Abstract
Cancer, if not in essence a genetic disease, is at least to a large extent determined in its behaviour by the interaction of a number of genetically coded products, which may enhance its growth (oncogenes) or suppress it (tumour suppressor genes or anti-oncogenes). However, the genetic changes of various cancers show considerable individual variations some of which maybe determined by geographic or aetiological factors. Overall, 50%–96% of oral carcinomas have abnormal karyotypes (Owen et al. 1992; Hittelman et al. 1993), and there is a high frequency of breakpoints and deletions (Owen et al. 1992; Patel et al. 1993; Partridge et al. 1994; Füzesi et al. 1994). All chromosomes may be involved, and it is noteworthy that those chromosomes encoding some of the well-known oncogenes (or tumour suppressor genes) are frequently altered, such as chromosome 1, 3, 7 (epidermal growth factor receptor, EGFR), 8 (myc), 9 (MTS), 11 (ras, bcll, intl), 13 (erb), 17 (neu, p53) and 18 (Patel et al. 1993; Voravud 1993; Tsuji et al. 1994). Details are outlined in the chapter by Scholes and Field in this volume.
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Dedicated to Professor Dr. Gerhard Seifert, ordinarius emeritus of Pathology, University of Hamburg, on the occasions of his 75th birthday who so decisively influenced the endeavours of Oral Pathology in Germany and the scientific work of the author.
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Burkhardt, A. (1996). Oncogenes and Growth Factor Receptors As Diagnostic and Prognostic Markers in Precancers and Cancers of the Oral Mucosa. In: Seifert, G. (eds) Oral Pathology. Current Topics in Pathology, vol 90. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-80169-3_8
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