Researchers have taken an important first step towards finding a better treatment for one type of T-cell acute lymphocytic leukemia, a severe form of childhood leukemia, for which the cure rate is only 50% with the main treatment - i.e. chemotherapy. In the quest for finding a better drug, Ottawa researchers have uncovered a weak spot that triggers this aggressive form of childhood cancer, and have also identified a possible new treatment that exploits this vulnerability.
T-cell acute lymphoblastic leukemia, or T-ALL, accounts for 15% of childhood acute lymphocytic leukemia cases. A common form of T-ALL involves a gene called TAL-1, which under certain circumstances can transform the T-cells into cancer cells. As you may know T-cells in our body play a key role in the human immune response.
In preclinical studies with mouse models, the researchers at The Ottawa Hospital and the University of Ottawa found that TAL-1 required an enzyme called UTX in order to transform the T-cells into cancer cells. The growth of TAL-1 type cancer cells was completely stopped when the enzyme UTX was turned off using an experimental compound GSK-J4, developed by GlaxoSmithKline plc (GSK).
As part of the research, mouse models were injected with cells from human TAL-1 type leukemia and then treated with GSK-J4 for over three weeks. At the end of the study period, it was found that the number of cancer cells in the bone marrow of the mouse models were down by 80%. The healthy cells were untouched by GSK-J4, and there were no short-term effects on other organs of the body associated with that compound.
GSK-J4 specifically worked only for TAL-1 subtype, and not any other types of T-ALL, say the researchers.
Commenting on the findings, senior author Marjorie Brand who led the study said, "Learning how a disease works at a molecular level needs to happen before any kind of successful drug can be developed. You need to do laboratory studies to find the right treatment and prove it works."
The study is published in Genes & Development.
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