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In the last decades the improvements in cancer treatments were an important challenge both for physicians and researchers. The major aim was to obtain a targeted therapy that selectively destroys tumor cells, without affecting the normal tissues. For a very long period of time, the classical methods of treatment were surgery, chemotherapy and radiotherapy. Nevertheless, in most cases, the classical therapies are efficient only in the incipient stages and the solid tumors are often resistant to treatment. Two thirds of the patients are discovered in advanced stages of the disease. Even treated, their death occurs because of relapses and metastases. A quarter of the patients with a tumor in an operable stage can not benefit from the treatment because of their age and co-morbidities. They can only receive palliative therapy with a high relapse percentage. The concept of cellular death determined by the interaction of light with certain drugs was developed a century ago. The first to describe this process was Oscar Raab, in 1900. von Tappeiner and a dermatologist, Jesionek, used a combination between topically applied eosin and white light for the treatment of cutaneous tumors. In fact, Hermann von Tappeiner was the one who introduced the term “Photodynamic Therapy” (PDT) in clinical use, demonstrating the necessary presence of oxygen for the photosensitizing reaction to take place. In 1942, Auler and Banzer injected hematoporphyrin in tumor-bearing animals and observed that, after exposure to a halogen lamp fluorescence, the tumor necrosis appeared. The purification of hematoporphyrin, the use of its derivatives, and especially the introduction of LASER as a light source by Maiman led to improvements in the effects of this therapy. The modern era of PDT began in 1960 with the studies of Lipson and Schwartz, when they observed the red fluorescence of neoplasic lesions after the injection of hematoporphyrin compounds. Since then, considerable efforts have been made to improve the effects of this therapy. 5-aminolevulinic acid was used in 1990 by Kennedy and represented a major advancement in PDT. The first approved photosensitizer to be used on humans was Photofrin. Today, PDT is a non-invasive cancer therapy that associates the use of three components: the photosensitizer (PS), the light, and oxygen. PDT consists of the administration of a PS which accumulates in the lesion and the irradiation of the affected area with light in order to activate the drug. Thus, PDT becomes a treatment with double specificity. On one hand, PS accumulates selectively in the tumor, on the other hand the irradiation is targeted at the tumor. Several factors favor the selective accumulation of PS in tumor cells, including their high proliferation rate, the increased number of low density lipoprotein receptors, the increased vascular permeability, and the production of collagen which can bind the PS (Nowis et al, 2005).

Skin tumors in humans represent about 30% of all new cancers reported annually (Yusuf et al, 2007); their incidence is expected to increase substantially because of increased recreational exposure to sunlight and depletion of the ozone layer. The main factor incriminated in skin cancer is represented by the ultraviolet radiation, especially type B (UVB), which accounts for 90% of the skin cancer cases (Azis, 2005). Currently, between 2 and 3 million non-melanoma skin cancers and 132.000 melanoma skin cancers occur each year and one in every three cancers diagnosed is a skin cancer according to World Health Organization (WHO, 2004). Further more so, it is estimated that one in five persons will develop a basal cell or squamous cell carcinoma in its life time (Robinson, 2005). The identification of the critical molecular targets and signaling pathways involved in the development of premalign and malign lesions UV-induced and the development of agents that modulate these targets are important steps in the management of skin cancer. In 1894 Paul Gerson Unna established that there was a direct causal relationship between exposure to sunlight and the development of the skin carcinomas (Unna, 1894). The acute exposure to UV radiation leads to erythema, edema, burns, pain, thickening and pigmentation of the skin (Afaq & Mukhtar, 2001) while chronic exposure induces immunosuppression (Aziz, 2005), premature aging (Jurkiewicz et al, 1995; LopezTorres et al, 1998) and skin cancers (Katiyar & Mukhtar, 2001; Katiyar, 2008; Taylor et al, 1990). The sunlight UV spectrum can be separated into three wavelengths: UVA (320-400 nm), UVB (280-320 nm) and UVC (200-280 nm). Primarily UVA and UVB reach the earth’s surface as UVC is filtered out by the ozone layer (Shae & Parrish, 1991). Though the UVB radiations is a small part of UV emissions (4 5%), they are extremely aggresive being 1000 times more carcinogenic than UVA (Bowden, 2004; Mukhtar & Elmets, 1996). UVB directly or through the reactive oxygen species (ROS) affects the genetic material of exposed cells forming photoproducts such as DNA cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone (Afaq et al, 2007) respective 8-oxo-7, 8-dihydroguanine (8-oxo-dG) and 8-hydroxy20-deoxyguanosine (8-OHdG) (Kawachi et al, 2008). Multistage carcinogenesis is a widely accepted hypothesis for the development of skin cancer. Skin carcinogenesis is divided into three stages namely: initiation, promotion and progression. Both UVA and UVB radiation have been shown to be complete carcinogens, capable of initiation, promotion and progression of carcinogenetic process (Aziz et al, 2005; Brash et al, 1996; Elmets et al, 2001). Actually, UV has dual actions in the development of skin cancers, it damages DNA and induces mutations of cellular genes crucial for oncogenesis; it induces immunosuppresion, which prevents tumor rejection by the host. To exert its biological effects, UV must be first absorbed by cellular