Research over the past decades has firmly established the genetic basis
of cancer. In particular, studies on animal tumour viruses and
chromosome rearrangements in human tumours have concurred to identify
so-called 'proto-oncogenes' and 'tumour suppressor genes', whose
deregulation promotes carcinogenesis. These important findings not only
explain the occurrence of certain hereditary tumours, but they also set
the stage for the development of anti-cancer drugs that specifically
target activated oncogenes. However, in spite of tremendous progress
towards the elucidation of key signalling pathways involved in
carcinogenesis, most cancers continue to elude currently available
therapies. This stands as a reminder that "cancer" is an extraordinarily
complex disease: although some cancers of the haematopoietic system show
only a limited number of characteristic chromosomal aberrations, most
solid tumours display a myriad of genetic changes and considerable
genetic heterogeneity. This is thought to reflect a trait commonly
referred to as 'genome instability', so that no two cancers are ever
likely to display the exact same genetic alterations. Numerical and
structural chromosome aberrations were recognised as a hallmark of human
tumours for more than a century. Yet, the causes and consequences of
these aberrations still remain to be fully understood. In particular,
the question of how genome instability impacts on the development of
human cancers continues to evoke intense debate.