Abstract
Checkpoints are surveillance mechanisms that block cell cycle transitions, for instance in response to DNA damage. We summarise here recent progress in the molecular characterisation of the G2 checkpoint which controls the entry into mitosis, and review new evidence which implicates deregulated expression of checkpoint proteins and proteins involved in DNA damage repair in cancer development. There now exists good evidence that individuals who have inherited mutations in genes involved in G2 checkpoint and DNA damage repair are predisposed to the development of various types of cancer, their cells having a strong tendency to accumulate additional mutations. However, the occurrence of mutations of most of these genes in sporadic tumors has yet to be analysed more accurately.