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Tanning bed users have more melanomas in uncommonly diagnosed areas, according to new research.

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The mutation burden of melanocytes in tanning bed users was nearly twofold that of melanocytes from control donors [median mutations per megabase (mut/Mb) of 5.69 versus 2.86] (Fig. 2B). This trend remained significant when we separately compared melanocytes by anatomic site (median mut/Mb of 8.82 versus 4.60 in upper back and 5.19 versus 2.05 in lower back) (Fig. 2C). The mutation burdens of cells from both control groups were less than the cells in the tanning cohort (fig. S2A).

We developed a linear mixed-effects (LME) model to determine whether tanning bed users had higher mutation burdens after adjusting for anatomic site and outliers (18). Specifically, we compared the tanning and control cohorts at the cell level while introducing a variable for anatomic site and including a random effect for different donors (fig. S3). In this analysis, the cells from tanning bed users had a significantly higher mutation burden (P = 1.3 × 10⁻²). However, we noted that cells from one donor (donor 59) had an extremely high mutation burden. To ensure that this donor was not entirely responsible for the differences observed, the analyses were repeated with a robust linear mixed-effects (RLME) model, which is less sensitive to outliers, heavy-tailed distributions, and model violations (19). In this analysis, the cells from tanning bed users continued to have a significantly higher mutation burden (P = 6.1 × 10⁻⁵).

We also compared mutation burdens at the biopsy level. We defined the mutation burden of a biopsy as the median mutation burden of its constituent melanocytes. Our statistical power was more limited in these comparisons because there were fewer independent biopsies than individual cells. On the lower back, tanning bed biopsies had significantly higher mutation burdens than control biopsies (Fig. 2D and fig. S2B). The difference was not statistically significant on the upper back (Fig. 2E and fig. S2C), although cell-level differences were significant at this site (Fig. 2C). The upper back is the most common site of sunburn (20) and melanoma (21), indicating that natural sunlight can induce high mutation burdens at this site, even without the additional influence of tanning beds. Since tanning bed–induced mutations would be expected to contribute to a smaller proportion of mutations in the underlying skin cells from the upper back, we would need a larger sample size to detect a statistically significant difference at the biopsy level.

Tanning bed use is tied to almost a three-fold increase in melanoma risk, and for the first time, scientists have shown how these devices cause melanoma-linked DNA damage across nearly the entire skin surface, reports a new study led by Northwestern Medicine and University of California, San Francisco.

The findings are published in Science Advances.

Melanoma, the deadliest skin cancer, kills about 11,000 in the U.S. each year. Despite decades of warnings, the precise biological mechanism behind tanning beds’ cancer risk remained unclear. The indoor tanning industry, which is making a comeback, has used that uncertainty to argue that tanning beds are no more harmful than sunlight.

Chen, W., Wang, Y., Yao, Z. et al. ECT2⁺ cell group acts as cancer stem cell in malignant pleomorphic adenoma. npj Precis. Onc. 9, 189 (2025). https://doi.org/10.1038/s41698-025-00974-x.

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Background: The identification of clinical factors affecting the gray-scale median (GSM) and determination of GSM diagnostic utility for differentiating between symptomatic and asymptomatic internal carotid artery (ICA) stenosis. Methods: This study included 45 patients with asymptomatic and 40 patients with symptomatic ICA stenosis undergoing carotid endarterectomy (CEA). Echolucency of carotid plaque was determined using computerized techniques for the GSM analysis. Study groups were compared in terms of clinical risk factors, coexisting comorbidities, and used pharmacotherapy. Results: Mean GSM values in the symptomatic group were significantly lower than in the asymptomatic group (p < 0.001). Both in the univariate as well as in the multiple regression analysis, GSM was significantly correlated with D-dimers and fasting plasma glucose levels and tended to correlate with β-adrenoceptor antagonist use in the symptomatic group. In asymptomatic patients, GSM was associated with the presence of grade 2 and grade 3 hypertension, and tended to correlate with the use of metformin, sulfonylureas, and statin. Independent factors for GSM in this group remained as grade 3 hypertension and statin’s therapy. The receiver operating characteristic (ROC) analysis revealed that GSM differentiated symptomatic from asymptomatic ICA stenosis with sensitivity and specificity of 73% and 80%, respectively. Conclusion: The completely diverse clinical parameters may affect GSM in symptomatic and asymptomatic patients undergoing CEA, whose clinical characteristics were similar in terms of most of the compared parameters. GSM may be a clinically useful parameter for differentiating between symptomatic and asymptomatic ICA stenosis.