https://scholars.lib.ntu.edu.tw/handle/123456789/544473
標題: | Comparative genomic hybridization study of arsenic-exposed and non-arsenic-exposed urinary transitional cell carcinoma | 作者: | Hsu L.-I. Chiu A.W. YEONG-SHIAU PU Wang Y.-H. Huan S.K. Hsiao C.-H. Hsieh F.-I. Chen C.-J. |
關鍵字: | Arsenic; Comparative genomic hybridization; p53 immunohistochemistry; Urinary transitional cell carcinoma | 公開日期: | 2008 | 卷: | 227 | 期: | 2 | 起(迄)頁: | 229-238 | 來源出版物: | Toxicology and Applied Pharmacology | 摘要: | To compare the differences in DNA aberrations between arsenic-exposed and non-arsenic-exposed transitional cell carcinoma (TCC), we analyzed 19 arsenic-exposed and 29 non-arsenic-exposed urinary TCCs from Chi-Mei Hospital using comparative genomic hybridization. DNA aberrations were detected in 42 TCCs including 19 arsenic-exposed and 23 non-arsenic-exposed TCCs. Arsenic-exposed TCCs had more changes than unexposed TCCs (mean ± SD, 6.6 ± 2.9 vs. 2.9 ± 2.2). Arsenic exposure was significantly associated with the number of DNA aberrations after adjustment for tumor stage, tumor grade and cigarette smoking in multiple regression analysis. The most frequent DNA gains, which were strikingly different between arsenic-exposed and non-arsenic-exposed TCCs, included those at 1p, 4p, 4q and 8q. A much higher frequency of DNA losses in arsenic-exposed TCCs compared with non-arsenic-exposed TCCs was observed in 10q, 11p and 17p. Chromosomal loss in 17p13 was associated not only with arsenic exposure, but also with tumor stage and grade. The p53 immunohistochemistry staining showed that chromosome 17p13 loss was associated with either p53 no expression (25%) or p53 overexpression (75%). The findings suggest that long-term arsenic exposure may increase the chromosome abnormality in TCC, and 17p loss plays an important role in arsenic-induced urinary carcinogenesis. ? 2007. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-39149104017&doi=10.1016%2fj.taap.2007.10.024&partnerID=40&md5=883046bb1d4a0a79305b0ba54ac79db1 https://scholars.lib.ntu.edu.tw/handle/123456789/544473 |
ISSN: | 0041-008X | DOI: | 10.1016/j.taap.2007.10.024 | SDG/關鍵字: | arsenic; protein p53; article; cancer cell; cancer staging; carcinogenesis; chromosome 17p; chromosome 1p; chromosome 4p; chromosome 4q; chromosome 8q; chromosome aberration; chromosome loss; cigarette smoking; comparative genomic hybridization; controlled study; DNA strand breakage; exposure; gene frequency; gene overexpression; human; human cell; immunohistochemistry; major clinical study; multiple regression; transitional cell carcinoma; Adult; Arsenic; Carcinoma, Transitional Cell; Chromosome Aberrations; Chromosomes, Human, Pair 17; DNA; Female; Gene Dosage; Genes, p53; Humans; Hybridization, Genetic; Immunohistochemistry; Male; Poisons; Regression Analysis; Smoking; Taiwan; Urinary Bladder Neoplasms; Water Supply |
顯示於: | 醫學系 |
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