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      Bowen’s disease – a review of newer treatment options

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          Abstract

          Bowen’s disease (squamous cell carcinoma in situ) has a 3%–5% risk to develop into invasive squamous cell carcinoma. Non-melanoma skin cancer is the most common cancer among Caucasians and its incidence has increased during the last decades dramatically. Multiple treatment options for Bowen’s disease have been described and are established with advantages and disadvantages. Bowen’s disease occurs more often in elderly patients (with a higher risk of comorbidities) and is frequently located on body sites with poor wound healing. Therefore there is need for non-invasive/non-destructive but effective treatment options.

          We would like to give an overview of established therapies and more detailed information about the newer treatment options for Bowen’s disease with topical diclofenac, topical imiquimod and photodynamic therapy.

          Most cited references122

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          Small anti-viral compounds activate immune cells via the TLR7 MyD88-dependent signaling pathway.

          The imidazoquinoline compounds imiquimod and R-848 are low-molecular-weight immune response modifiers that can induce the synthesis of interferon-alpha and other cytokines in a variety of cell types. These compounds have potent anti-viral and anti-tumor properties; however, the mechanisms by which they exert their anti-viral activities remain unclear. Here we show that the imidazoquinolines activate immune cells via the Toll-like receptor 7 (TLR7)-MyD88-dependent signaling pathway. In response to the imidazoquinolines, neither MyD88- nor TLR7-deficient mice showed any inflammatory cytokine production by macrophages, proliferation of splenocytes or maturation of dendritic cells. Imidazoquinoline-induced signaling events were also abolished in both MyD88- and TLR7-deficient mice.
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            Antiangiogenic and antitumor activities of cyclooxygenase-2 inhibitors.

            We provide evidence that cyclooxygenase (COX)-2-derived prostaglandins contribute to tumor growth by inducing newly formed blood vessels (neoangiogenesis) that sustain tumor cell viability and growth. COX-2 is expressed within human tumor neovasculature as well as in neoplastic cells present in human colon, breast, prostate, and lung cancer biopsy tissue. COX-1 is broadly distributed in normal, as well as in neoplastic, tissues. The contribution of COX-2 to human tumor growth was indicated by the ability of celecoxib, an agent that inhibits the COX-2 enzyme, to suppress growth of lung and colon tumors implanted into recipient mice. Mechanistically, celecoxib demonstrated a potent antiangiogenic activity. In a rat model of angiogenesis, we observe that corneal blood vessel formation is suppressed by celecoxib, but not by a COX-1 inhibitor. These and other data indicate that COX-2 and COX-2-derived prostaglandins may play a major role in development of cancer through numerous biochemical mechanisms, including stimulation of tumor cell growth and neovascularization. The ability of celecoxib to block angiogenesis and suppress tumor growth suggests a novel application of this anti-inflammatory drug in the treatment of human cancer.
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              Treatment recommendations for pyoderma gangrenosum: an evidence-based review of the literature based on more than 350 patients.

              Because the incidence of pyoderma gangrenosum (PG) is low, no prospective randomized controlled trials and only a few studies with case numbers of more than 15 patients have been published. To date no guidelines for treatment of PG have been established far. The aim of the study was to provide an evidence-based review of the literature and an evaluation of recommendations for PG treatment. We performed an electronic search using the PubMed database and the term "pyoderma-gangrenosum." Literature published in the English language during the past two decades was reviewed. All relevant studies that could be obtained regardless of the study design were evaluated for grades of recommendation and levels of evidence. Data on patient characteristics including severity of the disease, localization of lesions, associated diseases, and treatment procedures were abstracted and evaluated for therapeutic outcome. We conclude that therapeutic efficacy of systemic treatment with corticosteroids and cyclosporine is best documented in the literature for disseminated as well as for localized disease and should be considered first-line therapy. In cases that do not respond to this treatment, we recommend alternative therapeutic procedures (eg, systemic treatment with corticosteroids and mycophenolate mofetil; mycophenolate mofetil and cyclosporine; tacrolimus; infliximab; or plasmapheresis), considering additional factors including associated diseases.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                October 2008
                October 2008
                : 4
                : 5
                : 1085-1095
                Affiliations
                Zentrum für Dermatologie, Allergologie und Umweltmedizin, Helios Klinikum Wuppertal, Klinikum, der Universität Witten-Herdecke, Wuppertal, Germany
                Author notes
                Correspondence: Thorsten Neubert, Zentrum für Dermatologie, Allergologie und Umweltmedizin, Helios Klinikum Wuppertal, Klinikum der Universität Witten-Herdecke, Heusnerstr. 40, D-42283Wuppertal, Germany, Tel +49 202 896 3507, Email thorsten.neubert@ 123456helios-kliniken.de
                Article
                tcrm-4-1085
                2621408
                19209288
                3b3fd5fb-7187-493d-888e-4df11ed88e45
                © 2008 Dove Medical Press Limited. All rights reserved
                History
                Categories
                Review

                Medicine
                imiquimod,photodynamic therapy,bowen’s disease,diclofenac
                Medicine
                imiquimod, photodynamic therapy, bowen’s disease, diclofenac

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