作者: A. Burkhardt
DOI: 10.1007/978-3-642-80169-3_8
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摘要: Cancer, if not in essence a genetic disease, is at least to large extent determined its behaviour by the interaction of number genetically coded products, which may enhance growth (oncogenes) or suppress it (tumour suppressor genes anti-oncogenes). However, changes various cancers show considerable individual variations some maybe geographic aetiological factors. Overall, 50%–96% oral carcinomas have abnormal karyotypes (Owen et al. 1992; Hittelman 1993), and there high frequency breakpoints deletions Patel 1993; Partridge 1994; Fuzesi 1994). All chromosomes be involved, noteworthy that those encoding well-known oncogenes (or tumour genes) are frequently altered, such as chromosome 1, 3, 7 (epidermal factor receptor, EGFR), 8 (myc), 9 (MTS), 11 (ras, bcll, intl), 13 (erb), 17 (neu, p53) 18 (Patel Voravud Tsuji Details outlined chapter Scholes Field this volume.