For example, a gene that causes a cell to divide in two will never set that process in motion unless turned on by an outside stimulus. Once turned on, it will continue to promote proliferation until another signal turns it off. Most of the signals the genes rely on come from molecules outside the cell, however, and many of those molecules are unable to pierce the cell's sturdy lipid membrane. The only way such a molecule can get its message to the nucleus is by fitting into a receptor on the cell's surface and then prompting a cascade of chemicals called signaling molecules and transcription factors to carry the message along. That cascade is called signal transduction.
Many cancers are a case of signal transduction gone wrong.
In cancer cells, this programmed cell death is inhibited. Somehow, the cancer cells are producing proteins that stop the cellular death machinery from being activated. Under normal circumstances, NFKB's role in the body is to help set up the process of inflammation. And once it is on, it is the consummate cell death-blocker. Because NFKB is such an important transcription factor, Zandi has been focusing on just how it is controlled.