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  1. NTU Scholars
  2. 醫學院
  3. 醫學系
Please use this identifier to cite or link to this item: https://scholars.lib.ntu.edu.tw/handle/123456789/542061
Title: Acrolein contributes to urothelial carcinomas in patients with chronic kidney disease
Authors: JIAN-HUA HONG 
Lee, Priscilla Ann Hweek
YU-CHUAN LU 
CHAO-YUAN HUANG 
CHUNG-HSIN CHEN 
Chiang, Chih-Hung
PO-MING CHOW 
Jaw, Fu-Shan
Wang, Chung-Chieh
Huang, Chao-Yuan
Wang, Tse-Wen
Liu, Jin-Hui
FU-SHAN JAW 
Issue Date: 2020
Publisher: Elsevier Inc.
Journal Volume: 38
Journal Issue: 5
Start page/Pages: 465-475
Source: Urologic Oncology: Seminars and Original Investigations
Abstract: 
Background: Urothelial carcinomas (UCs) are highly prevalent in patients with end-stage renal disease. Chronic kidney disease (CKD) is the predecessor of end-stage renal disease, and it is also associated with UC. However, the interplay between CKD and UC lacks solid evidence. Acrolein is produced by polyamines and has been suggested to be the uremic “toxin.” The level of acrolein correlates well with chronic renal failure. We recently found that acrolein-induced DNA damage and inhibited DNA repair in urothelial cells, which contribute to bladder cancer. Therefore, we hypothesize that acrolein is involved in the formation of UC in patients with CKD. Materials and methods: A total of 62 UC patients and 43 healthy control subjects were recruited. Acrolein-DNA (Acr-dG) adducts and p53 gene mutations in UC tissues, plasma acrolein-protein conjugates (Acr-PC) and S-(3-hydroxypropyl)-N-acetylcysteine levels, and urinary Acr metabolites were analyzed in these patients. Results: Acr-dG levels were statistically correlated with CKD stages in UC patients (P < 0.01). Most p53 mutations were G to A and G to T mutations in these patients, and 50% of mutations at G:C pairs occurred in CpG sites, which is similar to the mutational spectra induced by Acr-dG adducts. Acr-PC levels in the plasma of UC patients with CKD were significantly higher than those of control subjects (P < 0.001). Altered urinary S-(3-hydroxypropyl)-N-acetylcysteine was also found in UC patients with CKD compared to control subjects (P < 0.005). Conclusion: These results indicate that acrolein acts as an endogenous uremic toxin and contributes to UC formation in patients with CKD. ? 2020 Elsevier Inc.
URI: https://www.scopus.com/inward/record.uri?eid=2-s2.0-85081950514&doi=10.1016%2fj.urolonc.2020.02.017&partnerID=40&md5=c198a5df5e03a0b6374051e4e81753bf
https://scholars.lib.ntu.edu.tw/handle/123456789/542061
ISSN: 1078-1439
DOI: 10.1016/j.urolonc.2020.02.017
SDG/Keyword: (3 hydroxypropyl) n acetylcysteine; acetylcysteine; acrolein; DNA; protein p53; unclassified drug; acrolein; aged; Article; blood level; cancer patient; cancer tissue; chronic kidney failure; controlled study; DNA adduct; DNA damage; DNA repair; female; gene mutation; human; human tissue; major clinical study; male; metabolite; priority journal; transitional cell carcinoma; urine level; chronic kidney failure; complication; DNA damage; drug effect; genetics; middle aged; mutation; transitional cell carcinoma; tumor cell culture; tumor suppressor gene; urinary tract tumor; Acrolein; Aged; Carcinoma, Transitional Cell; DNA Damage; Female; Genes, p53; Humans; Male; Middle Aged; Mutation; Renal Insufficiency, Chronic; Tumor Cells, Cultured; Urologic Neoplasms
[SDGs]SDG3
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臺大位居世界頂尖大學之列,為永久珍藏及向國際展現本校豐碩的研究成果及學術能量,圖書館整合機構典藏(NTUR)與學術庫(AH)不同功能平台,成為臺大學術典藏NTU scholars。期能整合研究能量、促進交流合作、保存學術產出、推廣研究成果。

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