Jean Claude Dusingize

Cigarette Smoking and the Risks of Basal Cell Carcinoma and Squamous Cell Carcinoma

Sunlight is the principal environmental risk factor for keratinocyte cancers, but other carcinogens have also been implicated, including tobacco smoke. Findings have been conflicting, however. We investigated associations between cigarette smoking and incidence of basal cell carcinoma (BCC) or squamous cell carcinoma (SCC) in QSkin, a prospective study of skin cancer (Nxa0= 43,794). Smoking history was self-reported at baseline; newly diagnosed BCCs and SCCs were ascertained through data linkage and verified by histopathology reports. We restricted analyses to white participants who at baseline reported no past history of skin cancer excisions and no more than five destructively treated actinic skin lesions. We fitted Cox proportional hazards models, adjusted for known confounders. Compared with never smokers, current smokers had significantly lower risks of BCC (hazard ratioxa0= 0.6; 95% confidence intervalxa0= 0.4-0.9) but significantly higher risks of SCC (hazard ratioxa0= 2.3; 95% confidence intervalxa0= 1.5-3.6). Former smokers had similar risks for BCC and SCC as never smokers. Among smokers, we observed no dose-response trends with duration of smoking, intensity, or time since quitting. On further analysis, current smokers had fewer skin examinations and procedures than never smokers, suggesting greater opportunities for detection among never smokers. Strengths include large sample size, prospective design, and virtually complete follow-up; however, histologic details were missing for a proportion of excised tumors. In conclusion, current smokers had a lower incidence of BCC (possibly because of detection bias) but higher rates of SCC.

Risk stratification for melanoma: models derived and validated in a purpose-designed prospective cohort.

BackgroundnRisk stratification can improve the efficacy and cost-efficiency of screening programs for early detection of cancer. We sought to derive a risk stratification tool for melanoma that was suitable for the general population using only self-reported information.nnnMethodsnWe used melanoma risk factor information collected at baseline from QSKIN, a prospective cohort study of Queensland adults age 40 to 69 years at recruitment (n = 41 954). We examined two separate outcomes: 1) invasive melanomas and 2) all melanomas (invasive + in situ) obtained through data linkage to the cancer registry. We used stepwise Cox proportional hazards modeling to derive the risk models in a randomly selected two-thirds sample of the data set and assessed model performance in the remaining one-third validation sample.nnnResultsnAfter a median follow-up of 3.4 years, 655 (1.6%) participants developed melanoma (257 invasive, 398 in situ). The prediction model for invasive melanoma included seven terms. At baseline, the strongest predictors of invasive melanoma were age, sex, tanning ability, number of moles at age 21 years, and number of skin lesions treated destructively. The model for all melanomas (ie, invasive and in situ) included five additional terms. Discrimination in the validation data set was high for both models (C-index = 0.69, 95% confidence interval [CI] = 0.62 to 0.76, and C-index = 0.72, 95% CI = 0.69 to 0.75, respectively), and calibration was acceptable.nnnConclusionsnSuch a tool could be used to target surveillance activities to those at highest predicted risk of developing melanoma over a median duration of 3.4 years.

Association between phenotypic characteristics and melanoma in a large prospective cohort study

To delineate causal pathways for melanoma, it is essential to derive unbiased estimates of risk. Extant knowledge derives largely from case-control studies with potential for bias. In a population-based prospective study (QSkin, nxa0= 38,854), we assessed melanoma risks associated with pigmentation characteristics and other phenotypes, and we explored additive interactions. We fitted Cox proportional hazards models to adjust for other factors to estimate the independent effects of each characteristic on melanoma risk. During a mean follow-up of 3.5 years, 642 (1.5%) participants developed melanoma (253 invasive, 389 in situ). The characteristics most strongly associated with invasive melanoma were self-reported nevus density at age 21 years (many vs. no moles hazard ratio [95% confidence interval]xa0= 4.91 [2.81-8.55]), inability to tan (no tan vs. deep tan, hazard ratio [95% confidence interval]xa0= 3.39 [1.85-6.20]), and red hair color (vs. black, hazard ratio [95% confidence interval]xa0= 3.11 [1.50-6.43]). Propensity to sunburn was not associated with melanoma after tanning inability was adjusted for. People with both high nevus density and a history of multiple keratinocyte cancers had significantly higher melanoma risks than those with only one of those traits. We infer that melanoma risk is more strongly related to nevus density and inability to tan than susceptibility to sunburn.

Smoking and Cutaneous Melanoma: Findings from the QSkin Sun and Health Cohort Study

Background: Previous studies suggest that smokers have lower risks of cutaneous melanoma than nonsmokers, but data from population-based prospective studies are scarce. We investigated associations between smoking and melanoma in a cohort study purpose-designed to investigate skin cancer outcomes. Methods: Participants with no prior history of melanoma (n = 38,697) completed a risk factor survey at baseline (2011). Patients were followed through linkage to the cancer registry. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between smoking (including intensity, duration, time since quitting) and melanoma using multivariate Cox proportional hazards regression, accounting for death as a competing event. Results: During a mean follow-up of 3.5 years, invasive melanomas developed in 247 participants. Compared with never smokers, former smokers (but not current smokers) had lower risks of invasive melanoma (HR 0.76; 95% CI, 0.57–1.01). Among former smokers, risks were lower with greater quantity of cigarettes smoked (HR 0.75; 95% CI, 0.56–0.98 per 10 cigarettes/day). No association was observed with duration of smoking while longer time since quitting was associated with a relative risk of melanoma that was not significantly different from the null (HR 1.18; 95% CI, 0.91–1.51, for every 10 years since quitting). Conclusions: We observed complex associations between smoking and melanoma, with some suggestion that former smokers had lower risks than never or current smokers. The apparent inverse association among former smokers may be due to residual confounding, although surveillance bias or biological effects cannot be excluded entirely. Impact: Smoking does not increase the risk of cutaneous melanoma. Cancer Epidemiol Biomarkers Prev; 27(8); 874–81. ©2018 AACR.

Hormonal and reproductive factors and incidence of basal cell carcinoma and squamous cell carcinoma in a large, prospective cohort

To the Editor: Previous research suggests that hormonal factors might influence the development of keratinocyte cancers (KCs), but the evidence is inconsistent. A potential mechanism for the association is photosensitization with use of estrogen, a hormone included in menopausal hormone therapy (MHT). We examined the association between hormonal and reproductive factors and subsequent risk for first histologically confirmed primary basal cell carcinoma (BCC) or squamous cell carcinoma (SCC) in a large cohort of women that was well-characterized with respect to important potential confounding factors, as well as clinical factors that might inform about possible detection bias. White women from the QSkin Sun and Health Study with no history of melanoma, excisions for skin cancer, or [5 self-reported ablations for sunspots or skin cancers (n 1⁄4 11,152) were eligible for the study. The latter criterion was stipulated to minimize potential bias caused by including women with prior disease in the analyses, considering that KCs can be ablated without a histologically confirmed diagnosis. Information on hormonal and reproductive factors was self-reported at baseline (2011). KC outcomes were identified from the administrative medical claims data (Medicare, Australia’s universal health insurance scheme) until June 30, 2014, and exact diagnoses of BCC and SCC were determined through linked pathology records. We used Cox proportional hazards models to estimate the hazard ratios (HRs) associated with oral contraceptives (OCs) andMHT, age atmenarche, menopausal status, age atmenopause andparity, and first histologically confirmed BCC or SCC while taking into account the effects of age, sun exposure, and phenotypic and lifestyle characteristics. Selected characteristics of the study cohort, overall and amongst postmenopausal women stratified by MHT use, are provided in Supplemental Table I (available at http://www.jaad.org). During a median follow-up of 3 years, 336 women developed

Physician skin checks before the diagnosis of melanoma correlate with tumor characteristics

1 BCCs (mean age 55.0 years) and 85 women,

Hormonal and reproductive factors and incidence of basal cell carcinoma in a population-based cohort - eScholarship

1 SCCs (mean age 55.6 years). We found no association between incidence of BCC or SCC and OC use (ever or never, duration), parity, or age at menarche or menopause (Tables I and II). Among postmenopausal women, ever (vs never) use of MHT at baseline was associated with an increased risk for BCC (adjusted HR 1.46; 95% confidence interval 1.07-1.97), but there was no dose response with duration of use (Ptrend 1⁄4 .2; Table I). MHT use was not associated with SCC (adjusted HR 0.79; 95% confidence interval 0.45-1.38). We investigated detection bias as a possible explanation for the positive association between MHT use and BCC through analyses stratified by self-reported history of skin checks by a doctor and number of Medicare claims for doctor consultations, biopsies, and cryotherapy treatments during follow-up; we observed no material difference in the effect estimates according to these factors. The association between MHT use and BCC did not differ materially across strata of sun exposure variables (data not shown). Our findings in relation to both OC and MHT use and risk for BCC accord with findings from 2 other prospective studies, the US Radiologic Technologists Study and the Danish Diet, Cancer, and Health cohort, although a significant trend with durationofMHTusewasobserved in theUSRadiologic Technologists Study cohort. Limitations of our study was the relatively short follow-up and constrained sample size that limited analyses for SCC. In summary, we did not observe an association between OC use or reproductive factors and incidence of BCC or SCC, but we did find a modest positive association between ever use of MHT and BCC only. Although we found no conclusive evidence of detection bias or confounding to explain the latter finding, in view of the lack of a dose-response relationship, we counsel cautious interpretation until further longitudinal studies have explored these associations.