Keeping Cells on Schedule
At any given moment, cells in your body are being created. But more importantly-others are dying.
Although it may seem that this biological ebb and flow has the potential for extremely negative consequences, the balance is crucial to good health. In fact, the balance becomes most obvious when diseases like cancer strike. In those cases, cells multiply uncontrollably without dying. As a result, they are violating a process called apoptosis, an important regulatory mechanism that programs cells to die at certain times.
The precise biochemical steps underlying apoptosis remain unknown. But researchers are sure that those steps include the key to the causes-and possibly the treatments-of ailments driven by unchecked cell growth.
Tak Mak has begun to shed new light on the many dimensions of apoptosis and other mechanisms the body uses to maintain the order of its systems. His work has created an entirely new understanding of T cells, which lie at the heart of the body's immune system response. He and his colleagues were the first to identify the intricate chemical receptors on the surface of these cells, which enable them to distinguish a harmful agent and then neutralize it.
In making such progress, Mak has honed methods of determining which genes are responsible for the function of T cells. Such genes take part in many different activities within the body, such as repairing the DNA that is necessary for cells to pass on their characteristics. However, Mak has concentrated on the role of these genes with respect to regulatory actions such as apoptosis, and the fact that diseases such as cancer can move in when that role is not fulfilled.
As the holder of a Canada Research Chair, Mak will continue to unravel the details of these molecular pathways, which govern the growth, activation, and death of cells. Ultimately, he anticipates the resulting insights will point the way to new strategies for diagnosing and treating a host of health problems that currently present some of our greatest challenges.