Fig. 1.13. a Well-differentiated squamous cell carcinoma. b Moderately differentiated squamous cell carcinoma. c Poorly differentiated squamous cell carcinoma

oropharynx, larynx and hypopharynx. Less frequently, it arises in the nasopharynx, nasal cavities and paranasal sinuses. The predilection sites in the oral cavity are the lateral tongue and floor of the mouth. In the oropharynx, the most commonly involved sites are the base of the tongue and the tonsils. In the larynx, there are geographic differences in the topographic distribution, the glottis being the most frequent location in some countries, and the supraglottis in others [20, 117].

Smoking and alcohol abuse are the greatest risk factors for the development of SCCs of the head and neck. Much attention has been paid to the possible role of viral infection, particularly the Epstein-Barr virus (EBV), and the human papillomavirus (HPV), in the pathogenesis of the head and neck carcinoma.

The EBV is aetiopathogenetically strongly related to nasopharyngeal carcinomas [265], and to rare cases of lymphoepithelial carcinoma of the salivary glands [153, 160]. HPV has been aetiologically linked to SCCs of the tonsil [97, 214]. Apart from tonsillar SCC and nasopha-ryngeal SCC, it appears that EBV and HPV play little, if any, role in the pathogenesis of SCCs in other locations in the head and neck [93, 153, 227, 392].

The macroscopic appearance of invasive SCCs is variable, and includes flat lesions with a well-defined, raised edge, polypoid exophytic and papillary lesions, as well as endophytic infiltrative lesions. The surface of the tumour is frequently ulcerated.

Microscopically, SCCs are characterised by an invasive growth and evidence of squamous differentiation. Invasive growth is manifested by interruption of the basement membrane and the growth of islands, cords, or single (dyscohesive) tumour cells in the subepitheli-al stroma; large tumours may invade deeper structures, i.e. muscle, cartilage and bone. Perineural invasion and invasion of lymphatic and blood vessels may be present and are reliable proof of invasive cancer. Squamous differentiation is demonstrated by intercellular bridges and/or keratinisation, with keratin pearl formation.

Immunohistochemically, SCCs express epithelial markers, such as cytokeratins and epithelial membrane antigen (EMA). The patterns of expression of cytokera-tin subtypes are related to the degree of SCC differentiation and to the degree of keratinisation [229].

The pattern of cytokeratin expression in low-grade SCCs is similar to that observed in non-neoplastic squa-mous epithelium, and is characterised by medium and high molecular weight cytokeratins, and the lack of expression of the low molecular weight cytokeratins. Highgrade SCCs tend to lose the expression of medium and high molecular weight cytokeratins and express low molecular weight cytokeratins [229].

Of the various cytokeratin subtypes, cytokeratins 8, 18 and 19, recognised by the antibody CAM5.2, could be used as an indicator of malignant transformation. In a study by Mallofre et al., 40% of SCCs were positive for CAM5.2, but it was never positive in nonneoplastic squamous epithelium [229]. In poorly differentiated SCCs, expression of vimentin may appear [367].

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