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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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VEGF Antibody Plus Cisplatin Reduces Angiogenesis and Tumor Growth in a Xenograft Model of Ovarian Cancer

Volumen 29, Edición 1, 2010, pp. 17-30
DOI: 10.1615/JEnvironPatholToxicolOncol.v29.i1.50
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SINOPSIS

In our previous study, PAb, a VEGF polyclonal antibody was found to inhibit murine tumor growth significantly. The main objective of this study was to investigate the efficacy of combination therapy of (PAb) and cisplatin on human ovarian cancer xenograft. Effect of VEGF, PAb, PAb-cisplatin combination, and cisplatin alone on cultured human ovarian teratocarci-noma cell line PA-1 were assessed by measuring cell proliferation, matrigel invasion, MMP-9 expression, and MMP-9 secretion. In vivo, effect of PAb was observed in a xenograft model of ovarian cancer. Antitumor efficacy was monitored by assessment of tumor volume, MVD, serum NO, serum VEGF, and p53 expression. VEGF increased proliferation of PA-1 cell in a dose-dependent manner while addition of PAb inhibited cell proliferation, cell invasion as well as MMP-9 secretion in vitro. Tumor burden in PAb and PAb-cisplatin combination group was reduced by 41% (p < 0.05) and 66% (p < 0.01), respectively. A significant decrease in MVD, serum NO, serum VEGF, and p53 expression was also observed after PAb and PAb-cisplatin combination treatment when compared to normal mouse serum IgG-treated control mice. Thus, it was concluded that VEGF immunoneutralization may enhance cisplatin-in-duced apoptosis in human ovarian cancer and thus may be an effective way to reduce tumor growth in ovarian carcinoma.

CITADO POR
  1. Rocic Petra, Why is coronary collateral growth impaired in type II diabetes and the metabolic syndrome?, Vascular Pharmacology, 57, 5-6, 2012. Crossref

  2. Growdon Whitfield, Foster Rosemary, Bradford Leslie, Angiogenesis in Gynecologic Cancers, in Tumor Angiogenesis Regulators, 2013. Crossref

  3. Leng Ruobing, Zha Lang, Tang Liangdan, MiR-718 represses VEGF and inhibits ovarian cancer cell progression, FEBS Letters, 588, 12, 2014. Crossref

  4. Dodd Tracy, Jadhav Rashmi, Wiggins Luke, Stewart James, Smith Erika, Russell James C., Rocic Petra, MMPs 2 and 9 are essential for coronary collateral growth and are prominently regulated by p38 MAPK, Journal of Molecular and Cellular Cardiology, 51, 6, 2011. Crossref

  5. Ghosh Sonali, Basu Moitri, Roy Sib Sankar, ETS-1 Protein Regulates Vascular Endothelial Growth Factor-induced Matrix Metalloproteinase-9 and Matrix Metalloproteinase-13 Expression in Human Ovarian Carcinoma Cell Line SKOV-3, Journal of Biological Chemistry, 287, 18, 2012. Crossref

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