Case Number : Case 1107 - 19th September Posted By: Guest

Bowen's disease arising in a seborrhoeic keratosis.

Agree.

Yes, reticulated seborrheic keratosis with bowenoid transformation.

Yes, Bowen's arising in a seborrheic keratosis.

Agree

[img]https://dermpathpro.com/uploads/spot_diagnosis_comment_img/CASE1107_RAC6910x10_Ki67_Label.jpg[/img]

[img]https://dermpathpro.com/uploads/spot_diagnosis_comment_img/CASE1107_RAC6910x10_p16_Label.jpg[/img]

[img]https://dermpathpro.com/uploads/spot_diagnosis_comment_img/CASE1107_RAC6910x10_p53_Label.jpg[/img]

Yes this was a seborrhoeic keratosis with bowenoid dsyplasia (this is uncommon to rare in my experience but give that both lesions are common may be a chance association). Just shows you should keep your eyes open though even on apparently straight forward routine cases. p16 is actually highly sensitive for Bowen's including bowenoid actinic keratosis and I believe this is independant of high risk HPV but please if anyone has more information on that please do educate us. I know in penile / vulval lesions it is strongly associated with certain types including "warty" carcinomas.

Seems I was right but needs more study I guess.

Murao K1, Yoshioka R, Kubo Y. Human papillomavirus infection in Bowen disease: Negative p53 expression, not p16INK 4a overexpression, is correlated with human papillomavirus-associated Bowen disease.J Dermatol. 2014 Sep 9. doi: 10.1111/1346-8138.12613. [Epub ahead of print]

Author information 1Department of Dermatology, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima, Japan.
Abstract

Genital Bowen disease (BD) has been linked to the high-risk types of human papillomavirus (HPV) infection. Recently, it has been recognized that HPV also can be associated with extragenital BD. HPV oncoproteins E6 and E7 interfere with the function of p53 and pRb, respectively, leading carcinogenesis. p16INK 4a overexpression induced by inactivation of pRb is recognized as a surrogate marker for HPV-associated cervical cancer. In this study, we examined the presence of HPV DNA in 142 BD lesions by polymerase chain reaction (PCR), and determined the type of HPV by PCR restriction fragment length polymorphism or direct DNA sequencing. HPV DNA was detected in 66.7% of genital BD and 8.3% of extragenital BD. The types of HPV detected were HPV types 6, 16, 33, 52, 56, 58 and 59. We also investigated the expression of p16INK 4a , pRb and p53 by immunohistochemistry. Positive expression was detected in 88.6% for p16INK 4a , 25.2% for pRb, and 63.8% for p53. There was no significant difference in p16INK 4a and pRb expression between HPV-positive and -negative BD. However, a strong correlation of HPV positivity with p53 negativity was found. A total of 66.7% of HPV-positive BD showed no p53 expression, whereas the corresponding rate was 32.8% of HPV-negative BD. This study demonstrated that HPV can participate in the development of BD, not only in the genital lesion, but also in extragenital lesion. p16INK 4a overexpression is not a marker for HPV infection in BD. Instead, negative p53 expression is correlated with HPV-associated BD.