Tumor histology.

<p>A representative example of a virus-induced keratoacanthoma (A, C, E and G) and an epidermal carcinoma (B, D, F and H) is shown. Epidermal carcinomas appeared in one animal from the immunocompetent naturally infected colony and one animal from the immunocompetent experimentally infected colony. <b>Panel A:</b> Part of keratin filled craters (X) can be seen in the upper left. Irregular epidermal acanthotic proliferations (O) push into the dermis with preservation of a boundary (arrowheads). Apoptotic bodies can be seen (arrow). <b>Panel B:</b> Upper part of an epidermal carcinoma with ulceration, characterized by irregularly shaped strands of atypical keratinocytes invading the inflamed stroma. The inset shows deeper solid parts of tumor with high rates of mitosis and increased nuclear cytoplasmic ratios amongst other cellular atypical features. <b>Panel C:</b> At the lateral margin of a keratoacanthoma, a thickened highly proliferative basal layer can be seen by Ki-67 label. The upper layers also show some Ki-67 positivity. <b>Panel D:</b> In an epidermal carcinoma almost all cells are Ki-67-positive, showing the high proliferative rate of the tumor. Small tumor islets (X) invade the stroma. <b>Panel E:</b> Immunostaining against keratin 14 shows a succinct demarcation of proliferative epidermis from dermal stroma. <b>Panel F:</b> Keratin 14 immunohistology, showing the dropping off of tumor cells into the stroma (arrowheads). <b>Panel G:</b> By laminin immunohistochemistry, a separation of epidermal proliferation from the dermal stroma can be visualized. The inset shows a higher magnification. <b>Panel H:</b> Laminin staining is not continuous, constituting an additional criterion for the invasive nature of the epidermal carcinoma. Original magnification panels A, B and B-inset: 100×; panels C, D, G and H: 200×, panels E, F and G-inset: 400×.