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Leukemia Gets A New Drug

Researchers from the Flanders Interuniversity Institute for Biotechnology (VIB) affiliated to the Catholic University of Leuven say that Sorafenib (Nexavar) is a better drug than Glivec for Chronic Eosinophilic Leukemia //(CEL). They said that although Glivec has a good track record, it is known to cause resistance after some time and hence the need to use an alternative drug.

This finding is not only important for CEL patients, but it also provides a new approach for treating specific forms of leukemia. It is clear from this research that a combination of targeted drugs provides a greater chance of lifelong effective treatment. Chronic Eosinophilic Leukemia (CEL) Our body's white blood cells combat foreign intruders (such as viruses and bacteria). However, in chronic leukemia, the cells in the bone marrow that should develop into white blood cells multiply uncontrollably. These blood cells do not function properly, jeopardizing the production of normal blood cells. Among other consequences, this makes patients more susceptible to infections. Chronic leukemia appears in several forms − in CEL, a rare form of leukemia, the excessive increase of eosinophils (a certain type of white blood cell) can cause tissue damage in the heart, the skin, and the central nervous system. The mechanism behind the cause Under normal circumstances, our body regulates the production of white blood cells very precisely by means of a targeted activation of tyrosine kinases, which start this production. But sometimes defects in the DNA cause these tyrosine kinases to be active continuously, giving rise to diseases like leukemia. In 2003, Jan Cools and his colleagues under the direction of Peter Marynen, along with colleagues Elizabeth Stover and Gary Gilliland from Boston, discovered that CEL is caused by this kind of defective activation of the tyrosine kinase FIP1L1-PDGFRá. Now, with additional research, they have uncovered the molecular mechanism behind the abn
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