Continuing to illuminate the mechanisms underlying UV-mediated melanomagenesis

Dellinger, Ryan W.; Liu‐Smith, Feng; Meyskens, Frank L.

doi:10.1016/j.jphotobiol.2014.06.006

Cited by 10 publications

(9 citation statements)

References 62 publications

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“…It is well documented that UV radiation and oxidative stress are linked [37], both of which can be differentially impacted by sex hormones. As redox biology is unique in melanocytes (evidenced by its regulation via melanocytic master regulator MiTF [38,39]), melanocytes may undergo a lineage-specific UV-induced DNA damage repair which is highly likely impacted by hormones and thus result in differential mutation rates.…”

Section: Discussionmentioning

confidence: 99%

Race-, Age-, and Anatomic Site-Specific Gender Differences in Cutaneous Melanoma Suggest Differential Mechanisms of Early- and Late-Onset Melanoma

Yuan

Edwards

et al. 2019

IJERPH

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In order to explore melanoma risk factors through gender-, age-, race-, and site-specific incidence rates, malignant melanoma cases from the Caucasian whites and non-whites were retrieved from the US SEER database. Age-standardized, age-, and site-specific tumor rates were calculated. All races and both genders showed positive annual average percentage changes (AAPCs) over the years, but AAPCs varied at different body sites, with men’s trunk exhibiting the fastest increase. Non-whites were diagnosed at a significantly younger age than whites and showed a trend towards fewer gender differences in the age of diagnosis. However, non-whites and whites showed a similar pattern of age-specific gender differences in the incidence rate ratios. A consistent spiked difference (female vs. male, incidence rate ratio (IRR) >2) was observed at or near the age of 20–24 in all race groups and at all body sites. The highest female vs. male IRR was found in the hip and lower extremities, and the lowest IRR was found in the head and neck region in all races. These race-, gender-, and site-dependent differences suggest that age-associated cumulative sun exposure weighs significantly more in late-onset melanomas, while genetics and/or pathophysiological factors make important contributions to early-onset melanomas.

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Section: Discussionmentioning

confidence: 99%

Race-, Age-, and Anatomic Site-Specific Gender Differences in Cutaneous Melanoma Suggest Differential Mechanisms of Early- and Late-Onset Melanoma

Yuan

Edwards

et al. 2019

IJERPH

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“…Despite all the knowledge about melanoma biology, this cancer remains one of the greatest challenges of our day [1,5,32,33], mainly due to the acquired resistance to chemotherapy and radiation [5,30]. Therefore, melanoma treatment remains essentially surgical [1,6,7,10].…”

Section: Discussionmentioning

confidence: 99%

“…There are some established risk factors for melanoma development, like family history [9,10], genetic and hereditary factors, as well as environmental factors [1,2,3]. Nowadays, nutritional factors have emerged as possible modifiable risk factors for cutaneous melanoma, since a growing number of studies have shown that a balanced diet, rich in fruits and vegetables, is associated with lower risks for several types of cancer, including cutaneous melanoma.…”

Section: Introductionmentioning

confidence: 99%

Vitamin A Enhances Macrophages Activity Against B16-F10 Malignant Melanocytes: A New Player for Cancer Immunotherapy?

Oliveira¹,

Costa²,

Faria³

et al. 2019

Medicina

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Background and objectives: The incidence of cutaneous melanoma has been increasing. Melanoma is an aggressive form of skin cancer irresponsive to radiation and chemotherapy, rendering this cancer a disease with poor prognosis: In order to surpass some of the limitations addressed to melanoma treatment, alternatives like vitamins have been investigated. In the present study, we address this relationship and investigate the possible role of vitamin A. Materials and Methods: We perform a co-culture assay using a macrophage cell model and RAW 264.7 from mouse, and also a murine melanoma cell line B16-F10. Macrophages were stimulated with both Escherichia coli lipopolysaccharides (LPS) as control, and also with LPS plus vitamin A. Results: Using B16-F10 and RAW 264.7 cell lines, we were able to demonstrate that low concentrations of vitamin A increase cytotoxic activity of macrophages, whereas higher concentrations have the opposite effect. Conclusion: These findings can constitute a new point of view related to immunostimulation by nutrients, which may be considered one major preventive strategy by enhancing the natural defense system of the body.

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“…Although the causal network of melanoma has not yet been fully elucidated [ 17 ], UV exposure is the most tangible environmental risk factor that can be readily modified by behavioral precautions [ 18 ]. Therefore, the purpose of this study was to explore the relationship between the hypothesized photobiological pathway and risk of melanoma.…”

Section: Introductionmentioning

confidence: 99%

A Case-Control Study of the Genetic Variability in Reactive Oxygen Species—Metabolizing Enzymes in Melanoma Risk

Yuan

Yourk

Farhat

et al. 2018

IJMS

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Recent studies have shown that ultraviolet (UV)-induced chemiexcitation of melanin fragments leads to DNA damage; and chemiexcitation of melanin fragments requires reactive oxygen species (ROS), as ROS excite an electron in the melanin fragments. In addition, ROS also cause DNA damages on their own. We hypothesized that ROS producing and metabolizing enzymes were major contributors in UV-driven melanomas. In this case-control study of 349 participants, we genotyped 23 prioritized single nucleotide polymorphisms (SNPs) in nicotinamide adenine dinucleotide phosphate (NADPH) oxidases 1 and 4 (NOX1 and NOX4, respectively), CYBA, RAC1, superoxide dismutases (SOD1, SOD2, and SOD3) and catalase (CAT), and analyzed their associated melanoma risk. Five SNPs, namely rs1049255 (CYBA), rs4673 (CYBA), rs10951982 (RAC1), rs8031 (SOD2), and rs2536512 (SOD3), exhibited significant genotypic frequency differences between melanoma cases and healthy controls. In simple logistic regression, RAC1 rs10951982 (odds ratio (OR) 8.98, 95% confidence interval (CI): 5.08 to 16.44; p < 0.001) reached universal significance (p = 0.002) and the minor alleles were associated with increased risk of melanoma. In contrast, minor alleles in SOD2 rs8031 (OR 0.16, 95% CI: 0.06 to 0.39; p < 0.001) and SOD3 rs2536512 (OR 0.08, 95% CI: 0.01 to 0.31; p = 0.001) were associated with reduced risk of melanoma. In multivariate logistic regression, RAC1 rs10951982 (OR 6.15, 95% CI: 2.98 to 13.41; p < 0.001) remained significantly associated with increased risk of melanoma. Our results highlighted the importance of RAC1, SOD2, and SOD3 variants in the risk of melanoma.

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Continuing to illuminate the mechanisms underlying UV-mediated melanomagenesis

Cited by 10 publications

References 62 publications

Race-, Age-, and Anatomic Site-Specific Gender Differences in Cutaneous Melanoma Suggest Differential Mechanisms of Early- and Late-Onset Melanoma

Race-, Age-, and Anatomic Site-Specific Gender Differences in Cutaneous Melanoma Suggest Differential Mechanisms of Early- and Late-Onset Melanoma

Vitamin A Enhances Macrophages Activity Against B16-F10 Malignant Melanocytes: A New Player for Cancer Immunotherapy?

A Case-Control Study of the Genetic Variability in Reactive Oxygen Species—Metabolizing Enzymes in Melanoma Risk

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