Jun 6, 2012
New Clues About the Origin of Cancer
"Whether or not a tumor develops depends on the moment of the cell cycle in which the damage occurs, which repair pathways components are affected, and which others are impaired in terms of apoptosis and cell cycle arrest," explains the North-American Travis H. Stracker, head of the "Genomic Instability and Cancer" group and an expert in DNA repair pathways and its implications on human health. In this study, H. Stracker and his team report on some of these combinations for the initiation of cancer and in different kinds of tissue. "The paper points out that our understanding of which aspects of damage response promote tumorigenesis and where they play a role in the process needs to be investigated further because it shows that it has been generalized and that there is a lot of specifics that are not at all clear."
The researchers utilized mice carrying mutations in key DNA repair genes involved in cancer. Next, they combined them with other mutations affecting cell cycle checkpoints or apoptosis until they hit upon the combinations that are sufficient to initiate tumorigenesis or to generate certain types of tumors. "It is like deconstructing cancer to find the factors responsible for it appearing," says H. Stracker. During DNA replication in a dividing cell there is a series of checkpoints to test that duplication is taking place properly. If the cell detects errors in any of these phases, cell growth is halted and highly complex DNA repair processes are triggered. If the repair is defective and the cell accumulates many genomic errors, "watch-out" proteins step in, such as tumor suppressor p53. Such proteins activate programmed cell death (apoptosis) or cell cycle arrest (senescence). "A very complex network of pathways and proteins are involved," explains the researcher.
Read more at Science Daily