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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sunscreens are employed to mitigate the adverse effects of sunlight on skin but are primarily designed to prevent ultraviolet-B-associated burning and damage. The increasingly recognized role of ultraviolet A in aging, and possibly melanoma, highlights the need to include ultraviolet A screens; however, validation remains difficult. We have used a novel method to establish the efficacy of sunscreens, by measuring ultraviolet-A-induced free-radical production (thought to contribute towards ultraviolet-A-related aging and malignant change). Electron spin resonance spectroscopy was used to detect free radicals directly in human Caucasian skin during irradiation with levels of ultraviolet comparable to solar intensities. Using this system the protection afforded by three high factor sunscreens (sun protection factor 20+) that claim ultraviolet A protection was examined. Each sunscreen behaved similarly: at recommended application levels (> or = 2 mg per cm2) the ultraviolet-induced free radicals were reduced by only about 55%, and by about 45% at 0.5-1.5 mg per cm (0.5 mg per cm2 reported for common usage). A "free-radical protection factor" calculated on the basis of these results was only 2 at the recommended application level, which contrasts strongly with the erythema-based sun protection factors (mainly indicative of ultraviolet B protection) quoted by the manufacturers (20+). The disparity between these protection factors suggests that prolonged sunbathing (encouraged by use of these creams) would disproportionately increase exposure to ultraviolet A and consequently the risk of ultraviolet-A-related skin damage.
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PMID:Sunscreens inadequately protect against ultraviolet-A-induced free radicals in skin: implications for skin aging and melanoma? 1463 6

The Skin Cancer Foundation is the only national and international organization devoted exclusively to malignancies of the skin. It conducts public and medical education programs andprovides support for research and professional training to reduce the incidence, morbidity, and mortality of skin cancers. The following article is reprinted from The Melanoma Letter, Vol. 22, No. 3. Outstanding articles from the Foundation's award-winning publications, The Skin Cancer Foundation Journal, The Melanoma Letter, and Sun & Skin News will regularly appear here in upcoming issues. The Skin Cancer Foundation Journal, published annually, is a major part of the Foundation's professional and public education programs. Directed primarily to dermatologists, it also has an extensive readership among the general public. The Melanoma Letter, a widely respected quarterly newsletter for clinicians and researchers, focuses on the diagnosis, treatment, and prevention of the deadliest form of skin cancer. Sun & Skin News, a quarterly newsletter for the lay public, covers a broad range of topics related to skin health, including prevention and treatment of skin cancers and other sun-induced skin damage, the effectiveness of new sunscreen formulas, sunglasses, and the danger of tanning parlors.
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PMID:Consideration of statins for chemoprevention of cutaneous melanoma. 1569 98

Previous studies showed that long-wave ultraviolet (UVA) radiation induces severe skin damage through the generation of reactive oxygen species and the depletion of endogenous antioxidant systems. Recent results from our laboratory indicate a dramatic increase of both lipid peroxidation products (TBARS) and abnormal L-isoaspartyl residues, marker of protein damage, in UVA-irradiated human melanoma cells. In this study, the effects of hydroxytyrosol (DOPET), the major antioxidant compound present in olive oil, on UVA-induced cell damages, have been investigated, using a human melanoma cell line (M14) as a model system. In UVA-irradiated M14 cells, a protective effect of DOPET in preventing the uprise of typical markers of oxidative stress, such as TBARS and 2'7'-dichlorofluorescein (DCF) fluorescence intensity, was observed. In addition, DOPET prevents the increase of altered L-isoAsp residues induced by UVA irradiation. These protective effects are dose dependent, reaching the maximum at 400 microM DOPET. At higher concentrations, DOPET causes an arrest of M14 cell proliferation and acts as a proapoptotic stimulus by activating caspase-3 activity. In the investigated model system, DOPET is quantitatively converted into its methylated derivative, endowed with a radical scavenging ability comparable to that of its parent compound. These findings are in line with the hypothesis that the oxidative stress plays a major role in mediating the UVA-induced protein damage. Results suggest that DOPET may exerts differential effects on melanoma cells according to the dose employed and this must always be taken into account when olive oil-derived large consumer products, including cosmetics and functional foods, are employed.
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PMID:Hydroxytyrosol, a natural antioxidant from olive oil, prevents protein damage induced by long-wave ultraviolet radiation in melanoma cells. 1574 87

The C60-fullerene derivatives are expected, as novel and potent anti-oxidants, to more effectively protect skin cells against oxidative stress. UVA-induced oxidative stress is considered to promote melanogenesis and serious skin damage. The effect of any fullerene derivatives on UVA-induced melanogenesis is still unknown. Here, we evaluated effects of a water-soluble polyvinylpyrrolidone (PVP)-wrapped fullerene derivative (named "Radical Radical Sponge" because of its anti-oxidant ability) on melanogenesis, which was promoted by UVA-irradiation to human melanocytes and skin tissues. Radical Sponge markedly scavenged UVA-induced reactive oxygen species (ROS) inside human melanocytes as shown by fluorometry using the redox indicator CDCFH-DA. After treatment with Radical Sponge or other agents, human melanocytes and skin tissues were irradiated by UVA. Then, cellular melanin content, tyrosinase activity and the ultrastructural change of skin melanosomes were examined. Radical Sponge showed to significantly inhibit UVA-promoted melanogenesis in normal human epidermis melanocytes (NHEM) and human melanoma HMV-II cells within a non-cytotoxicity dose range. As compared with two whitening agents, arbutin and L-ascorbic acid, Radical Sponge demonstrated the stronger anti-melanogenic potential according to spectrophotometric quantification for extracted melanin. In human skin cultures also, UVA-promoted melanin contents were repressed by Radical Sponge according to Fontana-Masson stain, suggesting its ability to repress UVA-induced tanning. Transmission electron microscopic ultrastructural images also proved that UVA-increased melanosomes in human skin tissue were obviously reduced by Radical Sponge. The UVA-enhanced tyrosinase enzymatic activity in NHEM melanocytes was inhibited by Radical Sponge more markedly than by arbutin and L-ascorbic acid. The UVA-enhanced tyrosinase protein expression, together with cell-size fatness and dendrite-formation, was also inhibited more markedly by Radical Sponge according to immunostain and flow cytometry using anti-tyrosinase antibody. Thus the depigmentating action of Radical Sponge might be due to its down-regulating effect on the tyrosinase expression, which is initiated by UVA-caused ROS generation.
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PMID:Inhibitory effect of the water-soluble polymer-wrapped derivative of fullerene on UVA-induced melanogenesis via downregulation of tyrosinase expression in human melanocytes and skin tissues. 1733 22

It is widely known that ultraviolet light causes skin damage and melanoma. Different wavelengths of ultraviolet light penetrate the skin at different depths, causing varying levels of damage. Higher wavelengths tend to penetrate deeper and, consequently, are thought to induce a myriad of skin conditions, thereby playing a significant role in the photoaging process. Sunscreens containing the ultraviolet A blocker Mexoryl are important in impeding ultraviolet A light, potentially reducing many of the characteristics of skin aging and preventing biochemical changes that can lead to nonmelanoma carcinoma. Until now, sunscreen products sold in the United States focused on blocking ultraviolet B light. Those that did provide ultraviolet A filtering contained physical blocks (zinc oxide or titanium dioxide) or the chemical block Parsol 1789 (avobenzone). These broad-spectrum sunscreens have limitations, such as degradation under ultraviolet exposure, that resulted in decreased effectiveness. Mexoryl, a novel ultraviolet A filter, provides efficient ultraviolet A coverage, better photostability, and enhanced water resistance. Sunscreens containing Mexoryl are widely used in Europe and Canada. It was not until July 24, 2006, that the U.S. Food and Drug Association approved the compound.
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PMID:Mexoryl: a review of an ultraviolet a filter. 1780 38

Exposure to ultraviolet radiation is the main modifiable risk factor for melanoma. Strong epidemiologic and molecular evidence links sun exposure to the development of melanoma. Given the ubiquitous abundance of ultraviolet radiation, prevention aimed at blocking sun exposure is recommended by the American Academy of Dermatology, the Skin Cancer Foundation, the American Cancer Society, the Centers for Disease Control, and the Environmental Protection Agency. However, in contrast to other forms of skin damage, controversial data regarding sunscreen use and increased melanoma risk, possibly secondary to more overall sun exposure in melanoma patients, requires clarification. Primary care physicians may not be as adept at identifying worrisome lesions, but they have more opportunity to make the diagnosis. False positive identification of lesions and biopsy does not lead to extreme morbidity. Counseling patients to perform self skin examinations also contributes to important early detection.
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PMID:Melanoma: prevention and early detection. 1808 69

Ultraviolet radiation is estimated to be one of the most important risk factors for nonmelanoma and melanoma skin cancers. Athletes practicing outdoor sports receive considerable UV doses because of training and competition schedules with high sun exposure, and in alpine sports, by altitude-related increase of UV radiation and reflection from snow- and ice-covered surfaces. Extreme UV exposure in outdoor sports such as skiing, mountaineering, cycling, or triathlon has been documented in a series of dosimetric studies. Sweating because of physical exercise may contribute to UV-related skin damage as it increases the individual photosensitivity of the skin, facilitating the risk of sunburns. Large epidemiological studies showed that recreational activities such as sun exposure on the beach or during water sports were associated with an increased risk of basal cell carcinoma, whereas skiing has been shown to be at increased risk for squamous cell carcinoma. Risk factors of cutaneous melanoma such as the number of melanocytic nevi and solar lentigines have been found to be more frequent in subjects practicing endurance outdoor sports. An increased risk for cutaneous melanoma may be assumed for these athletes. In addition to the important sun exposure, exercise-induced immunosuppression may increase the risk for nonmelanoma skin cancer and cutaneous melanoma in athletes. Frequently, athletes seem to know little about the risk of sun exposure. Protective means such as avoiding training and competition with considerable sun exposure, choosing adequate clothing, and applying water-resistant sunscreen still need to be propagated in the community of outdoor sportsmen.
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PMID:Outdoor sports and skin cancer. 1828 Aug 99

Ultraviolet (UV) irradiation is a major environmental factor responsible for a high incidence of premature skin aging, referred to as photoaging, as well as skin cancer and melanoma. UVA irradiation represents 90% of the solar UV light reaching the earth's surface, and yet the mechanisms by which it exerts its biological effects are not clear. UVA penetrates into the skin tissue, reaching the basal layers of the active dividing cells and, therefore, the contribution of UVA to skin damage may be significant. The majority of UVA energy is absorbed by unidentified photosensitizers in the cells which are postulated to generate reactive oxygen species (ROS). It has been believed that both chronological aging and photoaging share the same molecular features and, as such, it is very common to utilize UV irradiation for induction of skin aging. To determine the involvement of protein kinase isoforms in chronological aging and photoaging, we utilized in vitro aging model systems of primary murine fibroblasts and primary fibroblasts isolated from PKC null mice. We show for the first time distinct involvement of PKC isoforms PKCdelta and PKCalpha in photoaging versus cellular senescence. While chronological aging is accompanied by overexpression and activation of PKCalpha, UV irradiation and ROS production are associated with photoaging accompanied by PKCdelta downregulation and nuclear translocation.
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PMID:UV irradiation increases ROS production via PKCdelta signaling in primary murine fibroblasts. 1852 85

UV solar radiation is the major environmental risk factor for malignant melanoma. A great effort is currently posed on the search of new compounds able to prevent or reduce UV-mediated cell damage. Ferulic acid is a natural compound recently included in the formulation of solar protecting dermatological products. The purpose of the present work was to assess whether its ethyl ester derivative, FAEE, could protect skin melanocytes from UV-induced oxidative stress and cell damage. Experiments on human melanocytes irradiated with UVB showed that FAEE treatment reduced the generation of ROS, with a net decrease of protein oxidation. FAEE treatment was accompanied by an induction of HSP70 and heme oxygenase, by a marked suppression of PARP activation and a significant suppression of apoptosis. Moreover FAEE prevented iNOS induction, thus suppressing the secondary generation of NO-derived oxidizing agents. FAEE may represent a potentially effective pharmacological approach to reduce UV radiation-induced skin damage.
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PMID:Protective effect of ferulic acid ethyl ester against oxidative stress mediated by UVB irradiation in human epidermal melanocytes. 1927 91

The current study examined the chemopreventive potential of the dual-function JAK3/EGFR tyrosine kinase inhibitor WHI-P131 (CAS 202475-60-3) in photocarcinogenesis of non-melanoma skin cancer (NMSC). Prophylactic WHI-P131 exhibited significant anti-inflammatory activity in the SKH-1 mouse model of sunburn and afforded significant protection against the inflammatory skin damage that results from UVB exposure. UVB exposure (400 mJ/cm2) increased the mutation rate of the transgene target in UVB-exposed skin of BigBlue mice by a factor of 3.7 from 8.6 x 10(-5) to 31.7 x 10(-5) but this genotoxicity was almost completely prevented by topically administered prophylactic WHI-Pl31 (1.5 mg/cm2). Chronic and repetitive exposure of vehicle-treated SKH-1 mice to 35 mJ/cm2 UVB, three times per week for 20 weeks resulted in appearance of a spectrum of lesions from actinic keratoses and squamous cell carcinoma (SCC) in situ to invasive SCC. Both the number and size of the skin lesions progressively increased over time. Notably, topical administration of WHI-P131 (1.0 mg/cm2) over the UVB target skin area on the dorsal surface 15 min before each UVB exposure significantly suppressed the photocarcinogenesis as documented by a 4-week delay in the onset of visible skin lesions, decreased total lesion volume per mouse (1.9 +/- 0.5 mm3 vs. 2.5 +/- 0.5 mm3/lesion at 20 weeks), and decreased number (1.6 +/- 0.4/mouse vs. 4.2 +/- 1.6/mouse at 20 weeks, P < 0.05) as well as smaller size of lesions and consequently a smaller total lesion volume ("skin cancer burden") (10.6 +/- 4.3 mm3 vs. 3.2 +/- 0.9 mm3 at 20 weeks, P < 0.05). These experimental findings provide unprecedented evidence that WHI-P131 may be useful as a chemopreventive agent against NMSC.
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PMID:Prevention of UVB-induced skin inflammation, genotoxicity, and photocarcinogenesis in mice by WHI-P131, a dual-function inhibitor of Janus kinase 3 and EGF receptor kinase. 2048 73


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