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Journal of Environmental Pathology, Toxicology and Oncology

Published 4 issues per year

ISSN Print: 0731-8898

ISSN Online: 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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Immunohistochemical Study of Fibrosis and Adenocarcinoma in Dominant-Negative p53 Transgenic Mice Exposed to Chrysotile Asbestos and Benzo(a)pyrene

Volume 27, Issue 4, 2008, pp. 267-276
DOI: 10.1615/JEnvironPatholToxicolOncol.v27.i4.30
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ABSTRACT

We evaluated the mechanisms using immunohistochemistry whereby chrysotile asbestos and benzo(a)pyrene (BaP) instilled intratracheally into lung-specific dominant-negative p53 (dnp53) mice might interact in causing lung carcinomas and fibrosis. Chrysotile asbestos and benzo(a)pyrene (BaP) were instilled intratracheally into lung-specific dominant-negative p53 (dnp53) and control mice. The mice were sacrificed at 12 months and their lungs examined for lung carcinomas and fibrosis. Immunostains for proteins related to apoptosis, fibrogen-esis, matrix remodeling and inflammation were performed. The dnp53 mice had increased numbers of lung adenocarcinomas with BaP alone and the combination of chrysotile and BaP (the latter was additive but not significant). Several atypical adenomatous hyperplasia lesions were found in the combined treatment group. dnp53 and FVBN control mice developed nodular buds of fibrotic lung tissue after chrysotile asbestos exposure that were localized in respiratory bronchioles; these lesions had significant increases in immunohistochemical staining for TGF-β, MMP-7 and -9, MIG-1, and SDF-1. Fibrotic lesions in mice exposed to chrysotile had increased collagen demonstrated by picrosirius red staining. The dnp53 mice with adenocarcinomas had increased SDF-1, TGF-β, MMP-9 and -7, Cyclin D, and MIG-1 immunostaining in the chrysotile and combined treatment groups. We conclude that BaP and the combination of BaP plus chrysotile asbestos are potent inducers of adenocarcinoma in dnp53 mice and that the inflammatory cytokines and proteases MMP-7 and -9, MIG-1, and SDF-1, and growth factors Cyclin D and TGF-β are increased in the specific lesions.

CITED BY
  1. Cheresh Paul, Kim Seok-Jo, Tulasiram Sandhya, Kamp David W., Oxidative stress and pulmonary fibrosis, Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 1832, 7, 2013. Crossref

  2. Huang Sarah X. L., Jaurand Marie-Claude, Kamp David W., Whysner John, Hei Tom K., Role of Mutagenicity in Asbestos Fiber-Induced Carcinogenicity and Other Diseases, Journal of Toxicology and Environmental Health, Part B, 14, 1-4, 2011. Crossref

  3. Perkins T.N., Peeters P.M., Wouters E.F.M., Reynaert N.L., Mossman B.T., Pathogenesis and Mechanisms of Asbestosis and Silicosis, in Pathobiology of Human Disease, 2014. Crossref

  4. Sargent Linda M, Porter Dale W, Staska Lauren M, Hubbs Ann F, Lowry David T, Battelli Lori, Siegrist Katelyn J, Kashon Michael L, Mercer Robert R, Bauer Alison K, Chen Bean T, Salisbury Jeffrey L, Frazer David, McKinney Walter, Andrew Michael, Tsuruoka Shuji, Endo Morinobu, Fluharty Kara L, Castranova Vince, Reynolds Steven H, Promotion of lung adenocarcinoma following inhalation exposure to multi-walled carbon nanotubes, Particle and Fibre Toxicology, 11, 1, 2014. Crossref

  5. Gao Meili, Li Yongfei, Sun Ying, Shah Walayat, Yang Shuiyun, Wang Yili, Long Jiangang, Benzo[a]pyrene Exposure Increases Toxic Biomarkers and Morphological Disorders in Mouse Cervix, Basic & Clinical Pharmacology & Toxicology, 109, 5, 2011. Crossref

  6. Kasai Tatsuya, Umeda Yumi, Ohnishi Makoto, Mine Takashi, Kondo Hitomi, Takeuchi Tetsuya, Matsumoto Michiharu, Fukushima Shoji, Lung carcinogenicity of inhaled multi-walled carbon nanotube in rats, Particle and Fibre Toxicology, 13, 1, 2015. Crossref

  7. Di Ciaula Agostino, Asbestos ingestion and gastrointestinal cancer: a possible underestimated hazard, Expert Review of Gastroenterology & Hepatology, 11, 5, 2017. Crossref

  8. Jiang Y, Chen X, Yang G, Wang Q, Wang J, Xiong W, Yuan J, BaP-induced DNA damage initiated p53-independent necroptosis via the mitochondrial pathway involving Bax and Bcl-2, Human & Experimental Toxicology, 32, 12, 2013. Crossref

  9. Liu Gang, Cheresh Paul, Kamp David W., Molecular Basis of Asbestos-Induced Lung Disease, Annual Review of Pathology: Mechanisms of Disease, 8, 1, 2013. Crossref

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