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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

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Chemopreventive Action of Diclofenac in Dimethybenzanthracene Induced Lung Cancer in Female Wistar Rat

Volumen 29, Edición 3, 2010, pp. 255-265
DOI: 10.1615/JEnvironPatholToxicolOncol.v29.i3.80
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SINOPSIS

Nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to be effective antineoplastic agents that block prostaglandin formation by inhibiting the enzyme cyclooxygenase (COX), which exists in two isoforms, COX-1 and COX-2. COX-2 is over expressed in lung cancer. The present study evaluates the chemopreventive efficiency of diclofenac, which is a preferentially selective COX-2 inhibitor in lung cancer. Female Wistar rats were divided into 4 groups. Group 1 served as control and received saline intratracheally, once. In group 2 lung cancer was induced by a single intratracheal instillation of dimethybenz(a)anthracene (DMBA) (20 mg/kg body weight). Group 3 was given the intervention of diclofenac (8mg/kg body weight) daily by oral gavage, in addition to DMBA. Group 4 received diclofenac alone. After 18 weeks of treatment, animals were sacrificed and various studies done. COX-2 expression as seen by western immunoblot and immunohistochemistry (IHC) was increased in the DMBA group, while diclofenac intervention was able to bring down the levels of the enzyme. Apoptosis studies by DNA fragmentation, TUNEL and fluorescent dyes reveal the lowered number of apoptotic cells in group 2. The levels were restored by diclofenac treatment in group 3. There was also a significant reduction in tumor incidence in DMBA+Diclofenac treated animals. All these results indicate that diclofenac acts as an effective chemopreventive agent that mediates its effects by the induction of apoptosis in cancer tissue and suppression of COX-2 enzyme.

CITADO POR
  1. Setia Shruti, Sanyal Sankar Nath, Downregulation of NF-κB and PCNA in the regulatory pathways of apoptosis by cyclooxygenase-2 inhibitors in experimental lung cancer, Molecular and Cellular Biochemistry, 369, 1-2, 2012. Crossref

  2. Nadda N., Vaish V., Setia S., Sanyal S.N., Angiostatic role of the selective cyclooxygenase-2 inhibitor etoricoxib (MK0663) in experimental lung cancer, Biomedicine & Pharmacotherapy, 66, 6, 2012. Crossref

  3. Setia Shruti, Sanyal Sankar N., Upregulation of intrinsic apoptotic pathway in NSAIDs mediated chemoprevention of experimental lung carcinogenesis, Pharmacological Reports, 64, 3, 2012. Crossref

  4. Wójcik Marta, Ramadori Pierluigi, Blaschke Martina, Sultan Sadaf, Khan Sajjad, Malik Ihtzaz A., Naz Naila, Martius Gesa, Ramadori Giuliano, Schultze Frank C., Immunodetection of cyclooxygenase-2 (COX-2) is restricted to tissue macrophages in normal rat liver and to recruited mononuclear phagocytes in liver injury and cholangiocarcinoma, Histochemistry and Cell Biology, 137, 2, 2012. Crossref

  5. Avendaño Carmen, Menéndez J. Carlos, Cancer Chemoprevention, in Medicinal Chemistry of Anticancer Drugs, 2015. Crossref

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