학술논문

Overexpression of ribonucleotide reductase subunit M1 protein predicts shorter survival in metastatic bladder cancer patients treated with gemcitabine-containing combination chemotherapy.
Document Type
Article
Source
International Journal of Urology. Mar2017, Vol. 24 Issue 3, p230-235. 6p.
Subject
*GENETIC overexpression
*RIBONUCLEOSIDE diphosphate reductase
*BLADDER cancer
*BLADDER cancer treatment
*COMBINATION drug therapy
*CISPLATIN
*PROGNOSIS
Language
ISSN
0919-8172
Abstract
Objectives To identify biomarkers predicting prognosis in bladder cancer patients undergoing the gemcitabine and cisplatin regimen. Methods We studied 52 patients with metastatic bladder cancer treated with the gemcitabine and cisplatin regimen by evaluating the relationship between the expression of two biomarkers, ribonucleotide reductase subunit M1 and excision repair cross complementing 1, by immunohistochemistry and clinical outcomes. Results The patients with low expression of ribonucleotide reductase subunit M1 showed a higher objective response rate by the gemcitabine and cisplatin regimen than those with high expression of ribonucleotide reductase subunit M1 (80.0% and 45.5%, respectively). No differences were observed according to the expression level of excision repair cross complementing 1. Low expression of ribonucleotide reductase subunit M1 significantly prolonged overall survival and progression-free survival compared with the high expression group. Low expression of excision repair cross complementing 1 tended to prolong overall survival and progression-free survival, but there were no significant differences ( P = 0.07 and 0.10, respectively). Multivariate analysis showed that the expression of ribonucleotide reductase subunit M1 was the only independent prognostic factor ( P = 0.012). Conclusions The expressions of ribonucleotide reductase subunit M1 seem to be associated with clinical response and survival in patients with metastatic bladder cancer treated with gemcitabine and cisplatin-based chemotherapy. [ABSTRACT FROM AUTHOR]