Carcinogenesis can occur through a combination of mutational and epimutational events that disrupt key pathways regulating cellular growth and division. The DNA methylomes of cancer cells exhibit two striking differences from normal cells; a global reduction of DNA methylation levels and the aberrant hypermethylation of some sequences, particularly CpG islands (CGIs). Aberrant hypermethylation is often invoked as a silencing mechanism for inactivation of tumour suppressor genes that directly drives the carcinogenic process. However global analysis of cancer methylomes indicates that most affected CGI genes are already silenced prior to aberrant hypermethylation during cancer development. I will discuss how an altered epigenome can predicate cancer types.
The European Laboratory Research & Innovation Group
Our Vision : To provide outstanding, leading edge knowledge to the life sciences community on an open access basis