摘要
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.
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.
