Abstract
RecQ helicases represent a highly conserved family that is required for the maintenance of genome integrity. In humans, defects in any of three RecQ family members (BLM, WRN or RECQ4) give rise to cancer predisposition disorders. These are Bloom's, Werner's and Rothmund–Thomson syndromes, respectively. RecQ helicases are considered to be 'caretaker' tumour suppressors that suppress neoplastic transformation through control of chromosomal stability. Many other similar caretakers are functionally linked to the RecQ helicases, indicating a possible common molecular basis for tumorigenesis in several apparently distinct cancer predisposition disorders. Human RecQ helicases make multiple physical interactions with other nuclear proteins that are required for DNA metabolism. Many of these interactions have a functional effect on the activity of one or both partners. RecQ helicases are proposed to function at the interface between DNA replication and recombination to 'repair' damaged replication forks.