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Journal of Environmental Pathology, Toxicology and Oncology

Publicou 4 edições por ano

ISSN Imprimir: 0731-8898

ISSN On-line: 2162-6537

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 2.4 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.8 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.5 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00049 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.59 SJR: 0.429 SNIP: 0.507 CiteScore™:: 3.9 H-Index: 49

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Is Cyclooxygenase-2 Important in Skin Carcinogenesis?

Volume 21, Edição 2, 2002, 9 pages
DOI: 10.1615/JEnvironPatholToxicolOncol.v21.i2.120
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RESUMO

Our studies have focused on the role of arachidonic acid and its products in chemically and UV light-induced murine models of skin carcinogenesis, with an emphasis on determining the importance of prostaglandins (PGs), which are synthesized by the two isoforms ofcyclooxygenase (COX). Different types of tumor promoters elevate COX-2 expression in keratinocytes, with little change in COX-1, suggesting that there are multiple signaling pathways by which COX-2 expression can be regulated. We found that the expression of both COX isoforms is increased by treatment with PGs and that this autoregulation occurs via PG receptors linked to a cAMP signaling pathway. We also observed that COX-2 is constitutively upregulated in papillomas and carcinomas from either chemical initiation-promotion or UV-irradiation carcinogenesis experiments. We next investigated cis- and transacting factors required for COX-2 expression. Two regions of the COX-2 promoter, an E box and a nuclear factor-IL6 (NF-IL6) site, were identified as positive regulatory elements through transient transfection with luciferase reporter vectors containing various 5’-flanking regions of the promoter. We found that overexpression of COX-2 in tumors maybe caused by a dysregulation in the expression pattern of the CCAAT/enhancer binding protein (C/EBP) family of transcription factors. To demonstrate the importance of PG synthesis in the carcinogenesis process, several nonsteroidal anti-inflammatory (NSAIDs) drugs were administered either orally or topically during UV carcinogenesis. Dietary administration of indomethacin, piroxicam, or the selective COX-2 inhibitor celecoxib prevented the development of UV-induced skin cancers by up to 85%. In addition, celecoxib had therapeutic efficacy in that it caused regression of preexisting tumors. Topical administration ofindomethacin after each UV exposure was also effective, suggesting that a postexposure approach to skin cancer prevention maybe effective. Collectively, these studies suggest that prostaglandins play a critical role in skin cancer development.

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