“…Our previous studies have indicated that the immortal phenotype of neoplastic head and neck keratinocytes is showing examples of the LOH described above associated with p53 dysfunction (Burns et al, 1993;Edington et al, 1995), CDKN2A/p16 ink4A dysfunction (Loughran et al, 1994(Loughran et al, , 1996 and a high frequency of allele loss at other genetic loci indicative of multiple suppressor gene loss (Edington et al, 1995, see also Table 2). Therefore, since many other human chromosomal loci have been shown to have antiproliferative e ects reminiscent of replicative senescence when transferred into immortal cells Karlsson et al, 1996;Uejima et al, 1995;Rimessi et al, 1994;Ning et al, 1991;Sandhu et al, 1994Sandhu et al, , 1996Ogata et al, 1993;Koi et al, 1993;Casey et al, 1993;Sasaki et al, 1994;Wang et al, 1992) we decided to investigate the role of these loci in neoplastic human keratinocyte immortalization.…”