Assistant Professor Duyster and his team examined the dangerous protein "BCR-ABl" for such mutations. They discovered that in some patients, the specific docking site for the drug Glivec is deformed. Spontaneous genetic mutations had occurred in the area of this site. That has momentous consequences, because in such cases Glivec no longer has any effect.

Glivec was designed to fit exactly into the site of the protein “BCR-ABL” that sends out the signals for cell proliferation. That is one of the advantages of Glivec – it was specifically designed for the target. Thus, side effects could be avoided that would occur if Glivec were to dock on to other proteins in the cell as well.

But when the specific docking site for the drug is altered by mutation, Glivec can no longer adhere to "BCR-ABL".

The research work of Assistant Professor Duyster and his team is very important for the treatment of leukemia patients. Now strategies to make leukemia therapy even more successful can be searched for.
It could, for instance, be possible to implement additional treatment methods along with Glivec or develop drugs that would dock onto another site in the "BCR-ABL" protein.

Dr. Nikolas von Bubnoff from the Duyster team is currently studying new substances that like Glivec would adhere to "BCR-ABL" and inhibit the activity of the protein. In contrast to Glivec, these "second generation" substances are effective even when mutations already exist that prevent Glivec from attaching and having an effect. This group of drugs could also be used when Glivec is no longer capable of docking onto the site.