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  4. Comparative genomic hybridization study of arsenic-exposed and non-arsenic-exposed urinary transitional cell carcinoma
 
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Comparative genomic hybridization study of arsenic-exposed and non-arsenic-exposed urinary transitional cell carcinoma

Journal
Toxicology and Applied Pharmacology
Journal Volume
227
Journal Issue
2
Pages
229-238
Date Issued
2008
Author(s)
Hsu L.-I.
Chiu A.W.
YEONG-SHIAU PU  
Wang Y.-H.
Huan S.K.
Hsiao C.-H.
Hsieh F.-I.
Chen C.-J.
DOI
10.1016/j.taap.2007.10.024
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
Abstract
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.
Subjects
Arsenic; Comparative genomic hybridization; p53 immunohistochemistry; Urinary transitional cell carcinoma
SDGs

[SDGs]SDG3

Other Subjects
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
Type
journal article

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