Human papillomavirus (HPV) is an important causative agent of cervical carcinoma and some malignant cutaneous tumors. The integration of HPV DNA into the host genome is one of the most important risk factors for malignant transformation. Here, we report the case of a 53-year-old man with multiple, black-brown genital macules and nodules. Histological findings resembled those for Bowen’s disease, and we made a diagnosis of bowenoid papulosis. This condition is generally benign, but invasive squamous cell carcinoma (SCC) arising from bowenoid papulosis has been previously reported. Therefore, we took biopsy specimens from 10 lesions and tested them for the presence of HPV DNA. DNA sequencing identified HPV type 16 (HPV-16) DNA in all samples. Next, we excised 4 different relatively large lesions and performed an amplification of papillomavirus oncogene transcripts (APOT) assay. This assay showed that all samples had only episome-derived viral transcripts, indicating no integration of HPV DNA into the host genome. We have followed this case for 3 years, and no progression to Bowen’s disease or SCC has so far been observed. We conclude that the APOT assay is a feasible method for evaluating the malignant potential of bowenoid papulosis.
 S. Majewski and S. Jablonska, “Human PapillomavirusAssociated Tumors of the Skin and Mucosa,” Journal of the American Academy of Dermatology, Vol. 36, No. 5, 1997, pp. 659-685.
 T. M. Darragh, T. J. Colgan, J. Thomas Cox, D. S. Heller, M. R. Henry, R. D. Luff, T. R. Nayar, J. M. Palefsky, M. H. Stoler, E. J. Wilkinson, R. J. Zaino and D. C. Wilbur, “The Lower Anogenital Squamous Terminology Standardization Project for HPV-Associated Lesions: Background and Consensus Recommendations from the College of American Pathologists and the American Society for Colposcopy and Cervical Pathology,” The International Journal of Gynecological Pathology, Vol. 32, No. 1, 2013, pp. 76-115.
 A. Yoneta, T. Yamashita, H. Y. Jin, A. Iwasawa, S. Kondo and K. Jimbow, “Development of Squamous Cell Carcinoma by Two High-Risk Human Papillomaviruses (HPVs), a Novel HPV-67 and HPV-31 from Bowenoid Papulosis,” British Journal of Dermatology, Vol. 143, No, 3, 2000, pp. 604-608.
 R. Klaes, S. M. Woerner, R. Ridder, N. Wentzensen, M. Duerst, A. Schneider, B. Lotz, P. Melsheimer and M. von Knebel Doeberitz, “Detection of High-Risk Cervical Intraepithelial Neoplasia and Cervical Cancer by Amplification of Transcripts Derived from Integrated Papillomavirus Oncogenes,” Cancer Research, Vol. 59, No. 24, 1999, pp. 6132-6136.
 G. Nakanishi, K. Fujii, K. Asagoe, T. Tanaka T and K. Iwatsuki, “Human Papillomavirus Genome Integration in Multifocal Vulvar Bowen’s Disease and Squamous Cell Carcinoma,” Clinical and Experimental Dermatology, Vol. 34, No. 8, 2009, pp. e965-967.
 I. Kraus, C. Driesch, S. Vinokurova, E. Hovig, A. Schneider, M. von Knebel Doeberitz and M. Duerst, “The Majority of Viral-Cellular Fusion Transcripts in Cervical Carcinomas Cotranscribe Cellular Sequences of Known or Predicted Genes,” Cancer Research, Vol. 68, No. 7, 2008, pp. 2514-2522.