Expert Recommendations on the Evaluation of Sunscreen Efficacy and the Beneficial Role of Non-filtering Ingredients

The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.

Abstract Objective To systematically review and provide information on the incidence of psoriasis and quantify global, regional, and country specific estimates of its prevalence. Design Systematic review and meta-analysis. Data sources Medline, Embase, Web of Science, SciELO, Korean Journal Databases, Russian Science Citation Index, WPRIM, SaudiMedLit, Informit, IndMed, and HERDIN were searched systematically from their inception dates to October 2019. Methods Studies were included if they reported on the incidence or prevalence of psoriasis in the general population. Incidence data were summarised descriptively, whereas bayesian hierarchical models were fitted to estimate the global, regional, and country specific prevalence of psoriasis. Results 41 164 records were identified and 168 studies met the inclusion criteria. In adults, the incidence of psoriasis varied from 30.3 per 100 000 person years (95% confidence interval 26.6 to 34.1) in Taiwan to 321.0 per 100 000 person years in Italy. The prevalence of psoriasis varied from 0.14% (95% uncertainty interval 0.05% to 0.40%) in east Asia to 1.99% (0.64% to 6.60%) in Australasia. The prevalence of psoriasis was also high in western Europe (1.92%, 1.07% to 3.46%), central Europe (1.83%, 0.62% to 5.32%), North America (1.50%, 0.63% to 3.60%), and high income southern Latin America (1.10%, 0.36% to 2.96%). Conclusions Eighty one per cent of the countries of the world lack information on the epidemiology of psoriasis. The disease occurs more frequently in adults than in children. Psoriasis is unequally distributed across geographical regions; it is more frequent in high income countries and in regions with older populations. The estimates provided can help guide countries and the international community when making public health decisions on the appropriate management of psoriasis and assessing its natural history over time. Systematic review registration PROSPERO CRD42019160817.

Long-term exposure to ultraviolet irradiation from sunlight causes premature skin aging (photoaging), characterized in part by wrinkles, altered pigmentation, and loss of skin tone. Photoaged skin displays prominent alterations in the collagenous extracellular matrix of connective tissue. We investigated the role of matrix-degrading metalloproteinases, a family of proteolytic enzymes, as mediators of collagen damage in photoaging. We studied 59 whites (33 men and 26 women, ranging in age from 21 to 58 years) with light-to-moderate skin pigmentation, none of whom had current or prior skin disease. Only some of the participants were included in each of the studies. We irradiated their buttock skin with fluorescent ultraviolet lights under standard conditions and obtained skin samples from irradiated and nonirradiated areas by keratome or punch biopsy. In some studies, tretinoin and its vehicle were applied to skin under occlusion 48 hours before ultraviolet irradiation. The expression of matrix metalloproteinases was determined by in situ hybridization, immunohistology, and in situ zymography. Irradiation-induced degradation of skin collagen was measured by radioimmunoassay of soluble cross-linked telopeptides. The protein level of tissue inhibitor of matrix metalloproteinases type 1 was determined by Western blot analysis. A single exposure to ultraviolet irradiation increased the expression of three matrix metalloproteinases -- collagenase, a 92-kd gelatinase, and stromelysin -- in skin connective tissue and outer skin layers, as compared with nonirradiated skin. The degradation of endogenous type I collagen fibrils was increased by 58 percent in irradiated skin, as compared with nonirradiated skin. Collagenase and gelatinase activity remained maximally elevated (4.4 and 2.3 times, respectively) for seven days with four exposures to ultraviolet irradiation, delivered at two-day intervals, as compared with base-line levels. Pretreatment of skin with tretinoin (all-trans-retinoic acid) inhibited the induction of matrix metalloproteinase proteins and activity (by 70 to 80 percent) in both connective tissue and outer layers of irradiated skin. Ultraviolet irradiation also induced tissue inhibitor of matrix metalloproteinases-1, which regulates the enzyme. Induction of the inhibitor was not affected by tretinoin. Multiple exposures to ultraviolet irradiation lead to sustained elevations of matrix metalloproteinases that degrade skin collagen and may contribute to photoaging. Treatment with topical tretinoin inhibits irradiation-induced matrix metalloproteinases but not their endogenous inhibitor.