Archive for June, 2011
The AJCC (see abstract below) has come out with the first ever staging system for cutaneous SCC on its own. Previously it was staged with other non-melanoma skin cancers. Of course they have not actually defined what an SCC is; as some of you may be aware there is still great controversy about early SCC vs solar keratosis and keratoacanthoma versus SCC
The salient points for us are the T part of the TMN system which gives us an idea of the important local prognostic factors, some of which I did not realise. The depth is actually a Breslow depth which I did not know could be used for SCC.
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis Carcinoma in situ
T1 Tumor <2 cm in greatest dimension with< 2 high-risk features*
T2 Tumor > 2 cm in greatest dimension with or without one additional high-risk feature, or any size with >2 high-risk features
T3 Tumor with invasion of maxilla, mandible, orbit, or temporal bone
T4 Tumor with invasion of skeleton (axial or appendicular) or perineural invasion of skull base
High-risk features include depth (>2-mm thickness; Clark level >IV); perineural invasion; location (primary site ear; primary site nonglabrous lip); and differentiation (poorly differentiated or undifferentiated).
A new American Joint Committee on Cancer staging system for cutaneous squamous cell carcinoma: Creation and rationale for inclusion of tumor (T) characteristics
Sharifeh Farasat, BS,a Siegrid S. Yu, MD,b Victor A. Neel, MD, PhD,c Kishwer S. Nehal, MD,d Thomas Lardaro, BSc,a Martin C. Mihm, MD,e David R. Byrd, MD,f Charles M. Balch, MD,g,h,i Joseph A. Califano, MD,j Alice Y. Chuang, MD,i William H. Sharfman, MD,h,i Jatin P. Shah, MD, PhD,k Paul Nghiem, MD, PhD,l Clark C. Otley, MD,m Anthony P. Tufaro, DDS, MD,n Timothy M. Johnson, MD,o Arthur J. Sober, MD,c and Nanette J. Li_egeois, MD, PhDh,j,n Baltimore, Maryland; San Francisco, California; Boston, Massachusetts; New York, New York; Seattle,Washington; Rochester, Minnesota; and Ann Arbor, Michigan
Background: The incidence of cutaneous squamous cell carcinoma (cSCC) is increasing. Although mostpatients achieve complete remission with surgical treatment, those with advanced disease have a poor prognosis. The American Joint Committee on Cancer (AJCC) is responsible for the staging criteria for all
cancers. For the past 20 years, the AJCC cancer staging manual has grouped all nonmelanoma skin cancers,including cSCC, together for the purposes of staging. However, based on new evidence, the AJCC has determined that cSCC should have a separate staging system in the 7th edition AJCC staging manual.
Objective: We sought to present the rationale for and characteristics of the new AJCC staging system specific to cSCC tumor characteristics (T).
Methods: The Nonmelanoma Skin Cancer Task Force of AJCC reviewed relevant data and reached expert consensus in creating the 7th edition AJCC staging system for cSCC. Emphasis was placed on prospectively accumulated data and multivariate analyses. Concordance with head and neck cancer staging system was also achieved.
Results: A new AJCC cSCC T classification is presented. The T classification is determined by tumor diameter, invasion into cranial bone, and high-risk features, including anatomic location, tumor thickness and level, differentiation, and perineural invasion.
Limitations: The data available for analysis are still suboptimal, with limited prospective outcomes trials and few multivariate analyses.
Conclusions: The new AJCC staging system for cSCC incorporates tumor-specific (T) staging features and will encourage coordinated, consistent collection of data that will be the basis of improved prognostic systems in the future. ( J Am Acad Dermatol 2011;64:1051-9.)
Long-Term Use of Nonsteroidal Anti-inflammatory Drugs Decreases the Risk of Cutaneous Melanoma: Results of a United States Case–Control Study
Clara Curiel-Lewandrowski1,2, Tamar Nijsten3, Maria L. Gomez1, Loes M. Hollestein4, Michael B. Atkins5 and Robert S. Stern1
Experimental and observational studies continue to demonstrate conflicting results regarding the role of several commonly used drugs as melanoma chemopreventive agents. This case–control study was designed to assess the associations between cutaneous melanoma (CM) and exposure to nonsteroidal anti-inflammatory drugs(NSAIDs) and statins in current users.
A total of 400 CM and 600 eligible age- and gender-matched community based controls were prospectively recruited and interviewed. We assessed participants’ demographic characteristics, CM risk factors, and current and previous use of medications. Multivariable conditional logistic regression models were used to estimate adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for associations between NSAIDs and/or aspirin (ASA), statin exposure, and CM risk. Half of the subjects were men (mean age 60 years). After adjusting for confounders, use of any type of NSAIDs for more than 5 years significantly reduced the risk of melanoma development compared with the low-exposure group adjusted OR¼0.57; 95% CI¼0.43–0.77). Subgroup analyses showed that the observed risk reduction was primarily driven by continuous ASA use (45 years adjusted OR¼0.51, 95% CI¼0.35–0.75). No significant protective effect was observed with statin exposure (OR¼0.97, 95% CI¼0.73–1.29).
Long-term use of NSAIDs, especially ASA, is associated with a significantly decreased risk of CM development. Clinical intervention studies are warranted to further investigate the potential role of ASA and other NSAIDs as chemopreventive agents for CM.
Journal of Investigative Dermatology (2011) 131, 1460–1468; doi:10.1038/jid.2011.58; published online 10 March 2011
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Have a look at this commentary and abstract. Obviously something we knew already. Fascinating the stats about the current risk of melanoma (in USA obviously) vs 1935. I can get you a copy of the article if you would like.
Baby’s Sun Exposure Could Mean Cancer Later.
According to a review in the July issue of Pediatrics, it could be setting a child up for melanoma or other skin cancers later in life. UV radiation can suppress the immune system and damage skin cells – a process that may happen more quickly in babies than in adults, the authors note.
Young skin is delicate and thinner. It produces less melanin, a skin protecting pigment. UV rays can reach the pigment producing melanin cells, called melanocytes, and damage them. Damage to those cells is a “precursor to melanoma,” says Robin Gehris, M.D., the chief of pediatric dermatologic surgery at the Children’s Hospital of Pittsburgh. “Infant skin may be even more prone to sun damage than we had thought, and that might be important later on for melanoma and other cancer risk,” says Gehris, who was not involved in the new review.
Sun exposure earlier in life, from infancy through adolescence, seems to be associated with different cell changes and an earlier diagnosis of melanoma than exposure in the adult years, the article points out. One study cited in the review has projected that 1 in 33 babies born today will develop melanoma during their lives, versus 1 in 1,500 babies born in 1935.
The American Academy of Pediatrics (AAP), which publishesPediatrics, advises parents to keep children 6 months or younger out of the sun completely. For older babies, the AAP recommends dressing infants in brimmed hats and sun-protective clothing, applying sunscreen to any small patches of exposed skin, and minimizing sun exposure during the midday hours, when the sun is at its hottest.
In light of the comments made on the weekend at the skin cancer conference at the Gold Coast about how the future of sunscreens is not only sun-protection but also DNA protection and DNA repair, I was fascinated to come across this article from “The Healthy Skeptic” : How effective are skin products with DNA-repairing enzymes?
By Chris Woolston, Special to the Los Angeles Times
The UV rays blasting down from the sun do more than burn your skin. They attack you right down to your DNA. That’s why there’s such a strong link between sun exposure and skin cancer. If you could somehow repair the sun-damaged DNA in your skin, you could go a long way toward reducing your risk of skin cancer. As a bonus, your skin would look younger and healthier. Every skin cell has a toolbox of enzymes that fix broken DNA, but what can you do when natural repairs aren’t enough? If you’re willing to reach into your wallet, you might be tempted to try a relatively pricey sunscreen or skin cream that contains DNA-repairing enzymes.
One option is a Neova DNA Damage Control sunscreen from PhotoMedex. Along with antioxidants, zinc oxide and other familiar ingredients, the sunscreens contain an enzyme called UV-endonuclease that’s harvested from an extract of ocean bacteria. This extract, called micrococcus lysate, is enclosed in a tiny package of fat (called a liposome) that supposedly helps deliver the enzyme deep into the skin. A 3-ounce tube of Neova Active (SPF 45) costs $46 on the company website. A 2.5-ounce tube of Neova Everyday (SPF 43) costs $39.
DNA EGF Renewal is a line of skin-care products developed by Dr. Ronald Moy, a professor of dermatology at UCLA’sDavid Geffen School of Medicine. These products contain “the highest concentrations of DNA repair enzymes” derived from a variety of sources, including plankton, micrococcus and botanical sources, Moy says. They also include epidermal growth factor, a protein isolated from barley by a biotech company in Iceland. The company website sells a 1.7-ounce tube of the sunscreen (SPF 30) for $45. A single ounce of the company’s DNA Intensive Renewal lotion costs $125.
DNA Repair Serum from Skin Care Heaven contains DNA repair enzymes from micrococcus lysate along with antioxidants and caffeine, which are said to fight redness. A 1.7-ounce tube costs about $112 on the company website.
The claims The Neova website says that “smart” sunscreens are the “newest, most powerful” therapy for sun-damaged skin. Barbara Hayes, vice president of marketing for PhotoMedex, says that the sunscreens will lighten age spots, reduce fine lines and even out skin tone within about four weeks. “It’s really quite amazing when you see someone who has used this product,” she says. The DNA EGF Renewal website says that the products offer a “futuristic approach to skin renewal and protection.” Moy, the dermatologist who founded the company, says that many studies have shown that DNA-repairing enzymes in lotions and creams really can revitalize skin, reverse sun damage and reduce the risk of skin cancer. He recommends the products for his patients at heightened risk for skin cancer, including those with very fair skin. The Skin Care Heaven website says DNA Repair Serum will “delay the signs of aging and stimulate the natural recovery process of your skin.” Kathy Everett, a medical esthetician with the company who sells the product at a spa in Carlsbad, says the enzymes work “synergistically” with antioxidants to remove fine lines and lighten age spots with several weeks of use. “My clients are impressed with the results,” she says.
The bottom line the idea that anything in a lotion could actually repair something as fragile and complicated as DNA may sound far-fetched, but DNA-repairing enzymes have a proven ability to heal and protect, says Dr. Steven Q. Wang, director of dermatologic surgery and dermatology at Memorial Sloan-Kettering Cancer Center in Basking Ridge, N.J. In simple terms, endonucleases work by cutting out the damaged bits of DNA, which are then regenerated. Many studies in the last decade have shown that adding extra enzymes to the skin “enhances the body’s innate mechanisms for repairing DNA damage,” Wang says.
For one example, a 2010 study in the Journal of Drugs in Dermatology by Moy and colleagues at UCLA found that using a cream with DNA repair enzymes for 48 weeks significantly reduced actinic keratoses (scaly precancerous growths) in 17 people with severely sun-damaged skin. (The product used in the study is not commercially available.) But because Neova and similar products haven’t been thoroughly tested in clinical trials, Wang says he has some questions about their real-world benefits. His main concern is that the products may not deliver enzymes deeply enough to have any noticeable effect on fine lines and age spots.
“If you have money and want to try it, I say go for it,” he says. “But it may not be worth it.” Dr. Suzanne Kilmer, a board member of the American Society for Dermatologic Surgery who runs a clinic in Sacramento, has used Neova herself and recommends it for her patients. She believes DNA-repairing enzymes could be the next big advance in sunscreens. If they catch on, she says, they could help reduce the incidence of skin cancer 10 to 20 years from now. “Zinc oxide already blocks almost all of the UV, and the enzymes help repair the damage from any UV that manages to get through,” Kilmer says. “It’s my hope that all sunscreens will eventually have this stuff.” When discussing the products with patients, Kilmer mainly talks about preventing wrinkles and age spots, not melanoma. “They don’t always jump on board if you make it all about skin cancer,” she says.