Photodynamic therapy (PDT) involves the activation of a photosensitizing drug, which preferentially localizes to diseased skin, by irradiation with light to cause selective cytotoxic damage. Since its discovery in the early 20th century and the development of topical photosensitizers 2 decades ago, PDT is increasingly being used in dermatology for a wide range of neoplastic, inflammatory, and infectious cutaneous conditions. Topical 5-aminolevulinic acid and methyl aminolevulinic acid, the most commonly used agents in PDT, have received Food and Drug Administration approval for the treatment of actinic keratoses, and many second-generation photosensitizers are under investigation. Compared with conventional therapies, PDT has the advantage of being noninvasive and capable of field treatment. It is also associated with quicker recovery periods and excellent cosmetic results. Because of these benefits, PDT is being evaluated as a potential treatment option for many dermatologic conditions and has been shown to be effective for certain nonmelanoma skin cancers. Although research is still limited, PDT might also have a therapeutic benefit for cutaneous T-cell lymphoma, acne, psoriasis, leishmaniasis, and warts, among others. This article is a review of the clinical applications of PDT in dermatology and summarizes the current evidence in literature describing its efficacy, safety, and cosmetic outcome.
"Photodynamic therapy (PDT) is a therapeutical approach directed towards destruction of tumoral cells, with increasing use in various medical fields such as urology, gastroenterology, pneumology and ophthalmology. The anti-tumoral effect of PDT is widely used in dermatology, in the treatment of several muco-cutaneous tumors, such as basal and squamous cell carcinoma, Bowen disease, leucoplakia and oral dysplasia
[1, 2]. "
[Show abstract][Hide abstract] ABSTRACT: Background: Photodynamic therapy is an alternative treatment of muco-cutaneous tumors that uses a light source able to photoactivate a chemical compound that acts as a photosensitizer. The phthalocyanines append to a wide chemical class that encompasses a large range of compounds; out of them aluminium-substituted disulphonated phthalocyanine possesses a good photosensitizing potential.
Results: The destructive effects of PDT with aluminium-substituted disulphonated phthalocyanine are achieved by induction of apoptosis in tumoral cells as assessed by flow cytometry analysis. Using protein microarray we evaluate the possible molecular pathways by which photodynamic therapy activates apoptosis in dysplastic oral keratinocytes cells, leading to the tumoral cells destruction. Among assessed analytes, Bcl-2, P70S6K kinase, Raf-1 and Bad proteins represent the apoptosis related biomolecules that showed expression variations with the greatest amplitude.
Conclusions: Up to date, the intimate molecular apoptotic mechanisms activated by photodynamic therapy with this type of phthalocyanine in dysplastic human oral keratinocytes are not completely elucidated. With protein microarray as high-throughput proteomic approach a better understanding of the manner in which photodynamic therapy leads to tumoral cell destruction can be obtained, by depicting apoptotic molecules that can be potentially triggered in future anti-tumoral therapies.
Biological research 07/2014; 47(1):33. DOI:10.1186/0717-6287-47-33 · 1.48 Impact Factor
"Most SCCs arise from actinic keratoses, and various progression rates have been reported. These lesions often occur in multiples and are generally associated with alteration of surrounding skin (field) in a phenomenon known as “field cancerization”.55,56 Topical 5-fluorouracil (5%, 1%, 0.5%), imiquimod cream (5%, 3.75%), ingenol mebutate (0.05%, 0.015%), diclofenac sodium gel 3% with 2.5% hyaluronic gel, topical retinoids, chemical peels, lasers (ablative resurfacing with carbon dioxide) or erbium:yttrium aluminum garnet (YAG) and PDT are aimed at treating multiple lesions. "
[Show abstract][Hide abstract] ABSTRACT: In photodynamic therapy (PDT) a photosensitizer - a molecule that is activated by light - is administered and exposed to a light source. This leads both to destruction of cells targeted by the particular type of photosensitizer, and immunomodulation. Given the ease with which photosensitizers and light can be delivered to the skin, it should come as no surprise that PDT is an increasingly utilized therapeutic in dermatology. PDT is used commonly to treat precancerous cells, sun-damaged skin, and acne. It has reportedly also been used to treat other conditions including inflammatory disorders and cutaneous infections. This review discusses the principles behind how PDT is used in dermatology, as well as evidence for current applications of PDT.
Clinical, Cosmetic and Investigational Dermatology 05/2014; 7:145-163. DOI:10.2147/CCID.S35334
"Currently, PDT is applied in the palliative treatment of small tumors and/or surface tumors (Fayter et al. 2010; Gao et al. 2010), as well as in non-malignant skin diseases (Lee and Baron 2011), in precancerous lesions such as Barrett's esophagus (Fayter et al. 2010), and in age-related macular degeneration (Shah et al. 2009; Lee and Baron 2011). It has also been applied successfully as antimicrobial treatment (Cassidy et al. 2009). "
[Show abstract][Hide abstract] ABSTRACT: It is generally accepted that compounds of nanomolecular size penetrate into cells by different endocytic processes. The vehiculization strategy of a compound is a factor that could determine its uptake mechanism. Understanding the influence of the vehicle in the precise mechanism of drug penetration into cells makes possible to improve or modify the therapeutic effects. In this study, using human A-549 cells, we have characterized the possible internalization mechanism of the photosensitizer Zn(II)-phthalocyanine (ZnPc), either dissolved in dimethylformamide (ZnPc-DMF) or included in liposomes of dipalmitoyl-phosphatidyl-choline. Specific inhibitors involved in the main endocytic pathways were used. Co-incubation of cells with ZnPc-liposomes and dynasore (dinamin-mediated endocytosis inhibitor) resulted in a significant decrease of photodamage, whereas other inhibitors did not alter the photodynamic effect of ZnPc. On the contrary, cells treated with ZnPc-DMF in the presence of dynasore, genistein (caveolin-mediated endocytosis inhibitor) or cytochalasin D (macropinocytosis and caveolin-mediated endocytosis inhibitor) showed a significant decrease in ZnPc uptake and photodynamic damage. These results suggest that ZnPc-DMF penetrates into cells mainly by caveolin-mediated endocytosis, whereas ZnPc-liposomes are internalized into cells preferentially by clathrin-mediated endocytosis. We conclude that using different drug vehiculization systems, it is possible to modify the internalization mechanism of a therapeutic compound, which could be of great interest in clinical research.
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