Management of nonmelanoma skin cancer in 2007

As the incidence of nonmelanoma skin cancer (NMSC) increases, so does the number of modalities used to treat this condition. Surgery is the most frequent approach used to treat NMSC, and clinicians usually perform Mohs micrographic surgery, conventional excision, electrodesiccation and curettage or cryosurgery. The 'gold standard' for treatment continues to be Mohs micrographic surgery, but owing to the time and expense involved with this procedure, it is indicated only in patients with aggressive tumors or those where disfigurement or functional impairment is a risk. Although radiation therapy is effective, its use is limited because of the side effects induced; radiation therapy can be used in certain patients who are not surgical candidates. Newer noninvasive options for NMSC include topical chemotherapeutics, biological-immune-response modifiers, retinoids, and photodynamic therapy, which can be used particularly in patients with superficial tumors. Treatments should be tailored to tumor type, location, size, and histological pattern, and although surgical methods remain the most frequently used, newer noninvasive treatments can be used in select tumors and may reduce morbidity.     

Repair capacity for UV light induced DNA damage associated with risk of nonmelanoma skin cancer and tumor progression.

PURPOSE: To examine the role of suboptimal DNA repair capacity (DRC) for UV light-induced DNA damage in the development of nonmelanoma skin cancer (NMSC) and tumor progression. EXPERIMENTAL DESIGN: We conducted a hospital-based case-control study of 255 patients with newly diagnosed NMSC [146 with basal cell carcinoma (BCC) and 109 with squamous cell carcinoma (SCC)] and 333 cancer-free controls. We collected information on demographic variables and risk factors from questionnaires, tumor characteristics from medical records, and lymphocytic DRC phenotype by the host-cell reactivation assay. Multivariable logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (95% CI). RESULTS: Overall, there was a relative 16% reduction in DRC in NMSC patients compared with controls (P < 0.001 for BCC and for SCC, respectively). DRC below the controls' median value was associated with increased risk significantly for BCC (OR, 1.62; 95% CI, 1.07-2.45) but borderline for SCC (OR, 1.63; 95% CI, 0.95-2.79) after adjustment for age, sex, and other assay-related covariates. When the highest tertile of controls' DRC was used as the reference, the intermediate and low DRC were associated with a statistically significant trend for increasing risk for both BCC (P(trend) = 0.007) and SCC (P(trend) = 0.020). However, patients with aggressive or multiple SCC tended to have a higher DRC than those with nonaggressive or single SCC. CONCLUSIONS: Reduced DRC is an independent risk factor for BCC and single or nonaggressive SCC but not for multiple primaries, local aggressiveness, or recurrence of NMSC.     

Serum carotenoids and alpha-tocopherol and risk of nonmelanoma skin cancer.

BACKGROUND: Carotenoids and tocopherols have been hypothesized to protect against cancer. METHODS: We prospectively evaluated associations of several carotenoids and alpha-tocopherol with risk of nonmelanoma skin cancer using serum collected at baseline from 302 subjects in the Isotretinoin-Basal Cell Carcinoma Prevention Trial. All subjects had at least two BCCs in the 5 years prior to randomization. During 5 years of follow-up, 70 subjects did not develop a nonmelanoma skin cancer, 221 developed a BCC, and 85 developed a squamous cell carcinoma (SCC). Cox proportional hazards models were used to estimate risk ratios. Models were stratified by clinical center and gender and adjusted for age, solar damage, skin type, number of prior BCCs and/or SCCs, treatment group, body mass index, and serum low-density lipoprotein-cholesterol and high-density lipoprotein-cholesterol. RESULTS: Risk of developing a subsequent BCC was not related to serum levels of any of the carotenoids measured or to alpha-tocopherol. Serum levels of alpha-carotene, beta-carotene, lycopene, and alpha-tocopherol also were not independently related to risk of a subsequent SCC. However, serum lutein, zeaxanthin, and beta-cryptoxanthin were positively related to SCC risk; risk ratios for subjects in the highest versus lowest tertiles of these micronutrients were 1.63 [95% confidence interval (95% CI) 0.88-3.01; P for trend = 0.01], 2.40 (95% CI 1.30-4.42; P for trend = 0.01), and 2.15 (95% CI 1.21-3.83; P for trend = 0.09), respectively. CONCLUSION: Additional research is needed on the relationship of carotenoids to SCC risk in the general population and in subsets of the population who are at increased risk.     

Association of nonmelanoma skin cancer with second malignancy

BACKGROUND: Heightened risks of second cancers have been reported in patients with nonmelanoma cancer of the skin (NMSC), but this association has not been studied in a large, ethnically diverse, multigeographic population. METHODS: This cross-sectional study assessed the association of NMSC with another malignancy in the Women's Health Initiative Observational Study, a study that was conducted in 40 communities throughout the U.S. and involved 93,676 postmenopausal women ages 50-79 years. Cancer history, demographics, and previous and current risk exposures were determined by questionnaire at a baseline examination. Logistic regression was used to assess the association (odds ratio) of a history of NMSC with a history of other (non-NMSC) cancers controlling for age and potential confounding factors. Complete cancer data were available in 92,658 women. RESULTS: In age-adjusted analyses, women with a history of NMSC (n = 7554 women) were 2.30 times as likely to report a history of another cancer, other than NMSC, compared with women who had no history of NMSC (95% confidence interval [95% CI], 2.18-2.44). In a subgroup analysis, black women with NMSC had 7.46 times the odds (95% CI, 3.08-18.0) of reporting a second malignancy compared with black women without NMSC. CONCLUSIONS: This study provides additional evidence of an association between NMSC and another malignancy in a large, multiethnic population.     

XPD polymorphism and risk of subsequent cancer in individuals with nonmelanoma skin cancer.

BACKGROUND: Individuals with nonmelanoma skin cancer (NMSC) are at increased risk of developing subsequent cancers. Genetic predisposition to reduced DNA repair capacity may be an underlying susceptibility factor explaining the excess risk of malignancies. To test this hypothesis, a cohort study was conducted to examine the association between XPD Lys751Gln polymorphism and risk of a second primary cancer in individuals with NMSC. METHODS: A subgroup of 481 individuals with a history of NMSC who participated in the CLUE II community-based cohort was followed for the development of a second primary cancer. Blood specimens donated in 1989 were genotyped for the XPD Lys751Gln polymorphism using the 5' nuclease assay. Cox proportional regression with delayed entry was used to calculate the incidence rate ratio (IRR) and 95% confidence interval (95% CI) for risk of developing a second primary cancer according to XPD genotype. All statistical tests were two sided. RESULTS: Eighty individuals developed a second primary cancer. The most frequent occurring cancers were of the prostate (18%), lung (15%), and breast (15%). Persons with at least one Gln allele had an increased risk of a second primary cancer compared with the reference Lys/Lys genotype (adjusted IRR 2.22, 95% CI 1.30-3.76). When the reference category was limited to never smokers with the Lys/Lys genotype, the risk of developing a second primary cancer associated with having at least one Gln allele was increased >3-fold in both never smokers (IRR 3.93, 95% CI 1.36-11.36) and ever smokers (IRR 6.14, 95% CI 2.17-17.37). CONCLUSION: These findings suggest that individuals with NMSC who have the variant XPD Gln allele are at increased risk of developing a second primary cancer.     

Daily coffee consumption and prevalence of nonmelanoma skin cancer in Caucasian women.

The purpose of this study was to assess the relationship between daily coffee consumption and nonmelanoma skin cancer. This study was a cross-sectional analysis of women enrolled in the Women's Health Initiative Observational Study (n=93 676). As nearly all cases of self-reported nonmelanoma skin cancer occurred among Caucasian women (97.8%), we focused our analyses on this group. Compared with nondrinkers, women drinking only caffeinated coffee on a daily basis had a 10.8% lower prevalence of nonmelanoma skin cancer. Consumption of six or more cups of caffeinated coffee per day was associated with a 36% reduction in nonmelanoma skin cancer. After adjusting for various demographic and life style variables, daily consumption of six or more cups was associated with a 30% reduced prevalence of nonmelanoma skin cancer. In contrast to caffeinated coffee, daily consumption of decaffeinated coffee was not associated with a significant change in self-reported nonmelanoma skin cancer for Caucasian women. Daily caffeinated coffee consumption was associated with a dose-related decreased prevalence of nonmelanoma skin cancer in Caucasian women.     

Treatment of nonmelanoma skin cancer at a large Australian center

One thousand one hundred fifty-four cases of nonmelanoma skin cancer (NMSC) referred to the Consultative Skin Clinic at Peter MacCallum Cancer Institute (PMCI) (Melbourne, Australia) in 1980 were reviewed. The median age was 68 years, and the male to female ratio was 1.5:1. Final diagnosis was basal cell carcinoma (BCC) in 901 patients (78%), squamous cell carcinoma (SCC) in 242 patients (21%), and basosquamous carcinoma in 11 patients (1%). Seven hundred twelve (62%) were biopsy proven. Comparison of clinical and histologic diagnoses showed that BCC were correctly diagnosed clinically in 85% of cases but only 53% of SCC were correctly diagnosed. The distribution of sites was as follows: head and neck 871 (75%), limbs 131 (11%), trunk 50 (4%), and multiple sites 102 (9%). One thousand eighty-nine (94%) had primary lesions and 65 (6%) had recurrent lesions. The lesions were treated with surgery in 55% of cases, superficial radiotherapy in 39%, other types of radiotherapy in 3%, cryotherapy in 1%, and 5-fluorouracil in 0.2%. Recurrent lesions, lesions on the eyelids, ears or nose, and T4 lesions were significantly associated with increased failure rates. Superficial radiotherapy was associated with a 2.3-fold increase in failure rate compared to surgery when other prognostic factors were taken into account (P = 0.01, 95% confidence interval = 1.2-4.3). Nonsuperficial radiotherapy was associated with an 11.5-fold increase in failure rate compared to surgery (P less than 0.0001, 95% confidence interval = 4.9-27.1), but several of these cases were treated for palliative purposes only. The results of, and indications for treatment with surgery or radiotherapy at PMCI are discussed.     

Seroreactivity to cutaneous human papillomaviruses among patients with nonmelanoma skin cancer or benign skin lesions.

Cutaneous human papillomaviruses (HPV) are common in nonmelanoma skin cancers, benign skin lesions, and healthy skin. Increased seroprevalences for cutaneous HPV among nonmelanoma skin cancer patients have been described. To determine whether antibodies to cutaneous HPV are related to presence of the virus and/or to skin disease, we collected serum and biopsies from both lesions and healthy skin from 434 nonimmunosuppressed patients (72 squamous cell carcinomas, 160 basal cell carcinomas, 81 actinic keratoses, and 121 benign lesions). Biopsies were analyzed for HPV DNA by PCR, cloning, and sequencing. Serum antibodies to the major capsid protein L1 of HPV 1, 5, 6, 8, 9, 10, 15, 16, 20, 24, 32, 36, 38, and 57 as well as to the oncoproteins E6 and E7 of HPV 8 and 38 were detected using a multiplexed fluorescent bead-based assay. Type-specific seroprevalence among patients with the same type of HPV DNA (sensitivity of serology) varied from 0% to at most 28%. Presence of HPV DNA and antibodies to the same HPV type was not significantly correlated. However, seropositivity to any HPV type was significantly more common among patients positive for HPV DNA of any HPV type (odds ratio, 1.90; 95% confidence interval, 1.55-2.34). Seroprevalences were similar among the different patient groups but was, for most HPV types, somewhat higher among squamous cell carcinoma patients than among basal cell carcinoma patients (P < 0.01). In conclusion, additional studies are required to clarify the biological meaning of seropositivity as a marker of cutaneous HPV infection and skin disease.     

Prospective study of genital human papillomaviruses and nonmelanoma skin cancer

Genital high‐risk human papillomaviruses (HPVs) cause cervical cancer and are also found in a small proportion of nonmelanoma skin cancers (NMSCs). We used cancer registry linkages to follow the 856,000 serum donors included in the Southern Sweden Microbiology Biobank or the Janus Biobank in Norway, for incident skin cancers occurring up to 30 years after serum donation. Serum samples taken before diagnosis of squamous cell carcinoma (SCC) (N = 633), basal cell carcinoma (BCC) (N = 1990) or other NMSC (N = 153) and matched samples from control donors were tested for antibodies to the genital HPV types 16 and 18. Both HPV 16 and 18 were associated with increased risk for SCC [odds ratio (OR) 1.6, 95% confidence interval (CI) 1.1–2.6 and OR 1.7, 95% CI 1.1–2.5, respectively] and other NMSC (OR 2.3, 95% CI 1.0–5.2 and OR 3.5, 95% CI 1.4–8.7, respectively), but not for BCC. Tumor blocks from HPV16 or 18 seropositive cases were tested with real‐time polymerase chain reaction for presence of HPV16 or 18 DNA. No HPV18 DNA was found and only four of 79 SCC cases (two of which were from the perineum/perianal area), one of 221 BCC cases and zero of five cases with other NMSC contained HPV16 DNA. In conclusion, we found prospective evidence that HPV16 and 18 antibodies associate with SCC and other NMSC risk, but not with BCC risk. As only a small proportion of seropositive subjects had evidence of the corresponding HPV DNA in the tumor, most of this excess risk is likely to be due to confounders associated with genital HPV infection.     

Biological amplification factor for sunlight-induced nonmelanoma skin cancer at high latitudes

Data for the incidence of basal cell carcinomas (BCCs) and squamous cell carcinomas (SCCs) of the skin, registered for six regions of Norway during 10 years (1976-1985), were used to evaluate the biological amplification factor Ab for induction of these cancers by sunlight. Ab is the ratio of the increment in skin cancer production to the increment in causative sunlight exposure. Two different approximations were used for the action spectrum for carcinogenesis: an erythema action spectrum; and an action spectrum for mutagenesis of cells in the basal layer of the skin. These two fundamentally different approaches yielded Ab values that were similar to within about 10%: 2.1-2.3 for BCCs; and 1.6-1.8 for SCCs. Using a radiation amplification factor for ozone depletion of 0.8-1.1, we find that the total amplification factor for BCCs is within the range 1.6-2.1 and that that for SCCs is within the range 1.3-1.7 at northern latitudes of 60-70 degrees. Thus, an ozone depletion of 1% will result in an increase in the incidence of BCCs by 1.6-2.1% and of SCCs by 1.3-1.7%. There were no significant differences between the values for men and women. Neither was there any significant difference between Ab values found for skin commonly exposed to sunlight (face) and for skin sites normally covered by clothes and therefore receiving much lower exposures, in spite of the fact that the tumor density per unit skin area was a factor of 20 or more larger at the former sites. This observation, as well as the curves relating cancer incidence with annual exposure to carcinogenic sunlight, supports a power law relationship between cancer incidence and annual sun exposure. Sunlight appears to be the main cause of BCCs and SCCs even at the high latitudes of Northern Norway. All over, BCCs were found to be about 6 times more frequent than SCCs. The ratio of the incidence of BCCs to that of SCCs seemed to be independent of the latitude. Finally, BCCs were found to be equally frequent among men and women, while SCCs were found to be about twice as frequent among men as among women.     

光动力联合冷冻对非黑色素瘤性皮肤癌的临床疗效

目的探究光动力联合冷冻对非黑色素瘤性皮肤癌(NMSC)患者的临床疗效。方法根据治疗方案的不同将96例NMSC患者分为研究组(n=50)和对照组(n=46),对照组采用5-氨基酮戊酸光动力疗法(ALAPDT)治疗,研究组采用ALA-PDT联合冷冻治疗。比较两组患者的视觉模拟评分量表(VAS)评分、外观满意度、临床疗效、不良反应发生情况和3年无进展生存情况。结果研究组患者的VAS评分略高于对照组,但差异无统计学意义(P﹥0.05)。研究组患者的外观满意度、治疗总有效率均高于对照组,差异均有统计学意义(P﹤0.05)。研究组患者的不良反应总发生率略高于对照组,但差异无统计学意义(P﹥0.05)。两组患者的3年无进展生存时间和3年无进展生存率比较,差异均无统计学意义(P﹥0.05)。结论光动力联合冷冻治疗非黑色素瘤性皮肤癌的临床疗效较好,有利于皮损外观的恢复,患者的满意度高,不良反应少,患者的无进展生存期较长,可为不适宜行手术治疗的非黑色素瘤性皮肤癌患者提供新的治疗思路。     

Altered expression of bcl-2 family member proteins in nonmelanoma skin cancer

BACKGROUND: Differentiation, proliferation, and cell death are coordinated tightly within the epidermis. Alterations within keratinocytes that disrupt these processes are believed to contribute to the development of nonmelanoma skin cancers (NMSC). In the current study the authors examined the expression of selected members of the bcl-2 gene family in the skin and in case-matched samples of NMSC. METHODS: Immunohistochemistry was performed on tissue sections using antibodies against bcl-2, bcl-x, bax, and bak. Case-matched frozen nonneoplastic skin samples and tumor tissues were used for Western blot analysis. RESULTS: In normal epidermis, bcl-2 oncoprotein is expressed in keratinocytes of the basal layer but is down-regulated in suprabasal layers. The proapoptotic bax protein is expressed at low levels in basal keratinocytes and is up-regulated in suprabasal layers. The bcl-x and bak proteins both are expressed in the basal and spinous strata but are down-regulated in the granular cell layer. Both bcl-2 and bax were diffusely cytosolic whereas bcl-x and bak exhibited a distinct perinuclear distribution. Squamous cell carcinomas (SCC) were negative for bcl-2 whereas bcl-2 increased 5.5-fold in basal cell carcinomas (BCC). The distribution of bcl-x and bax proteins within BCC and SCC overlapped and were associated with squamous differentiation. Bax protein was increased twofold to threefold in NMSC. An increase in bak protein also was observed in SCC. However, bak was diffusely cytosolic within BCC in contrast to the perinuclear distribution in nonneoplastic keratinocytes. CONCLUSIONS: These findings suggest that altered expression of bcl-2 family members may play a role in the pathogenesis of NMSC.     

Surface mold brachytherapy for nonmelanoma skin cancer: Canadian patterns of practice

PurposeWe sought to describe the use of surface mold brachytherapy (SMBT) for nonmelanoma skin cancer in Canada.Methods and MaterialsA list of Canadian Association of Radiation Oncologists membership and provincial registries were used for a preliminary survey to identify radiation oncologists and physicists involved in the practice of SMBT. A detailed survey was sent electronically to individuals involved in treating with SMBT.ResultsOf 41 centers in Canada, 39 responded, with 7 centers indicating use of SMBT. Seven radiation oncologists and 5 physicists from 6 of 7 treating centers responded to the detailed survey, with an overall 75% individual response rate (12/16). General agreement was found regarding indications for SMBT which included irregular or curved surfaces, avoidance of deep structures, and requirement for small fields. There was consensus regarding some contraindications for SMBT such as tumor depth and size. Hypofractionated schedules were used in 5 of 6 centers and doses ranged from 50 Gy in 5 fractions once per week to 30 Gy in 10 fractions twice a day over 5 days. The most common dosimetric parameters for plan evaluation included D₉₀, D₉₅, D_100, and maximum skin dose.ConclusionsA minority of Canadian centers practice SMBT. In centers practicing SMBT, general agreement exists on general indications for its use. Given the wide variation in dose and fractionation used and the rarity of the indication a phase 2 Canadian protocol would be invaluable.     

Selenium supplementation and secondary prevention of nonmelanoma skin cancer in a randomized trial

The Nutritional Prevention of Cancer Trial was a double-blind, randomized, placebo-controlled clinical trial designed to test whether selenium as selenized yeast (200 microg daily) could prevent nonmelanoma skin cancer among 1312 patients from the Eastern United States who had previously had this disease. Results from September 15, 1983, through December 31, 1993, showed no association between treatment and the incidence of basal and squamous cell carcinomas of the skin. This report summarizes the entire blinded treatment period, which ended on January 31, 1996. The association between treatment and time to first nonmelanoma skin cancer diagnosis and between treatment and time to multiple skin tumors overall and within subgroups, defined by baseline characteristics, was evaluated. Although results through the entire blinded period continued to show that selenium supplementation was not statistically significantly associated with the risk of basal cell carcinoma (hazard ratio [HR] = 1.09, 95% confidence interval [CI] = 0.94 to 1.26), selenium supplementation was associated with statistically significantly elevated risk of squamous cell carcinoma (HR = 1.25, 95% CI = 1.03 to 1.51) and of total nonmelanoma skin cancer (HR = 1.17, 95% CI = 1.02 to 1.34). Results from the Nutritional Prevention of Cancer Trial conducted among individuals at high risk of nonmelanoma skin cancer continue to demonstrate that selenium supplementation is ineffective at preventing basal cell carcinoma and that it increases the risk of squamous cell carcinoma and total nonmelanoma skin cancer.     

Nonsteroidal anti‐inflammatory drugs and the risk of nonmelanoma skin cancer

Nonsteroidal anti‐inflammatory drugs (NSAIDs) have been assigned a promising role in the chemoprevention of various malignancies. However, epidemiological data on the association between NSAID use and nonmelanoma skin cancer (NMSC) are limited. To explore whether patients regularly exposed to systemic NSAIDs are at a reduced risk of basal cell carcinoma (BCC) or squamous cell carcinoma (SCC), we conducted a population‐based case‐control analysis using the Clinical Practice Research Datalink, a United Kingdom primary care database. We identified 65,398 patients with incident BCC and 7,864 patients with incident SCC diagnosed between 1995 and 2013 and matched 1 and 4 NMSC‐free controls to each BCC and SCC case, respectively, on age, sex, general practice, calendar time and years of history in the database. We compared prior NSAID exposure between cases and controls using multivariate conditional logistic regression analyses controlling for several potential confounders. Overall, we found no association between NSAID use and BCC, but when looking exclusively at users of single NSAID substances there was a suggestion of a reduced BCC risk in regular users of aspirin and ibuprofen (adjusted odds ratio [adj. OR]: 0.92, 95% confidence interval [CI]: 0.85–0.99 and adj. OR: 0.61, 95% CI: 0.48–0.78, respectively). The risk of SCC was slightly decreased in regular users of any NSAIDs (adj. OR: 0.89, 95% CI: 0.82–0.97), with the strongest risk reduction observed in current users of coxibs (adj. OR: 0.77, 95% CI: 0.62–0.95). These findings provide evidence that patients predisposed to NMSC might benefit from chemoprevention with NSAIDs.     

Seroreactivity to epidermodysplasia verruciformis-related human papillomavirus types is associated with nonmelanoma skin cancer

DNA from epidermodysplasia verruciformis-related human papillomavirus (EV-HPV) types is frequently found in nonmelanoma skin cancer (squamous and basal cell carcinoma). Epidemiological studies that investigate the relation between EV-HPV infection and nonmelanoma skin cancer are scarce. We designed a case-control study in which we looked for HPV infection in 540 cases with a history of skin cancer and 333 controls. By measuring seroreactivity to L1 virus-like particles of EV-HPV types 5, 8, 15, 20, 24, and 38 and the genital type HPV16 and by estimating the skin cancer relative risk among HPV seropositives, we analyzed whether EV-HPV serorecognition is associated with nonmelanoma skin cancer. Seroreactivity to five of the six EV-HPV types tested (HPV5, 8, 15, 20, and 24) was significantly increased in the squamous cell carcinoma cases. After adjusting for age and sex, the estimated squamous cell carcinoma relative risk was significantly increased in HPV8 and HPV38 seropositives [odds ratio (OR) = 14.7 (95% confidence interval (CI), 1.6-135) and OR = 3.0 (95% CI, 1.1-8.4), respectively]. The estimated relative risk for nodular and superficial multifocal basal cell carcinoma was also significantly increased in the HPV8 seropositives [OR = 9.2 (95% CI, 1.1-78.2) and OR = 17.3 (95% CI, 2.1-143), respectively] and in the HPV20 seropositives [OR = 3.2 (95% CI 1.3-7.9) and OR = 3.4 (95% CI 1.2-9.5), respectively]. The relative risk of developing malignant melanoma was not increased among HPV seropositives, and no associations were found for HPV16. Restricted analyses among the HPV seropositives only, to exclude distortion by interindividual differences in seroresponsiveness, underscored the significance of our findings. Restricted analyses among patients with skin cancer only, however, revealed that EV-HPV seropositivity was not significantly more present in patients with nonmelanoma skin cancer than in those with melanoma skin cancer. Taken together, our results indicate that EV-HPV serorecognition is nonspecifically associated with nonmelanoma skin cancer and suggest that EV-HPV-directed seroresponses are induced upon skin cancer formation, rather than upon infection.     

Association of surface ultraviolet B radiation levels with melanoma and nonmelanoma skin cancer in United States blacks.

Ultraviolet B (UVB) radiation exposure increases the risk of skin cancer in whites. Motivated by indications that United States geographic variation of relative skin cancer risk in blacks approaches that in whites, we used Poisson regression to estimate the risk of skin cancer in blacks as a function of average annual surface-levels of UVB radiation, measured by Robertson-Berger meters. United States data were used on deaths in 506 state economic areas, 1970-1994, and on incident cases in the nine areas of the Surveillance, Epidemiology, and End Results Program, 1973-1994. For black males, the age-adjusted relative risk of mortality for a 50% increase in UVB radiation was significantly above one for malignant melanoma, 1970-1994 (1.16; 95% confidence interval, 1.02-1.32) and nearly so for nonmelanoma skin cancer, 1970-1981 (1.18; 95% confidence interval, 1.00-1.39), for which the time period was chosen to avoid AIDS-related deaths from Kaposi's sarcoma. However, for black females, the relative risk of mortality was not significantly elevated for either skin cancer, and, for both black males and females, the relative risk of incidence was not significantly elevated for melanoma in the period 1973-1994. Incidence data on nonmelanoma skin cancer were not available. Although the public health implication is uncertain because of the much lower absolute risk of skin cancer in blacks compared with whites, the findings suggest that sunlight exposure increases skin cancer risk in blacks.     

Merkel cell polyomavirus sequences are frequently detected in nonmelanoma skin cancer of immunosuppressed patients

Recently, a new human polyoma virus has been identified in Merkel cell carcinomas (MCC). MCC is a highly aggressive neuroendocrine nonmelanoma skin cancer (NMSC) associated with immunosuppression. Clonal integration of this virus which was termed Merkel cell polyoma virus (MCPyV) was reported in a number of MCC. Squamous cell carcinoma (SCC) and basal cell carcinoma (BCC) are also NMSC and are the most frequent cancers in the setting of immunosuppression. A unique group of 56 NMSC from 11 immunosuppressed patients and 147 NMSC of 125 immunocompetent patients was tested for MCPyV by DNA PCR, targeting the Large T Antigen and the structural Viral Protein 1. NMSC included SCC, BCC and Bowen's disease (BD). In addition, normal skin and 89 colorectal cancers were tested. MCPyV specific sequences were significantly more frequently found in NMSC of immunosuppressed patients compared to immunocompetent patients (p < 0.001). In particular BD and BCC revealed a significant increased association of MCPyV of immunosuppressed patients (p = 0.002 and p = 0.006). Forty‐seven of 147 (32%) sporadic NMSC were MCPyV positive. Interestingly, 37.5% (36/96) of sporadic BCC of immunocompetent patients were MCPyV positive. No MCPyV was detected within normal skin and only 3 out of 89 of additionally tested colorectal cancers were MCPyV positive. Our data show that MCPyV is a frequently reactivated virus in immunocompromized patients. How MCPyV contributes to the pathogenesis of NMSC, i.e., BD, SCC and BCC, in immunosuppressed patients and in addition, potentially to the pathogenesis of a subset of sporadic BCC needs further investigations. © 2009 UICC