When normal cells don’t die, cancer follows
T-cell acute lymphoblastic leukemia is an aggressive cancer that usually affects children—and recent research is paving the way for new treatments.
Standard acute lymphoblastic leukemia occurs in B-cells, which are white blood cells that use antibodies to “tag” invaders for destruction. In T-cell acute lymphoblastic leukemia (T-ALL), T-cells, which help coordinate attacks against invaders, are affected instead.
A characteristic of many cancers is cells that do not die when they are supposed to. Normal cells undergo a natural, pre-programmed life cycle that ends in death, a system that prevents the decay of genetic material and the problems that come with it. But in cancer cells this process has often stopped working.
In a recent Oncoscience editorial, researchers at the Institut Curie Research Center discussed potential methods of helping cells die when they are supposed to. Specifically, the researchers explored how altering the communication between cells could “switch-on” the processes that lead to normal cell death, also known as programmed cell death, thereby helping treat leukemia.
Programmed cell death: When killing cells is good
Modern chemotherapy, which combines multiple different drugs in a complicated cocktail, has led to large improvements in T-ALL survival, but overall survival rate is still below 25%. New treatments are sorely needed.
In many T-ALL patients, T-cells do not have properly functioning receptors on their surface. These receptors are critical to the communication between cells, and it is that communication that tells cells when to activate their death sequence.
If researchers can induce the proper cell signaling, it may be possible to trigger the normal cell death process, killing cancer cells and in turn improving the survival of cancer patients.
Early results in mice seem promising. Administering a treatment that targets cell surface receptors significantly limited cancer expansion and improved overall survival.
“Further dissection of this pathway to identify its intracellular effectors will provide alternatives to [T-cell receptor]-directed therapies,” said the authors. A new target for cancer treatment could play an important role in improving survival of leukemia patients.