期刊
TOXICOLOGIC PATHOLOGY
卷 44, 期 1, 页码 71-87出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/0192623315610820
关键词
renal cell carcinoma; renal tubular hyperplasia; global gene expression; microarray; vinylidene chloride; National Toxicology Program; carcinogenicity bioassay; quantitative PCR; immunohistochemistry; mutation analysis
资金
- Intramural NIH HHS [Z99 ES999999] Funding Source: Medline
Vinylidene chloride (VDC) has been widely used in the production of plastics and flame retardants. Exposure of B6C3F1 mice to VDC in the 2-year National Toxicology Program carcinogenicity bioassay resulted in a dose-dependent increases in renal cell hyperplasia, renal cell adenoma, and renal cell carcinomas (RCCs). Among those differentially expressed genes from controls and RCC of VDC-exposed mice, there was an overrepresentation of genes from pathways associated with chronic xenobiotic and oxidative stress as well as c-Myc overexpression and dysregulation of TP53 cell cycle checkpoint and DNA damage repair pathways in RCC. Trend analysis comparing RCC, VDC-exposed kidney, and chamber control kidney showed a conservation of pathway dysregulation in terms of overrepresentation of xenobiotic and oxidative stress, and DNA damage and cell cycle checkpoint pathways in both VDC-exposed kidney and RCC, suggesting that these mechanisms play a role in the pathogenesis of RCC in VDC-exposed mice.
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