Volume 24, Issue 1 pp. 8-13
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The inhibitory effect of UVB irradiation on the expression of p53 and Ki-67 proteins in arsenic-induced Bowen's disease

Chee-Yin Chai

Chee-Yin Chai

Department of Pathology, Veterans General Hospital-Taipei, National Yang-Ming University, School of Medicine, Taipei, Taiwan, Republic of China

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Hsin-Su Yu

Corresponding Author

Hsin-Su Yu

Department of Dermatology, Veterans General Hospital-Taipei, National Yang-Ming University, School of Medicine, Taipei, Taiwan, Republic of China

Hsin-Su Yu, Department of Dermatology, Kaohsiung Medical College, No. 100, Shih-Chuan 1st Road, Kaohsiung City 807, Taiwan, Republic of China.Search for more papers by this author
Huai-Tzu Yen

Huai-Tzu Yen

Graduates Institute of Medical Sciences, Kaohsiung Medical College, Kaohsiung, Taiwan

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Kun-Bow Tsai

Kun-Bow Tsai

Department of Pathology, Veterans General Hospital-Taipei, National Yang-Ming University, School of Medicine, Taipei, Taiwan, Republic of China

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Gwu-Shing Chen

Gwu-Shing Chen

Department of Dermatology, Veterans General Hospital-Taipei, National Yang-Ming University, School of Medicine, Taipei, Taiwan, Republic of China

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Chia-Li Yu

Chia-Li Yu

Department of Medicine, Veterans General Hospital-Taipei, National Yang-Ming University, School of Medicine, Taipei, Taiwan, Republic of China

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First published: 27 April 2006
Citations: 15

Abstract

The aim of this study is to evaluate the effect of ultraviolet B (UVB) on arsenic-induced Bowen's disease. Four patients were irradiated with 750 mJ/cm2 of UVB and biopsies were performed before treatment and 2 weeks later. Immunohistochemical stains of p53 and Ki-67 were compared by the labelled-streptavidin method before and after the UVB treatment. We found that the number of p53 and Ki-67 positive cells after the UVB treatment were significantly fewer than those of non-UVB-treated specimens. These results suggest that the UVB inhibitory effect in Bowen's disease needs further studies to clarify its value in potentially retarding the progression of the hyperproliferative status in overt skin cancer on a molecular basis.

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