary code is rarely billed in units unless you are doing two separate lesions. And a lot of insurance companies won't pay for two first stages on the same day." But if two separate lesions are addressed on the same day, continue to bill each one as a unit of the 17312 code.

Again, each additional stage is covered for up to five tissue blocks. Since 17312 is an add-on code, it is not subject to the multiple surgical reduction rules. "If your billing staff sees the payer reducing the fee on this code, they should appeal," Ms. Koger advised.

Code 17313 covers the first stage of Mohs surgery on the trunk, arms, or legs. Again, up to five tissue blocks are covered. The add-on code for additional stages is 17314, which should be billed in units and is not subject to the multiple surgical reduction rule.

"Sometimes you might get a lot of referred patients, who may or may not arrive with a biopsy slide and report," she said. "If you don’t have it, there are some rules as to whether you can bill for a biopsy and frozen section done on the same day as Mohs."

If a biopsy has been done in the previous 60 days and the surgeon has access to it, then no billing can be submitted for a same-day biopsy. "But if you've tried to get it and were not able to, document that and do another biopsy that day."

In order to get paid for that biopsy, however, the billing code modifier 59 is necessary. "This is very important because it's how you get paid for those same-day biopsies and frozen sections. If you bill 17311 without the 59 modifier [after a same-day biopsy] it will be denied because the payer will consider it bundled in."

If more than five tissue blocks are required for any stage, the billing code is 17315. This billing code should be listed separately in addition to the primary procedural code.

Three other important modifier codes are 58, 78 and 79, Ms. Koger said. Modifier 58 covers related procedures done by the same physician during the 90-day postoperative period, including major surgery. It also covers Mohs on a different site, or an incision or excision on the day of Mohs surgery.

If a patient needs to return for a related procedure to the operating room in an outpatient surgery center or hospital during the post-op period, code 78 is the one to use. "Modifier 79 is used if you are doing Mohs during the global period of a previous surgery; it tells the payer that the Mohs is unrelated to the prior work. You need to use that to tell them it’s unrelated to the work you did. For example, if you perform Mohs on the scalp and repair the defect and then 3 weeks later you excise a cyst somewhere else."

The patient who needs to go home overnight and have Mohs completed the next day can be a billing problem, she added. "It might not make sense, but if you have this situation, on the second day you have to start all over again with the stage I code, even though it’s not really a stage I procedure," she said. "Then you follow with the code for additional stages. It seems wrong but that is the only way you can get paid." Staggering patients to force them to come back the next day, to take advantage of this rule, is sometimes done by "unscrupulous" surgeons trying to increase their payment, she said.

Finally she offered a few caveats about billing propriety.

"Excising really small lesions or every basal or squamous cell lesion with Mohs is not a good idea; it looks really suspicious. And don't divide really small specimens into a lot of blocks to be able to bill that. That is definitely not a good idea," she said

Ms. Koger disclosed having no financial disclosures.

SAN DIEGO – To receive appropriate payment for Mohs surgery, using the correct codes is key.

While there are not many CPT codes for Mohs, it is crucial to use the right ones, and the right add-on codes, to get full payment for work and to avoid the headache of resubmission and third-payer arguments, Denise Harriman Koger said at a meeting sponsored by the American Society for Mohs Surgery.

One aspect of Mohs makes it unique among all other dermatologic surgeries, said Ms. Kroger, a billing specialist from San Diego. "You must act as both surgeon and pathologist for this, and if you don't, you are not doing Mohs, and you can’t use Mohs codes to bill. If either of these responsibilities is delegated to another physician who reports his services separately, these codes are not appropriate."

The money trail begins with clear documentation of why Mohs is the best treatment, she said. "You need to document this – whether it's an aggressive tumor, one with poorly defined margins – whatever it is. If you are subject to a post-review audit after submitting the claim, they will want to see your reasoning about why you chose Mohs rather than a simple excision."

CPT code 17311 is probably the "most-utilized code for stage I Mohs," she said. It covers procedures on the head, neck, hands, feet, genitals, or any other location that directly involves any of those areas – including muscle, cartilage, bone, tendon, major nerves, or blood vessels. "These are the areas where Mohs is most indicated, especially the face, because lesions on the face are where you want to preserve as much tissue as possible." This code covers up to five tissue blocks from stage I.

For every additional stage performed, use the 17312 code and bill it in units. "For example, if you do three more stages, you would bill 17312 times three," Ms. Koger said. Code 17312 is only used in conjunction with 17311. "That primary code is rarely billed in units unless you are doing two separate lesions. And a lot of insurance companies won't pay for two first stages on the same day." But if two separate lesions are addressed on the same day, continue to bill each one as a unit of the 17312 code.

Again, each additional stage is covered for up to five tissue blocks. Since 17312 is an add-on code, it is not subject to the multiple surgical reduction rules. "If your billing staff sees the payer reducing the fee on this code, they should appeal," Ms. Koger advised.

Code 17313 covers the first stage of Mohs surgery on the trunk, arms, or legs. Again, up to five tissue blocks are covered. The add-on code for additional stages is 17314, which should be billed in units and is not subject to the multiple surgical reduction rule.

"Sometimes you might get a lot of referred patients, who may or may not arrive with a biopsy slide and report," she said. "If you don’t have it, there are some rules as to whether you can bill for a biopsy and frozen section done on the same day as Mohs."

If a biopsy has been done in the previous 60 days and the surgeon has access to it, then no billing can be submitted for a same-day biopsy. "But if you've tried to get it and were not able to, document that and do another biopsy that day."

In order to get paid for that biopsy, however, the billing code modifier 59 is necessary. "This is very important because it's how you get paid for those same-day biopsies and frozen sections. If you bill 17311 without the 59 modifier [after a same-day biopsy] it will be denied because the payer will consider it bundled in."

If more than five tissue blocks are required for any stage, the billing code is 17315. This billing code should be listed separately in addition to the primary procedural code.

Three other important modifier codes are 58, 78 and 79, Ms. Koger said. Modifier 58 covers related procedures done by the same physician during the 90-day postoperative period, including major surgery. It also covers Mohs on a different site, or an incision or excision on the day of Mohs surgery.

If a patient needs to return for a related procedure to the operating room in an outpatient surgery center or hospital during the post-op period, code 78 is the one to use. "Modifier 79 is used if you are doing Mohs during the global period of a previous surgery; it tells the payer that the Mohs is unrelated to the prior work. You need to use that to tell them it’s unrelated to the work you did. For example, if you perform Mohs on the scalp and repair the defect and then 3 weeks later you excise a cyst somewhere else."

The patient who needs to go home overnight and have Mohs completed the next day can be a billing problem, she added. "It might not make sense, but if you have this situation, on the second day you have to start all over again with the stage I code, even though it’s not really a stage I procedure," she said. "Then you follow with the code for additional stages. It seems wrong but that is the only way you can get paid." Staggering patients to force them to come back the next day, to take advantage of this rule, is sometimes done by "unscrupulous" surgeons trying to increase their payment, she said.

Finally she offered a few caveats about billing propriety.

"Excising really small lesions or every basal or squamous cell lesion with Mohs is not a good idea; it looks really suspicious. And don't divide really small specimens into a lot of blocks to be able to bill that. That is definitely not a good idea," she said

Ms. Koger disclosed having no financial disclosures.

SAN DIEGO – To receive appropriate payment for Mohs surgery, using the correct codes is key.

While there are not many CPT codes for Mohs, it is crucial to use the right ones, and the right add-on codes, to get full payment for work and to avoid the headache of resubmission and third-payer arguments, Denise Harriman Koger said at a meeting sponsored by the American Society for Mohs Surgery.

One aspect of Mohs makes it unique among all other dermatologic surgeries, said Ms. Kroger, a billing specialist from San Diego. "You must act as both surgeon and pathologist for this, and if you don't, you are not doing Mohs, and you can’t use Mohs codes to bill. If either of these responsibilities is delegated to another physician who reports his services separately, these codes are not appropriate."

The money trail begins with clear documentation of why Mohs is the best treatment, she said. "You need to document this – whether it's an aggressive tumor, one with poorly defined margins – whatever it is. If you are subject to a post-review audit after submitting the claim, they will want to see your reasoning about why you chose Mohs rather than a simple excision."

CPT code 17311 is probably the "most-utilized code for stage I Mohs," she said. It covers procedures on the head, neck, hands, feet, genitals, or any other location that directly involves any of those areas – including muscle, cartilage, bone, tendon, major nerves, or blood vessels. "These are the areas where Mohs is most indicated, especially the face, because lesions on the face are where you want to preserve as much tissue as possible." This code covers up to five tissue blocks from stage I.

For every additional stage performed, use the 17312 code and bill it in units. "For example, if you do three more stages, you would bill 17312 times three," Ms. Koger said. Code 17312 is only used in conjunction with 17311. "That primary code is rarely billed in units unless you are doing two separate lesions. And a lot of insurance companies won't pay for two first stages on the same day." But if two separate lesions are addressed on the same day, continue to bill each one as a unit of the 17312 code.

Again, each additional stage is covered for up to five tissue blocks. Since 17312 is an add-on code, it is not subject to the multiple surgical reduction rules. "If your billing staff sees the payer reducing the fee on this code, they should appeal," Ms. Koger advised.

Code 17313 covers the first stage of Mohs surgery on the trunk, arms, or legs. Again, up to five tissue blocks are covered. The add-on code for additional stages is 17314, which should be billed in units and is not subject to the multiple surgical reduction rule.

"Sometimes you might get a lot of referred patients, who may or may not arrive with a biopsy slide and report," she said. "If you don’t have it, there are some rules as to whether you can bill for a biopsy and frozen section done on the same day as Mohs."

If a biopsy has been done in the previous 60 days and the surgeon has access to it, then no billing can be submitted for a same-day biopsy. "But if you've tried to get it and were not able to, document that and do another biopsy that day."

In order to get paid for that biopsy, however, the billing code modifier 59 is necessary. "This is very important because it's how you get paid for those same-day biopsies and frozen sections. If you bill 17311 without the 59 modifier [after a same-day biopsy] it will be denied because the payer will consider it bundled in."

If more than five tissue blocks are required for any stage, the billing code is 17315. This billing code should be listed separately in addition to the primary procedural code.

Three other important modifier codes are 58, 78 and 79, Ms. Koger said. Modifier 58 covers related procedures done by the same physician during the 90-day postoperative period, including major surgery. It also covers Mohs on a different site, or an incision or excision on the day of Mohs surgery.

If a patient needs to return for a related procedure to the operating room in an outpatient surgery center or hospital during the post-op period, code 78 is the one to use. "Modifier 79 is used if you are doing Mohs during the global period of a previous surgery; it tells the payer that the Mohs is unrelated to the prior work. You need to use that to tell them it’s unrelated to the work you did. For example, if you perform Mohs on the scalp and repair the defect and then 3 weeks later you excise a cyst somewhere else."

The patient who needs to go home overnight and have Mohs completed the next day can be a billing problem, she added. "It might not make sense, but if you have this situation, on the second day you have to start all over again with the stage I code, even though it’s not really a stage I procedure," she said. "Then you follow with the code for additional stages. It seems wrong but that is the only way you can get paid." Staggering patients to force them to come back the next day, to take advantage of this rule, is sometimes done by "unscrupulous" surgeons trying to increase their payment, she said.

Finally she offered a few caveats about billing propriety.

"Excising really small lesions or every basal or squamous cell lesion with Mohs is not a good idea; it looks really suspicious. And don't divide really small specimens into a lot of blocks to be able to bill that. That is definitely not a good idea," she said

Ms. Koger disclosed having no financial disclosures.

Regular use of sunscreen during a clinical trial of basal cell and squamous cell carcinomas was found to reduce the incidence of a different skin malignancy – new primary melanomas – up to 10 years later, according to a study published online Dec. 6 in the Journal of Clinical Oncology.

The number of invasive melanomas in particular decreased by 73%, but this was an exploratory finding "and should be interpreted cautiously," said Dr. Adéle C. Green and her associates at the Queensland Institute of Medical Research, Royal Brisbane (Australia) Hospital.

Photo copyright mark wragg/iStockphoto.com

The original clinical trial, conducted in 1992-1996 and involving 1,621 white Queensland residents aged 25-75 years at baseline, examined the effects of 5 years of sunscreen application and beta-carotene supplementation on the incidence of basal and squamous cell carcinoma.

Dr. Green and her colleagues new report focuses on the incidence of melanoma as a secondary end point in the same study population. "Despite the known etiologic role of sun exposure, the question regarding sunscreen use to prevent melanoma remains open and controversial," they noted.

During the trial, 812 patients were given a free, unlimited supply of SPF-16 sunscreen and instructed to use it daily on their head, neck, arms, and hands. A comparison group of 809 patients was randomly assigned to continue using sunscreen of any SPF at their own discretion, which included no use at all in 38% and infrequent use in another 35%.

The two groups were similar in established risk factors for skin cancer, degree of sun exposure, and use of sun protection measures other than sunscreen.

Between baseline in 1992 and the end of the extended follow-up in 2006, 36 study patients developed first primary melanomas. These were in-situ malignancies in 22 subjects and invasive in 14; none of the melanomas was metastatic. Three patients who had melanoma diagnosed in 1992 were excluded.

Only 11 subjects in the sunscreen group developed melanoma, compared with 22 in the comparison group. "Risk of melanoma overall was reduced in those randomly assigned to daily sunscreen compared with discretionary use, although the result was of borderline statistical significance," the investigators reported (J. Clin. Oncol. 2010 [doi:10.1200/JCO.2010.28.7078]).

The average melanoma thickness was 0.53 mm in the sunscreen group, compared with 1.2 mm in the comparison group. The incidence of invasive melanoma was decreased by 73% with sunscreen, while the incidence of in situ lesions was not significantly different between the two groups.

Melanoma incidence was decreased at all sites on the body, not just on the sites assigned to protection by sunscreen. This is probably because many study patients in the sunscreen group applied sunscreen to their trunks and lower limbs regularly, even though they had not been instructed to do so, Dr. Green and her associates noted.

"Our findings provide reassurance in view of the widespread uncertainty to date about sunscreen's ability to prevent melanoma," they reported.

"Although the results are directly relevant to people who live in sunny climates like Australia’s and who receive relatively high levels of ambient sun exposure as a matter of course, they also have implications for white people living in temperate climates in North America and Europe who are at increased risk of melanoma because of increased solar UV exposure caused by the predilection for holidays in sunny places," they concluded.

Regular use of sunscreen during a clinical trial of basal cell and squamous cell carcinomas was found to reduce the incidence of a different skin malignancy – new primary melanomas – up to 10 years later, according to a study published online Dec. 6 in the Journal of Clinical Oncology.

The number of invasive melanomas in particular decreased by 73%, but this was an exploratory finding "and should be interpreted cautiously," said Dr. Adéle C. Green and her associates at the Queensland Institute of Medical Research, Royal Brisbane (Australia) Hospital.

Photo copyright mark wragg/iStockphoto.com

The original clinical trial, conducted in 1992-1996 and involving 1,621 white Queensland residents aged 25-75 years at baseline, examined the effects of 5 years of sunscreen application and beta-carotene supplementation on the incidence of basal and squamous cell carcinoma.

Dr. Green and her colleagues new report focuses on the incidence of melanoma as a secondary end point in the same study population. "Despite the known etiologic role of sun exposure, the question regarding sunscreen use to prevent melanoma remains open and controversial," they noted.

During the trial, 812 patients were given a free, unlimited supply of SPF-16 sunscreen and instructed to use it daily on their head, neck, arms, and hands. A comparison group of 809 patients was randomly assigned to continue using sunscreen of any SPF at their own discretion, which included no use at all in 38% and infrequent use in another 35%.

The two groups were similar in established risk factors for skin cancer, degree of sun exposure, and use of sun protection measures other than sunscreen.

Between baseline in 1992 and the end of the extended follow-up in 2006, 36 study patients developed first primary melanomas. These were in-situ malignancies in 22 subjects and invasive in 14; none of the melanomas was metastatic. Three patients who had melanoma diagnosed in 1992 were excluded.

Only 11 subjects in the sunscreen group developed melanoma, compared with 22 in the comparison group. "Risk of melanoma overall was reduced in those randomly assigned to daily sunscreen compared with discretionary use, although the result was of borderline statistical significance," the investigators reported (J. Clin. Oncol. 2010 [doi:10.1200/JCO.2010.28.7078]).

The average melanoma thickness was 0.53 mm in the sunscreen group, compared with 1.2 mm in the comparison group. The incidence of invasive melanoma was decreased by 73% with sunscreen, while the incidence of in situ lesions was not significantly different between the two groups.

Melanoma incidence was decreased at all sites on the body, not just on the sites assigned to protection by sunscreen. This is probably because many study patients in the sunscreen group applied sunscreen to their trunks and lower limbs regularly, even though they had not been instructed to do so, Dr. Green and her associates noted.

"Our findings provide reassurance in view of the widespread uncertainty to date about sunscreen's ability to prevent melanoma," they reported.

"Although the results are directly relevant to people who live in sunny climates like Australia’s and who receive relatively high levels of ambient sun exposure as a matter of course, they also have implications for white people living in temperate climates in North America and Europe who are at increased risk of melanoma because of increased solar UV exposure caused by the predilection for holidays in sunny places," they concluded.

Regular use of sunscreen during a clinical trial of basal cell and squamous cell carcinomas was found to reduce the incidence of a different skin malignancy – new primary melanomas – up to 10 years later, according to a study published online Dec. 6 in the Journal of Clinical Oncology.

The number of invasive melanomas in particular decreased by 73%, but this was an exploratory finding "and should be interpreted cautiously," said Dr. Adéle C. Green and her associates at the Queensland Institute of Medical Research, Royal Brisbane (Australia) Hospital.

Photo copyright mark wragg/iStockphoto.com

The original clinical trial, conducted in 1992-1996 and involving 1,621 white Queensland residents aged 25-75 years at baseline, examined the effects of 5 years of sunscreen application and beta-carotene supplementation on the incidence of basal and squamous cell carcinoma.

Dr. Green and her colleagues new report focuses on the incidence of melanoma as a secondary end point in the same study population. "Despite the known etiologic role of sun exposure, the question regarding sunscreen use to prevent melanoma remains open and controversial," they noted.

During the trial, 812 patients were given a free, unlimited supply of SPF-16 sunscreen and instructed to use it daily on their head, neck, arms, and hands. A comparison group of 809 patients was randomly assigned to continue using sunscreen of any SPF at their own discretion, which included no use at all in 38% and infrequent use in another 35%.

The two groups were similar in established risk factors for skin cancer, degree of sun exposure, and use of sun protection measures other than sunscreen.

Between baseline in 1992 and the end of the extended follow-up in 2006, 36 study patients developed first primary melanomas. These were in-situ malignancies in 22 subjects and invasive in 14; none of the melanomas was metastatic. Three patients who had melanoma diagnosed in 1992 were excluded.

Only 11 subjects in the sunscreen group developed melanoma, compared with 22 in the comparison group. "Risk of melanoma overall was reduced in those randomly assigned to daily sunscreen compared with discretionary use, although the result was of borderline statistical significance," the investigators reported (J. Clin. Oncol. 2010 [doi:10.1200/JCO.2010.28.7078]).

The average melanoma thickness was 0.53 mm in the sunscreen group, compared with 1.2 mm in the comparison group. The incidence of invasive melanoma was decreased by 73% with sunscreen, while the incidence of in situ lesions was not significantly different between the two groups.

Melanoma incidence was decreased at all sites on the body, not just on the sites assigned to protection by sunscreen. This is probably because many study patients in the sunscreen group applied sunscreen to their trunks and lower limbs regularly, even though they had not been instructed to do so, Dr. Green and her associates noted.

"Our findings provide reassurance in view of the widespread uncertainty to date about sunscreen's ability to prevent melanoma," they reported.

"Although the results are directly relevant to people who live in sunny climates like Australia’s and who receive relatively high levels of ambient sun exposure as a matter of course, they also have implications for white people living in temperate climates in North America and Europe who are at increased risk of melanoma because of increased solar UV exposure caused by the predilection for holidays in sunny places," they concluded.

GOTHENBURG, SWEDEN – The popular practice of trying to improve serum vitamin D status through controlled sun exposure is a no-win proposition that's unlikely to result in adequate vitamin D levels year-round without compromising skin health, according to Brian L. Diffey, Ph.D.

"Failure to understand the nature of human exposure to sunlight has led to widespread misguided public health advice concerning the sun exposure necessary for adequate vitamin D status. Messages concerning sun exposure should remain focused on the detrimental effects of excessive sun exposure and avoid giving specific advice on what may be thought to be optimal sun exposure," said Dr. Diffey, professor emeritus of photobiology at the University of Newcastle (England) who has been publishing studies on the relationship between sun exposure and skin cancer for more than 20 years.

"The recommendation for short, casual sun exposure as adequate for a healthy vitamin D status is simply ubiquitous. We read it everywhere. It has become part of our conventional wisdom. Nobody really questions it. But there's been a gross oversight in all of these recommendations: These calculations relate only to exposure under a clear sky with no clouds, [while] lying horizontal in the middle of the day in midsummer with no shade and roughly 25% of our body surface exposed," he explained.

That's simply not how sun exposure occurs in contemporary life. A person walking around in an urban environment with shade from nearby buildings and trees receives a sun exposure on the vertical body surfaces that’s typically one-sixth of that of a sunbather lying horizontally, Dr. Diffey continued.

As examples of the widespread public health messages encouraging limited sun exposure to enhance vitamin D levels, he noted that the U.K.'s National Osteoporosis Society recommends trying to get 10 minutes of sun exposure once or twice a day without sunscreen between May and September for bone health. The U.K. Health Protection Agency states that short periods outdoors will produce sufficient vitamin D. And "The UV Advantage," by Dr. Michael Holick, professor of medicine at Boston University and winner of the 2009 Linus Pauling prize for health research, containing the "Holick formula for safe sun," is a brisk seller.

Dr. Diffey pointed to a recent large international study of serum vitamin D levels month-by-month for individuals living at various latitudes which concluded most people have adequate but suboptimal levels during the summer months, with a mean of 70 nmol/L. The investigators deemed a level greater than 75 nmol/L to be optimal. In the winter months, most people fall into the 'inadequate' range, with a mean serum vitamin D of 48 nmol/L (BMJ 2010;340:b5664. [doi: 10.1136/bmj.b5664].

In light of study data showing that most people in Europe and North America spend an average of 1-2 hours per day outdoors during the summer, they are generally regarded as having suboptimal vitamin D levels during those months and are vitamin D insufficient the rest of the year. A recommendation for 10-20 minutes of daily casual sun exposure followed by sun avoidance would be "grossly insufficient" to maintain adequate vitamin D levels, he said.

"In fact, if people really did follow the conventional public health advice, we would be much more vitamin D insufficient than we now are," according to the photobiologist.

The safe and effective ways to raise vitamin D levels, Dr. Diffey said, are more widespread fortification of foods or the use of supplements, especially during the winter months.

For dermatologists, he added, there's another effective option: "Pop into your UVB cabin once a week from November to February when nobody's looking and give yourself 1 SED [standard erythema dose], which is about one-third of the minimal erythema dose." His recently published mathematical model (Br. J. Dermatol. 2010; 162:1,342-8) predicts this modest UVB exposure, adding up to a little over one-tenth of a typical UVB treatment course for psoriasis, would keep the recipient in the adequate range for serum vitamin D throughout the dark months.

Dr. Diffey said he has no relevant financial conflicts of interests.

GOTHENBURG, SWEDEN – The popular practice of trying to improve serum vitamin D status through controlled sun exposure is a no-win proposition that's unlikely to result in adequate vitamin D levels year-round without compromising skin health, according to Brian L. Diffey, Ph.D.

"Failure to understand the nature of human exposure to sunlight has led to widespread misguided public health advice concerning the sun exposure necessary for adequate vitamin D status. Messages concerning sun exposure should remain focused on the detrimental effects of excessive sun exposure and avoid giving specific advice on what may be thought to be optimal sun exposure," said Dr. Diffey, professor emeritus of photobiology at the University of Newcastle (England) who has been publishing studies on the relationship between sun exposure and skin cancer for more than 20 years.

"The recommendation for short, casual sun exposure as adequate for a healthy vitamin D status is simply ubiquitous. We read it everywhere. It has become part of our conventional wisdom. Nobody really questions it. But there's been a gross oversight in all of these recommendations: These calculations relate only to exposure under a clear sky with no clouds, [while] lying horizontal in the middle of the day in midsummer with no shade and roughly 25% of our body surface exposed," he explained.

That's simply not how sun exposure occurs in contemporary life. A person walking around in an urban environment with shade from nearby buildings and trees receives a sun exposure on the vertical body surfaces that’s typically one-sixth of that of a sunbather lying horizontally, Dr. Diffey continued.

As examples of the widespread public health messages encouraging limited sun exposure to enhance vitamin D levels, he noted that the U.K.'s National Osteoporosis Society recommends trying to get 10 minutes of sun exposure once or twice a day without sunscreen between May and September for bone health. The U.K. Health Protection Agency states that short periods outdoors will produce sufficient vitamin D. And "The UV Advantage," by Dr. Michael Holick, professor of medicine at Boston University and winner of the 2009 Linus Pauling prize for health research, containing the "Holick formula for safe sun," is a brisk seller.

Dr. Diffey pointed to a recent large international study of serum vitamin D levels month-by-month for individuals living at various latitudes which concluded most people have adequate but suboptimal levels during the summer months, with a mean of 70 nmol/L. The investigators deemed a level greater than 75 nmol/L to be optimal. In the winter months, most people fall into the 'inadequate' range, with a mean serum vitamin D of 48 nmol/L (BMJ 2010;340:b5664. [doi: 10.1136/bmj.b5664].

In light of study data showing that most people in Europe and North America spend an average of 1-2 hours per day outdoors during the summer, they are generally regarded as having suboptimal vitamin D levels during those months and are vitamin D insufficient the rest of the year. A recommendation for 10-20 minutes of daily casual sun exposure followed by sun avoidance would be "grossly insufficient" to maintain adequate vitamin D levels, he said.

"In fact, if people really did follow the conventional public health advice, we would be much more vitamin D insufficient than we now are," according to the photobiologist.

The safe and effective ways to raise vitamin D levels, Dr. Diffey said, are more widespread fortification of foods or the use of supplements, especially during the winter months.

For dermatologists, he added, there's another effective option: "Pop into your UVB cabin once a week from November to February when nobody's looking and give yourself 1 SED [standard erythema dose], which is about one-third of the minimal erythema dose." His recently published mathematical model (Br. J. Dermatol. 2010; 162:1,342-8) predicts this modest UVB exposure, adding up to a little over one-tenth of a typical UVB treatment course for psoriasis, would keep the recipient in the adequate range for serum vitamin D throughout the dark months.

Dr. Diffey said he has no relevant financial conflicts of interests.

GOTHENBURG, SWEDEN – The popular practice of trying to improve serum vitamin D status through controlled sun exposure is a no-win proposition that's unlikely to result in adequate vitamin D levels year-round without compromising skin health, according to Brian L. Diffey, Ph.D.

"Failure to understand the nature of human exposure to sunlight has led to widespread misguided public health advice concerning the sun exposure necessary for adequate vitamin D status. Messages concerning sun exposure should remain focused on the detrimental effects of excessive sun exposure and avoid giving specific advice on what may be thought to be optimal sun exposure," said Dr. Diffey, professor emeritus of photobiology at the University of Newcastle (England) who has been publishing studies on the relationship between sun exposure and skin cancer for more than 20 years.

"The recommendation for short, casual sun exposure as adequate for a healthy vitamin D status is simply ubiquitous. We read it everywhere. It has become part of our conventional wisdom. Nobody really questions it. But there's been a gross oversight in all of these recommendations: These calculations relate only to exposure under a clear sky with no clouds, [while] lying horizontal in the middle of the day in midsummer with no shade and roughly 25% of our body surface exposed," he explained.

That's simply not how sun exposure occurs in contemporary life. A person walking around in an urban environment with shade from nearby buildings and trees receives a sun exposure on the vertical body surfaces that’s typically one-sixth of that of a sunbather lying horizontally, Dr. Diffey continued.

As examples of the widespread public health messages encouraging limited sun exposure to enhance vitamin D levels, he noted that the U.K.'s National Osteoporosis Society recommends trying to get 10 minutes of sun exposure once or twice a day without sunscreen between May and September for bone health. The U.K. Health Protection Agency states that short periods outdoors will produce sufficient vitamin D. And "The UV Advantage," by Dr. Michael Holick, professor of medicine at Boston University and winner of the 2009 Linus Pauling prize for health research, containing the "Holick formula for safe sun," is a brisk seller.

Dr. Diffey pointed to a recent large international study of serum vitamin D levels month-by-month for individuals living at various latitudes which concluded most people have adequate but suboptimal levels during the summer months, with a mean of 70 nmol/L. The investigators deemed a level greater than 75 nmol/L to be optimal. In the winter months, most people fall into the 'inadequate' range, with a mean serum vitamin D of 48 nmol/L (BMJ 2010;340:b5664. [doi: 10.1136/bmj.b5664].

In light of study data showing that most people in Europe and North America spend an average of 1-2 hours per day outdoors during the summer, they are generally regarded as having suboptimal vitamin D levels during those months and are vitamin D insufficient the rest of the year. A recommendation for 10-20 minutes of daily casual sun exposure followed by sun avoidance would be "grossly insufficient" to maintain adequate vitamin D levels, he said.

"In fact, if people really did follow the conventional public health advice, we would be much more vitamin D insufficient than we now are," according to the photobiologist.

The safe and effective ways to raise vitamin D levels, Dr. Diffey said, are more widespread fortification of foods or the use of supplements, especially during the winter months.

For dermatologists, he added, there's another effective option: "Pop into your UVB cabin once a week from November to February when nobody's looking and give yourself 1 SED [standard erythema dose], which is about one-third of the minimal erythema dose." His recently published mathematical model (Br. J. Dermatol. 2010; 162:1,342-8) predicts this modest UVB exposure, adding up to a little over one-tenth of a typical UVB treatment course for psoriasis, would keep the recipient in the adequate range for serum vitamin D throughout the dark months.

Dr. Diffey said he has no relevant financial conflicts of interests.

Darrell S. Rigel, MD

Malignant melanoma represents a significant and growing public health burden in the US and worldwide. It is estimated that 68, 130 cases of invasive malignant melanoma and at least 48,000 cases of melanoma in-situ will be diagnosed in the US this year. Melanoma is also one of the few remaining cancers with increasing US incidence. In the 1930s, the lifetime risk of an American developing invasive malignant melanoma was 1 in 1,500. Currently, that risk is 1 in 59. Deaths from malignant melanoma are also increasing. The mortality rate from malignant melanoma has risen about 2% annually since 1960. This year, it is estimated that 8,700 Americans will die from this cancer. The identification of individuals at high risk for malignant melanoma is important for the development of focused and efficient prevention efforts. Acute sun exposure resulting in sunburn remains a significant risk factor for the development of melanoma, but numerous other potential risk factors have been cited. Included among these are atypical mole syndrome/dysplastic nevus syndrome, blistering sunburns, immunosuppression, prior therapy with psoralen with ultraviolet A light (UVA) light, UV exposure at tanning salons, elevated socioeconomic status, and history of melanoma in a first-degree relative. With a better understanding of the reasons for the increasing rate of this cancer, and with enhanced early detection approaches, we may be able to decrease the incidence and mortality of malignant melanoma.

*For a PDF of the full article, click on the link to the left of this introduction.

Darrell S. Rigel, MD

Malignant melanoma represents a significant and growing public health burden in the US and worldwide. It is estimated that 68, 130 cases of invasive malignant melanoma and at least 48,000 cases of melanoma in-situ will be diagnosed in the US this year. Melanoma is also one of the few remaining cancers with increasing US incidence. In the 1930s, the lifetime risk of an American developing invasive malignant melanoma was 1 in 1,500. Currently, that risk is 1 in 59. Deaths from malignant melanoma are also increasing. The mortality rate from malignant melanoma has risen about 2% annually since 1960. This year, it is estimated that 8,700 Americans will die from this cancer. The identification of individuals at high risk for malignant melanoma is important for the development of focused and efficient prevention efforts. Acute sun exposure resulting in sunburn remains a significant risk factor for the development of melanoma, but numerous other potential risk factors have been cited. Included among these are atypical mole syndrome/dysplastic nevus syndrome, blistering sunburns, immunosuppression, prior therapy with psoralen with ultraviolet A light (UVA) light, UV exposure at tanning salons, elevated socioeconomic status, and history of melanoma in a first-degree relative. With a better understanding of the reasons for the increasing rate of this cancer, and with enhanced early detection approaches, we may be able to decrease the incidence and mortality of malignant melanoma.

*For a PDF of the full article, click on the link to the left of this introduction.

Darrell S. Rigel, MD

Malignant melanoma represents a significant and growing public health burden in the US and worldwide. It is estimated that 68, 130 cases of invasive malignant melanoma and at least 48,000 cases of melanoma in-situ will be diagnosed in the US this year. Melanoma is also one of the few remaining cancers with increasing US incidence. In the 1930s, the lifetime risk of an American developing invasive malignant melanoma was 1 in 1,500. Currently, that risk is 1 in 59. Deaths from malignant melanoma are also increasing. The mortality rate from malignant melanoma has risen about 2% annually since 1960. This year, it is estimated that 8,700 Americans will die from this cancer. The identification of individuals at high risk for malignant melanoma is important for the development of focused and efficient prevention efforts. Acute sun exposure resulting in sunburn remains a significant risk factor for the development of melanoma, but numerous other potential risk factors have been cited. Included among these are atypical mole syndrome/dysplastic nevus syndrome, blistering sunburns, immunosuppression, prior therapy with psoralen with ultraviolet A light (UVA) light, UV exposure at tanning salons, elevated socioeconomic status, and history of melanoma in a first-degree relative. With a better understanding of the reasons for the increasing rate of this cancer, and with enhanced early detection approaches, we may be able to decrease the incidence and mortality of malignant melanoma.

*For a PDF of the full article, click on the link to the left of this introduction.

Justin M. Ko, MD, MBA, Nicole F. Velez, MD, and Hensin Tsao, MD, PhD

Melanoma is one of the most aggressive and yet poorly understood of human malignancies. Advances in genomics has allowed a more nuanced understanding of the disease, moving beyond the traditional dysplastic nevus-to-melanoma model and identifying multiple divergent oncogenic pathways leading to melanoma. An understanding of the molecular mechanisms driving melanoma has opened the doors for the development of targeted therapeutic approaches. As we enter the era of personalized medicine, it will be critical for clinicians to both appreciate and be able to determine the molecular profile of their patients’ melanoma because this profile will guide risk stratification, genetic counseling, and treatment customization. A review of the divergent pathways of melanoma development is presented here, with a particular emphasis on recently identified mutations, and their implications for patient care.

*For a PDF of the full article, click on the link to the left of this introduction.

Justin M. Ko, MD, MBA, Nicole F. Velez, MD, and Hensin Tsao, MD, PhD

Melanoma is one of the most aggressive and yet poorly understood of human malignancies. Advances in genomics has allowed a more nuanced understanding of the disease, moving beyond the traditional dysplastic nevus-to-melanoma model and identifying multiple divergent oncogenic pathways leading to melanoma. An understanding of the molecular mechanisms driving melanoma has opened the doors for the development of targeted therapeutic approaches. As we enter the era of personalized medicine, it will be critical for clinicians to both appreciate and be able to determine the molecular profile of their patients’ melanoma because this profile will guide risk stratification, genetic counseling, and treatment customization. A review of the divergent pathways of melanoma development is presented here, with a particular emphasis on recently identified mutations, and their implications for patient care.

*For a PDF of the full article, click on the link to the left of this introduction.

Justin M. Ko, MD, MBA, Nicole F. Velez, MD, and Hensin Tsao, MD, PhD

Melanoma is one of the most aggressive and yet poorly understood of human malignancies. Advances in genomics has allowed a more nuanced understanding of the disease, moving beyond the traditional dysplastic nevus-to-melanoma model and identifying multiple divergent oncogenic pathways leading to melanoma. An understanding of the molecular mechanisms driving melanoma has opened the doors for the development of targeted therapeutic approaches. As we enter the era of personalized medicine, it will be critical for clinicians to both appreciate and be able to determine the molecular profile of their patients’ melanoma because this profile will guide risk stratification, genetic counseling, and treatment customization. A review of the divergent pathways of melanoma development is presented here, with a particular emphasis on recently identified mutations, and their implications for patient care.

*For a PDF of the full article, click on the link to the left of this introduction.

Helen C. Haliasos, MD, Iris Zalaudek, MD, Josep Malvehy, MD, Christoph Lanschuetzer, MD, Helmut Hinter, MD, Rainer Hofmann-Wellenhof, MD, Ralph Braun, MD, and Ashfaq A. Marghoob, MD

Dermoscopy is a noninvasive technique that enables visualization of subsurface colors and structures within the skin that are imperceptible to the naked eye. The dermatoscope allows the physician to examine both the macroscopic and microscopic primary morphology of skin lesions, identify subtle clinical clues, confirm naked-eye clinical diagnoses, and monitor treatment progress while posing little threat to the young patient. Dermoscopic findings have been formulated into diagnostic criteria that assist experienced clinicians in differentiating benign and malignant neoplasms. In this review, clinical morphology of melanocytic nevi and melanoma in the pediatric population is examined and the relevant dermoscopic findings and histopathologic correlates that aid in the diagnosis and management of these lesions are described.

*For a PDF of the full article, click on the link to the left of this introduction.

Helen C. Haliasos, MD, Iris Zalaudek, MD, Josep Malvehy, MD, Christoph Lanschuetzer, MD, Helmut Hinter, MD, Rainer Hofmann-Wellenhof, MD, Ralph Braun, MD, and Ashfaq A. Marghoob, MD

Dermoscopy is a noninvasive technique that enables visualization of subsurface colors and structures within the skin that are imperceptible to the naked eye. The dermatoscope allows the physician to examine both the macroscopic and microscopic primary morphology of skin lesions, identify subtle clinical clues, confirm naked-eye clinical diagnoses, and monitor treatment progress while posing little threat to the young patient. Dermoscopic findings have been formulated into diagnostic criteria that assist experienced clinicians in differentiating benign and malignant neoplasms. In this review, clinical morphology of melanocytic nevi and melanoma in the pediatric population is examined and the relevant dermoscopic findings and histopathologic correlates that aid in the diagnosis and management of these lesions are described.

*For a PDF of the full article, click on the link to the left of this introduction.

Helen C. Haliasos, MD, Iris Zalaudek, MD, Josep Malvehy, MD, Christoph Lanschuetzer, MD, Helmut Hinter, MD, Rainer Hofmann-Wellenhof, MD, Ralph Braun, MD, and Ashfaq A. Marghoob, MD

Dermoscopy is a noninvasive technique that enables visualization of subsurface colors and structures within the skin that are imperceptible to the naked eye. The dermatoscope allows the physician to examine both the macroscopic and microscopic primary morphology of skin lesions, identify subtle clinical clues, confirm naked-eye clinical diagnoses, and monitor treatment progress while posing little threat to the young patient. Dermoscopic findings have been formulated into diagnostic criteria that assist experienced clinicians in differentiating benign and malignant neoplasms. In this review, clinical morphology of melanocytic nevi and melanoma in the pediatric population is examined and the relevant dermoscopic findings and histopathologic correlates that aid in the diagnosis and management of these lesions are described.

*For a PDF of the full article, click on the link to the left of this introduction.

Marc D. Brown, MD

As the incidence of melanoma continues to increase, so does the role of the dermatologist as both medical and surgical oncologist for these patients. The  dermatologist holds a key role in all phases of care, including prevention, diagnosis, treatment, and follow-up. The dermatologist is best trained to complete a full and thorough skin examination and is best able to recognize a melanoma in its early stages of growth. Dermatologists have a unique opportunity to prevent melanoma through appropriate patient education concerning sun protection, self skin examinations, and the ABCDEs of melanoma recognition (ie, asymmetry, border irregularity, color variations, dimension and evolution). The dermatologist is well trained to obtain an appropriate full-thickness skin biopsy and is knowledgeable to interpret the pathologist report and understand the significance of the various histologic prognostic indexes. Most patients present with localized disease and with thinner Breslow depth and thus can be skillfully treated in an outpatient setting under local anesthesia by a dermatologist.

*For a PDF of the full article, click on the link to the left of this introduction.

Marc D. Brown, MD

As the incidence of melanoma continues to increase, so does the role of the dermatologist as both medical and surgical oncologist for these patients. The  dermatologist holds a key role in all phases of care, including prevention, diagnosis, treatment, and follow-up. The dermatologist is best trained to complete a full and thorough skin examination and is best able to recognize a melanoma in its early stages of growth. Dermatologists have a unique opportunity to prevent melanoma through appropriate patient education concerning sun protection, self skin examinations, and the ABCDEs of melanoma recognition (ie, asymmetry, border irregularity, color variations, dimension and evolution). The dermatologist is well trained to obtain an appropriate full-thickness skin biopsy and is knowledgeable to interpret the pathologist report and understand the significance of the various histologic prognostic indexes. Most patients present with localized disease and with thinner Breslow depth and thus can be skillfully treated in an outpatient setting under local anesthesia by a dermatologist.

*For a PDF of the full article, click on the link to the left of this introduction.

Marc D. Brown, MD

As the incidence of melanoma continues to increase, so does the role of the dermatologist as both medical and surgical oncologist for these patients. The  dermatologist holds a key role in all phases of care, including prevention, diagnosis, treatment, and follow-up. The dermatologist is best trained to complete a full and thorough skin examination and is best able to recognize a melanoma in its early stages of growth. Dermatologists have a unique opportunity to prevent melanoma through appropriate patient education concerning sun protection, self skin examinations, and the ABCDEs of melanoma recognition (ie, asymmetry, border irregularity, color variations, dimension and evolution). The dermatologist is well trained to obtain an appropriate full-thickness skin biopsy and is knowledgeable to interpret the pathologist report and understand the significance of the various histologic prognostic indexes. Most patients present with localized disease and with thinner Breslow depth and thus can be skillfully treated in an outpatient setting under local anesthesia by a dermatologist.

*For a PDF of the full article, click on the link to the left of this introduction.

Merrick I. Ross, MD

When detected and treated early, melanoma has an excellent prognosis. Unfortunately, as the tumor invades deeper into tissue the risk of metastatic spread to regional lymph nodes and beyond increases and the prognosis worsens significantly. Therefore, accurately detecting any regional lymphatic metastasis would significantly aid in determining a patient’s prognosis and help guide his or her treatment plan. In 1991, Don Morton and colleagues presented new paradigm in diagnosing regional lymphatic involvement of tumors termed sentinel lymph node biopsy (SLNB). By mapping the regional lymph system around a tumor and tracing the lymphatic flow, a determination of the most likely lymph node or nodes the cancer will spread to first is made. Then, a limited biopsy of the most likely nodes is performed rather than a more-invasive removal of the entire local lymphatic chain. In 20 years that have followed, a great deal of information has been gained as to its accuracy, prognostic value, appropriate candidates, and its impact on regional disease control and survival. The SLNB has been shown to accurately stage regional lymph node basins in stage I and II melanoma patients with minimal morbidity. More sensitive histologic techniques are now being applied that may allow even greater accuracy in the staging of melanoma patients. Although specific percent risk thresholds are still in question, recommendation for SLNB when melanomas are 1 mm or thicker has gained wide acceptance. SLNB may also be appropriate for patients with melanomas that are between 0.76 and 1 mm thick and have ulceration, high mitotic rates, or reach a Clark level IV. Therefore, melanomas with IB or greater staging should be considered for SLNB.

*For a PDF of the full article, click on the link to the left of this introduction.

Merrick I. Ross, MD

When detected and treated early, melanoma has an excellent prognosis. Unfortunately, as the tumor invades deeper into tissue the risk of metastatic spread to regional lymph nodes and beyond increases and the prognosis worsens significantly. Therefore, accurately detecting any regional lymphatic metastasis would significantly aid in determining a patient’s prognosis and help guide his or her treatment plan. In 1991, Don Morton and colleagues presented new paradigm in diagnosing regional lymphatic involvement of tumors termed sentinel lymph node biopsy (SLNB). By mapping the regional lymph system around a tumor and tracing the lymphatic flow, a determination of the most likely lymph node or nodes the cancer will spread to first is made. Then, a limited biopsy of the most likely nodes is performed rather than a more-invasive removal of the entire local lymphatic chain. In 20 years that have followed, a great deal of information has been gained as to its accuracy, prognostic value, appropriate candidates, and its impact on regional disease control and survival. The SLNB has been shown to accurately stage regional lymph node basins in stage I and II melanoma patients with minimal morbidity. More sensitive histologic techniques are now being applied that may allow even greater accuracy in the staging of melanoma patients. Although specific percent risk thresholds are still in question, recommendation for SLNB when melanomas are 1 mm or thicker has gained wide acceptance. SLNB may also be appropriate for patients with melanomas that are between 0.76 and 1 mm thick and have ulceration, high mitotic rates, or reach a Clark level IV. Therefore, melanomas with IB or greater staging should be considered for SLNB.

*For a PDF of the full article, click on the link to the left of this introduction.

Merrick I. Ross, MD

When detected and treated early, melanoma has an excellent prognosis. Unfortunately, as the tumor invades deeper into tissue the risk of metastatic spread to regional lymph nodes and beyond increases and the prognosis worsens significantly. Therefore, accurately detecting any regional lymphatic metastasis would significantly aid in determining a patient’s prognosis and help guide his or her treatment plan. In 1991, Don Morton and colleagues presented new paradigm in diagnosing regional lymphatic involvement of tumors termed sentinel lymph node biopsy (SLNB). By mapping the regional lymph system around a tumor and tracing the lymphatic flow, a determination of the most likely lymph node or nodes the cancer will spread to first is made. Then, a limited biopsy of the most likely nodes is performed rather than a more-invasive removal of the entire local lymphatic chain. In 20 years that have followed, a great deal of information has been gained as to its accuracy, prognostic value, appropriate candidates, and its impact on regional disease control and survival. The SLNB has been shown to accurately stage regional lymph node basins in stage I and II melanoma patients with minimal morbidity. More sensitive histologic techniques are now being applied that may allow even greater accuracy in the staging of melanoma patients. Although specific percent risk thresholds are still in question, recommendation for SLNB when melanomas are 1 mm or thicker has gained wide acceptance. SLNB may also be appropriate for patients with melanomas that are between 0.76 and 1 mm thick and have ulceration, high mitotic rates, or reach a Clark level IV. Therefore, melanomas with IB or greater staging should be considered for SLNB.

*For a PDF of the full article, click on the link to the left of this introduction.

Jose Lutzky, MD, FACP

During the past 3 decades, the incidence, morbidity, and mortality of malignant melanoma have increased dramatically. Advanced melanoma has remained a disease that is for the most part incurable and has challenged all therapeutic efforts to make a dent in its natural history. Recent advances in the understanding of the molecular alterations in melanoma and in the immunologic mechanisms playing a role in this malignancy have brought hope that significant progress can be achieved, as evidenced by early encouraging clinical data. This review will summarize these recent developments and their impact on current clinical practice.

*For a PDF of the full article, click on the link to the left of this introduction.

Jose Lutzky, MD, FACP

During the past 3 decades, the incidence, morbidity, and mortality of malignant melanoma have increased dramatically. Advanced melanoma has remained a disease that is for the most part incurable and has challenged all therapeutic efforts to make a dent in its natural history. Recent advances in the understanding of the molecular alterations in melanoma and in the immunologic mechanisms playing a role in this malignancy have brought hope that significant progress can be achieved, as evidenced by early encouraging clinical data. This review will summarize these recent developments and their impact on current clinical practice.

*For a PDF of the full article, click on the link to the left of this introduction.

Jose Lutzky, MD, FACP

During the past 3 decades, the incidence, morbidity, and mortality of malignant melanoma have increased dramatically. Advanced melanoma has remained a disease that is for the most part incurable and has challenged all therapeutic efforts to make a dent in its natural history. Recent advances in the understanding of the molecular alterations in melanoma and in the immunologic mechanisms playing a role in this malignancy have brought hope that significant progress can be achieved, as evidenced by early encouraging clinical data. This review will summarize these recent developments and their impact on current clinical practice.

*For a PDF of the full article, click on the link to the left of this introduction.