Development of squamous cell carcinoma by two high-risk human papillomaviruses (HPVs), a novel HPV-67 and HPV-31 from bowenoid papulosis.

We report a patient with bowenoid papulosis (BP) involving two high-risk human papillomaviruses (HPVs) and the development of invasive squamous cell carcinoma (SCC). Our patient showed verrucous lesions on the penis, perianal area and groin that had been noted over the previous 8 years and had recurred after all therapeutic approaches. The perianal and left inguinal lesions revealed invasive SCC on histology. HPV-31 and HPV-67 sequences were detected by polymerase chain reaction from BP lesions of the perianal area and the shaft of the penis. HPV-31 has already been reported in BP as a high-risk HPV for the development of SCC, but HPV-67 is a novel one that has never been reported in BP. As HPV-67 has sequence homology to HPV-52 and HPV-58, it belongs to the family of HPV-16, a high-risk HPV group. Thus our patient showed two high-risk HPVs, i.e. HPV-31 and the novel HPV-67, which may be directly involved in the development of SCC.

Downregulation of CXCR-2 but not CXCR-1 expression by human keratinocytes by UVB.

Interleukin-8 (IL-8) belongs to the CXC chemokine family. IL-8 exerts its biological activities by binding to specific cell surface receptors, CXCR-1 and CXCR-2. Both receptors bind IL-8 with high affinity but they have different affinities for MGSA/Groalpha and NAP-2. It has been shown that the expression of epidermal CXCR-2 is increased in psoriasis, suggesting that activation of KC mediated by CXCR-2 contributes to the characteristic epidermal changes observed in psoriasis. In order to examine the mechanism(s) by which UVB therapy is effective for several dermatoses including psoriasis, we sought to examine if UVB would modulate the expression of CXCR-1 and CXCR-2 in human keratinocytes (KC). Constitutive expression of CXCR-1 and CXCR-2 mRNA was detected by RT-PCR in normal cultured human KC. After 100 or 300 J/m(2) irradiation, a decrease in CXCR-2 mRNA was detectable from 12 h after irradiation; this downregulation was observed until 48 h after irradiation. In contrast, the CXCR-1 mRNA level was unchanged. Immunohistochemical studies and flow cytometry analysis confirmed the suppressive effect of UVB on the expression of CXCR-2 protein in cultured human keratinocytes. Immunohistochemical studies on two minimal erythema doses (2MED)-exposed and 2MED-unexposed skin from healthy volunteers revealed that CXCR-2 staining occurred over the whole layer of the epidermis but at 24 h after 2MED irradiation, the positive staining of CXCR-2 was decreased. A faint CXCR-1 staining was observed in the lower part of the epidermis both in unexposed and exposed skins. Our results indicate that UVB-induced growth inhibition of KC in hyperproliferative skin disorders may, in part, be related to downregulation of CXCR-2.