There are different kinds of leukemia. Some forms of leukemia occur because two DNA strands break apart and the repair systems of the cells link them together again in the wrong order. When the blueprints for important proteins are located at the breakage site, then they, too, will be falsely assembled.

This is how the dangerous protein "BCR-ABL" develops, which then triggers the uncontrolled proliferation of white blood corpuscles. It is made up of two protein parts: a "Bcr" part and an "Abl" part. Both proteins are to be found in healthy cells, too. However, in a certain kind of leukemia – chronic myeloid leukemia (CML) – both proteins are paired to each other (BCR+ABL = BCR-ABL). The white corpuscles containing the fused BCR-ABL can proliferate in an uninhibited fashion, and thus a leukemia (=“white blood”) develops.

Now a drug exists which targets this type of leukemia. It has been on the market since the end of 2001: Glivec (imatinib mesylate).

Glivec docks onto the abnormal protein "BCR-ABL" and disables it. The consequence: The sick blood cells can no longer proliferate and thus they die off. Within a very short time the number of white blood cells decreases to a normal level. In some patients unfortunately, the cancer cells become resistant to Glivec. Then the drug no longer helps.

Why is that so?

In the National Genome Network Assistant Professor Justus Duyster and Dr. Nikolaus von Bubnoff have been investigating this problem. The Munich scientists believed that changes in the hereditary material could be to blame for why the drug has no effect. And they were right in their assumption. 

Page 2: Why Glivec does not work in some patients