In the present study, the immunophenotype of basal cell carcinoma was analysed in comparison with human vellus hair follicular keratinocytes. We also established the lectin binding profile of basal cell carcinoma and human vellus hair follicles (VHF), using several lectins with different sugar specificities. Our findings showed an almost identical immunohistochemical profile for basal cell carcinoma and the suprabulbar region of the outer root sheath of VHF, whereas other follicular compartments such as the bulbar, the isthmus or the supraseboglandular regions did not correlate. In particular, homogeneous and constant expression of the basal differentiation markers CK 5 and CK 14 were found in both specimen, with no expression of the simple epithelium type keratin CK 8 and the suprabasal differentiation markers CK 1 and CK 10. CK 19 showed variable expression in basal cell carcinoma, with constant expression in the outer root sheath and the follicular bulge regions, but was always absent in interfollicular epidermal keratinocytes. In addition, the lectin binding profiles of basal cell carcinoma and the outer root sheath in the suprabulbar region of human VHF were comparable, with the presence of binding sites for PNA, Con A and WGA. These findings provide evidence for a histochemical relationship between basal cell carcinoma and the follicular epithelium of VHF which is closer than that with the epidermis, and suggest its possible origin from or possibly its differentiation pattern towards the cells of the outer root sheath and/or the follicular bulge region of the VHF.

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Patients with HPV-positive head and neck squamous cell carcinoma (HNSCC) show better survival rates than those with HPV-negative HNSCC. While an enhanced radiosensitivity of HPV-positive tumors is clearly evident from single modality treatment, cisplatin is never administered as monotherapy and therefore its contribution to the enhanced cure rates of HPV-positive HNSCC is not known. Both cisplatin and radiotherapy can cause severe irreversible side effects and therefore various clinical studies are currently testing deintensified regimes for patients with HPV-positive HNSCC. One strategy is to omit cisplatin-based chemotherapy or replace it by less toxic treatments but the risk assessment of these approaches remains difficult. In this study we have compared the cytotoxic effects of cisplatin in a panel of HPV-positive and -negative HNSCC cell lines alone and when combined with radiation.While cisplatin-treated HPV-positive strains showed a slightly stronger inhibition of proliferation, there was no difference regarding colony formation. Cellular responses to the drug, namely cell cycle distribution, apoptosis and γH2AX-induction did not differ between the two entities but assessment of cisplatin-DNA-adducts suggests differences regarding the mechanisms that determine cisplatin sensitivity. Combining cisplatin with radiation, we generally observed an additive but only in a minority of strains from both entities a clear synergistic effect on colony formation. In summary, HPV-positive and -negative HNSCC cells were equally sensitive to cisplatin. Therefore replacing cisplatin may be feasible but the substituting agent should be of similar efficacy in order not to jeopardize the high cure rates for HPV-positive HNSCC.