Epigenetic changes at the DNA level, ie., alterations in the distribution of 5-methylcytosine (m5C), play a critical role in carcinogenesis. These changes consist of both increases and decreases in cytosine methylation in different genomic sequences (Baylin and Herman, 2000; Dutrillaux, 2000; Ehrlich, 2002; Issa, 2000; Mitelman et al., 1997). Transmission of the oncogenic phenotype from cell to progeny cell also relies on epigenetic changes at the chromatin level, which may be mechanistically associated with or independent of DNA methylation changes (Momparler, 2003). During carcinogenesis, these epigenetic modifications supplement genetic changes (point mutagenesis, chromosomal rearrangements, aneuploidy, and polyploidy), the classic source of carcinogenic alterations inherited at the cellular, and sometimes, also the individual level. Both genetic and epigenetic changes associated with carcinogenesis occur at much higher frequency in cancer cells than in normal cells and appear early in many types of tumorigenesis. Furthermore, both type of changes tend to evolve in association with tumour progression (Heim and Teixeira, 2000; Hoglund et al., 2003; Itano et al., 2002; Salem et al., 2000; Widschwendter et al., 2004). At the gross chromosomal level, karyotypic instability involves a progressive alteration of the karyotype affecting a cell population (Dutrillaux, 2000). At the level of local mutagenesis, tumour progression is associated with an accumulation of mutations often linked to a mutator phenotype (Albor and Kulesz-Martin, 2000; Fearon et al., 1990). Tumour progression can be accompanied by the spreading in cis of DNA methylation changes or an increased frequency of these changes (Itano et al., 2002; Laird, 2003; Widschwendter et al., 2004). Moreover, cancers can display a