Why look for an alternative for Glivec?
To arrive at a definite diagnosis for GIST, a biopsy is needed to verify the presence of specific receptor proteins on the GIST cells. Cells contain certain receptors to which growth factors can bind, but GIST cells contain a defect in one of these receptors, the KIT receptor. The defective KIT receptor gives a continuous signal to the cancer cells to multiply, enabling the cancer cells to grow irrespective of the presence of the growth factors. However, the drug Glivec works by also binding to this KIT receptor and thus disabling its activity. As a consequence, the GIST cells stop growing and even die off. In contrast to chemotherapy or radiation treatment, Glivec is a highly targeted drug without many side effects. The problem is that often the tumor cells adapt themselves so that Glivec no longer has an effect on them. To find a solution for this problem is a great challenge in the treatment of GIST. KIT adapts and resists Peter Marynen, in collaboration with other Leuven researcher
