A team led by Dr David Huang from The Walter and Eliza Hall Institute of Medical Research (WEHI) has made significant advances in understanding the signalling pathways that affect the behaviour of cells. This discovery may assist in the eventual development of more refined therapies to combat a range of cancers, including blood-borne cancers such as lymphomas.
Under normal conditions of health, a process called apoptosis - or programmed cell death - ensures that old, damaged or unnecessary cells die at the right time. This process is essential to maintain a balance of normal cells required for good health.
Scientists have been aware that the balance between two competing classes of proteins - pro-survival and anti-survival - determines whether a cell lives or dies. It has been understood that the pro-survival proteins keep cells alive. When a cell is damaged or is no longer required, the anti-survival proteins act upon the pro-survival proteins to trigger cell death. If this normal and healthy program is faulty, then damaged cells persist and continue to divide uncontrollably, creating rogue collections of cells or cancer. Therefore, an attractive way to kill cancer cells may be to tip the balance against the pro-survival proteins, such as by harnessing the action of the anti-survival proteins. However, a potential danger of using anti-survival cells to kill cancer cells is the collateral damage to normal cells.
The WEHI team has discovered that the process is not as simple as "pro- versus anti-survival." Instead, they discovered that some of the anti-survival proteins have highly selective action on particular pro-survival proteins. This discovery of the cell's complexity will be useful in the eventual development of more specific cancer drugs that have fewer side effects.