Chromosomal rearrangement as the basis for human tumourigenesis.
OBJECTIVE
To develop a model for the initiation of human tumourigenesis that is consistent with various observations that are difficult to reconcile with current models.


CONCLUSIONS
A novel model of tumourigenesis was developed that includes three basic postulates: (1) tumourigenesis is initiated by recombinogenic DNA lesions, (2) potentially recombinogenic DNA lesions in transcribed regions of the genome can be converted into chromosomal rearrangements and (3) chromosomal rearrangements alone are insufficient for tumourigenesis but can initiate a mutator/recombinator phenotype.
Radford
I R
IR
Radiation Oncology Division, Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, Victoria 3002, Australia. ian.radford@petermac.org
D000782:Aneuploidy; D002273:Carcinogens / Q000633:toxicity; D002471:Cell Transformation, Neoplastic; D002869:Chromosome Aberrations; D004249:DNA Damage; D004305:Dose-Response Relationship, Drug; D006801:Humans; D009154:Mutation; D009369:Neoplasms / Q000209:etiology*; D011995:Recombination, Genetic
D002273:Carcinogens