Leuven Leukemia, or cancer of the bone marrow, strikes some 700 Belgians each year. Medical science has been at a total loss regarding the origin or cause of some forms of this disease − including T-cell acute lymphatic leukemia, or T-ALL. But now, researchers from the Flanders Interuniversity Institute for Biotechnology (VIB), connected to the Catholic University of Leuven, have discovered the possible cause of the disease in 6% of the T-ALL patients. The scientists have found small circular DNA fragments in the cells of these patients that contain the ABL1 cancer gene. ABL1 also plays an important role in other forms of leukemia. The good news is that ABL1 is counteracted with the drug Glivec, and so this medication can now also provide help to a number of T-ALL patients.
T-ALL: T-cell acute lymphatic leukemia
In normal circumstances, our white blood cells combat foreign intruders, like viruses and bacteria. However, in leukemia, there is a breakdown in the formation of white blood cells. The cells in the bone marrow that should develop into white blood cells multiply out of control without fully reaching maturity. These blood cells function inadequately, disrupting the production of normal blood cells. Among other effects, this makes patients more susceptible to infections. Leukemia appears in several forms − in the case of T-ALL, a large accumulation of immature white blood cells occurs within a very short time. This is the most common type of cancer in children under the age of 14 − striking children between two and three years of age, in particular. At present, an optimal treatment, with chemotherapy, cures over half of these children.
ABL1 plays a prominent role in several forms of leukemia
ABL1 is a kinase, a type of protein that catalyzes a number of processes in the cell − in the case of ABL1, this is the process of cell division. It is crucial that kinases function in a very controlled manner withi
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Contact: Sooike Stoops
sooike.stoops@vib.be
32-9-244-6611
VIB, Flanders Interuniversity Institute of Biotechnology
1-Oct-2004
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