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From the Department of Oncological Science (Surgery II) (TN, TS, SF, YU, ST), Oita Medical University, Oita, Japan; and the Institute of Pathology (WM), Heinrich-Heine University, Düsseldorf, Germany.
Correspondence: Address correspondence and reprint requests to: Shinsuke Takeno, MD, Department of Oncological Science (Surgery II), Oita Medical University, Idaigaoka 1-1, Hasama-machi, 879-5593 Oita, Japan; Fax: 81-97-549-4449; E-mail: surg2{at}oita-med.ac.jp
Background: It would be of considerable benefit to patients with esophageal cancer to be able to predict the effect of CRT before therapy, because critical side effects could be avoided and the therapeutic cost of CRT-resistant cases could be reduced. One of the biological parameters with the potential to indicate radioresponse is the DNA double-strand break repair enzyme DNA-PKcs. This study aims to clarify the correlation between DNA-PKcs expression and CRT effect.
Methods: Sixty-seven patients with progressive esophageal cancer treated with CRT were included in this study. The relationship between the expression of DNA-PKcs and the effect of CRT was examined by using immunohistochemistry. The relationships between DNA-PKcs expression, clinicopathologic parameters, and CRT effect were investigated statistically.
Results: A significant correlation was found between the expression of DNA-PKcs and the effect of CRT (P = .0149). The highDNA-PKcs expression group showed greater therapeutic sensitivity than the low-expression group. Clinicopathologic factors had no relationship with DNA-PKcs expression or CRT effect.
Conclusions: This study suggests that high expression of DNA-PKcs correlates with CRT effect. DNA-PKcs expression could, therefore, be useful for predicting the effect of CRT. In addition, these results may make it possible to plan therapy taking patients quality of life into consideration.
Key Words: DNA-PKcs Esophageal cancer Chemoradiotherapy Immunohistochemistry
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T. Y-K. Chow, M. A. Alaoui-Jamali, C. Yeh, L. Yuen, and D. Griller The DNA double-stranded break repair protein endo-exonuclease as a therapeutic target for cancer Mol. Cancer Ther., August 1, 2004; 3(8): 911 - 920. [Abstract] [Full Text] [PDF] |
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