The molecular mechanisms leading to human senescence are still not known mostly 
because of the complexity of the process. Different research approaches are used 
to study ageing including studies of monogenic segmental progeroid syndromes. 
None of the known progerias represents true precocious ageing. Some of them, 
including Werner (WS), Bloom (BS), and Rothmund-Thomson syndromes (RTS) as well 
as combined xeroderma pigmentosa-Cockayne syndrome (XP-CS) are characterised by 
features resembling precocious ageing and the increased risk of malignant 
disease. Such phenotypes result from the mutations of the genes encoding 
proteins involved in the maintenance of genomic integrity, in most cases DNA 
helicases. Defective functioning of these proteins affects DNA repair, 
recombination, replication and transcription. Other segmental progeroid 
syndromes, such as Hutchinson-Gilford progeria (HGPS) and Cockayne syndrome are 
not associated with an increased risk of cancer. In this paper we present the 
clinical and molecular features of selected progeroid syndromes and describe the 
potential implications of these data for studies of ageing and cancer 
development.