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Journal of Environmental Pathology, Toxicology and Oncology

Publicado 4 números por año

ISSN Imprimir: 0731-8898

ISSN En Línea: 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

Indexed in

Arsenic-Mediated Cellular Signal Transduction, Transcription Factor Activation, and Aberrant Gene Expression: Implications in Carcinogenesis

Volumen 21, Edición 4, 2002, 12 pages
DOI: 10.1615/JEnvironPatholToxicolOncol.v21.i4.20
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SINOPSIS

Arsenic is a common environmental and occupational pollutant and a wellknown human carcinogen that causes cancers in many human organs. The exact molecular mechanisms of arsenic carcinogenesis, however, are not well understood. It is generally acknowledged that arsenic does not act via a classic genotoxic or mutagenic mechanism, because it is not a direct mutagen. On the other hand, a growing amount of evidence has shown that arsenic shares many properties with tumor promoters by inducing intracellular signal transduction, activating transcription factors, and changing the expression of genes that are involved in promoting cell growth, proliferation, and malignant transformation. It is postulated that arsenic-induced mitogen-activated protein kinases (MAPKs) signal transduction, which leads to activation of transcription factors such as activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kB) (which in turn alter gene expression), is associated with the carcinogenicity of arsenic. In this article, we review the recent findings in arsenic-induced MAPKs, AP-1 and NF-kB activation, and aberrant gene expression; their implications in arsenic carcinogenesis are discussed. The elucidation of arsenic-induced signal transduction pathways that lead to aberrant gene expression involved in the arsenic-triggered malignant transformation could help to identify novel molecular targets for the treatment of human cancers resulting from arsenic exposure.

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