Of Squamous Cell Carcinoma

Malignant tumours arise clonally from transformed cells that have undergone specific genetic alterations in tumour suppressor genes and proto-oncogenes [117], as well as telomerase re-activation [225, 226, 256]. Loss of chromosomal region 9p21 is the most common genetic change in head and neck carcinogenesis with consequent inactivation of the p16 gene [168, 169]. A frequent event is also mutation of the p53 gene located at 17p13; it occurs in approximately 50% of patients with SCCs of the head and neck [255, 257, 270]. Loss of retinoblastoma gene (Rb1) expression is seen in less than 20% of cases, although LOH at 13q14 is present in 60% or more of SCCs, suggesting the existence of (an)other tumour suppressor gene(s) neighbouring Rb1 [256].

The activation of oncogenes also occurs, such as cyclin D1 amplification, which has been described in one-third of patients with SCCs of the head and neck, and is associated with advanced disease [167, 272]. Amplification of other oncogenes, e.g. c-myc and epidermal growth factor receptor, has also been described in 6-25% of patients with SCCs of the head and neck [119, 121, 269], while ras mutations probably do not play a significant role in the development of head and neck SCCs [119].

Molecular pathology has significantly deepened our insight into genetic alterations occurring in and being probably responsible for cancer development. Moreover, it offers the opportunity for tissue characterisation, i.e. detection of tumour cells, distinction between multiple primary tumours and metastatic disease, and the risk of progression of premalignant lesions, going beyond morphological techniques that have been used in pathology until now. The question remains, however, whether there is any practical impact of these new techniques regarding diagnosis, prognosis and management.

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