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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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Induction of Apoptosis as a Potential Chemopreventive Effect of Dual Cycloxygenase Inhibitor, Diclofenac, in Early Colon Carcinogenesis

Volume 29, Edição 1, 2010, pp. 41-53
DOI: 10.1615/JEnvironPatholToxicolOncol.v29.i1.70
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RESUMO

We evaluated the role of diclofenac, a dual cycloxygenase inhibitor, in chemoprevention of 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in rat model. In a six-week long treatment with DMH (initiation stage), colonic mucosa showed a rich presence of preneoplastic lesions, such as multiple plaque lesions (MPL), aberrant crypt foci (ACF), and histologically well-characterized dysplasia. Control animals were free from these features while simultaneous treatment of DMH and diclofenac resulted in a significant reduction of these. The Diclofenac-only group did not show any prominent carcinogenic feature. The colonic tissue showed increased COX-2 expression in the DMH group, immunohistochemically and by western blotting. Apoptosis was quantified in isolated colonocytes by fluorescent staining and by TUNEL assay in tissue sections. The number of apoptotic cells was few in the DMH group, while it was featured prominently in all the other groups. The dose of the diclofenac used in the present study was established at an anti-inflammatory dose by the carrageenan-induced rodent paw oedema test. Because ACF can be accepted as reliable prognostic biomarkers in colon carcinogenesis, its inhibition and also the induction of the apoptosis process may favorably indicate the preclinical promise for chemoprevention of colon cancer as demonstrated in the initiation phase of carcinogenesis.

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