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

Ling I. Hsu, Wen-Hsiang Chiou, Yeong Shiau Pu, Yuan Hung Wang, Steven K. Huan, Cheng Hsiang Hsiao, Fang I. Hsieh, Chien Jen Chen

Research output: Contribution to journalArticle

10 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)229-238
Number of pages10
JournalToxicology and Applied Pharmacology
Volume227
Issue number2
DOIs
Publication statusPublished - Mar 1 2008

Fingerprint

Comparative Genomic Hybridization
Transitional Cell Carcinoma
Arsenic
Cells
Aberrations
DNA
Tumors
Chromosomes
Neoplasms
Regression analysis
Tobacco Products
Chromosome Aberrations
Carcinogenesis
Smoking
Immunohistochemistry
Regression Analysis
Staining and Labeling

Keywords

  • Arsenic
  • Comparative genomic hybridization
  • p53 immunohistochemistry
  • Urinary transitional cell carcinoma

ASJC Scopus subject areas

  • Pharmacology
  • Toxicology

Cite this

Comparative genomic hybridization study of arsenic-exposed and non-arsenic-exposed urinary transitional cell carcinoma. / Hsu, Ling I.; Chiou, Wen-Hsiang; Pu, Yeong Shiau; Wang, Yuan Hung; Huan, Steven K.; Hsiao, Cheng Hsiang; Hsieh, Fang I.; Chen, Chien Jen.

In: Toxicology and Applied Pharmacology, Vol. 227, No. 2, 01.03.2008, p. 229-238.

Research output: Contribution to journalArticle

Hsu, Ling I. ; Chiou, Wen-Hsiang ; Pu, Yeong Shiau ; Wang, Yuan Hung ; Huan, Steven K. ; Hsiao, Cheng Hsiang ; Hsieh, Fang I. ; Chen, Chien Jen. / Comparative genomic hybridization study of arsenic-exposed and non-arsenic-exposed urinary transitional cell carcinoma. In: Toxicology and Applied Pharmacology. 2008 ; Vol. 227, No. 2. pp. 229-238.
@article{75be7148a7504b1aacda5057994628d4,
title = "Comparative genomic hybridization study of arsenic-exposed and non-arsenic-exposed urinary transitional cell carcinoma",
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.",
keywords = "Arsenic, Comparative genomic hybridization, p53 immunohistochemistry, Urinary transitional cell carcinoma, Arsenic, Comparative genomic hybridization, p53 immunohistochemistry, Urinary transitional cell carcinoma",
author = "Hsu, {Ling I.} and Wen-Hsiang Chiou and Pu, {Yeong Shiau} and Wang, {Yuan Hung} and Huan, {Steven K.} and Hsiao, {Cheng Hsiang} and Hsieh, {Fang I.} and Chen, {Chien Jen}",
year = "2008",
month = "3",
day = "1",
doi = "10.1016/j.taap.2007.10.024",
language = "English",
volume = "227",
pages = "229--238",
journal = "Toxicology and Applied Pharmacology",
issn = "0041-008X",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - Comparative genomic hybridization study of arsenic-exposed and non-arsenic-exposed urinary transitional cell carcinoma

AU - Hsu, Ling I.

AU - Chiou, Wen-Hsiang

AU - Pu, Yeong Shiau

AU - Wang, Yuan Hung

AU - Huan, Steven K.

AU - Hsiao, Cheng Hsiang

AU - Hsieh, Fang I.

AU - Chen, Chien Jen

PY - 2008/3/1

Y1 - 2008/3/1

N2 - 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.

AB - 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.

KW - Arsenic

KW - Comparative genomic hybridization

KW - p53 immunohistochemistry

KW - Urinary transitional cell carcinoma

KW - Arsenic

KW - Comparative genomic hybridization

KW - p53 immunohistochemistry

KW - Urinary transitional cell carcinoma

UR - http://www.scopus.com/inward/record.url?scp=39149104017&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=39149104017&partnerID=8YFLogxK

U2 - 10.1016/j.taap.2007.10.024

DO - 10.1016/j.taap.2007.10.024

M3 - Article

C2 - 18201742

AN - SCOPUS:39149104017

VL - 227

SP - 229

EP - 238

JO - Toxicology and Applied Pharmacology

JF - Toxicology and Applied Pharmacology

SN - 0041-008X

IS - 2

ER -