Glivec is a standard medication used for the treatment of chronic myeloid leukemia (CML). However, patients are often found to develop resistance to it. As an attempt towards combating this issue, scientists from The Institute of Cancer Research UK have developed a new method that apparently destroys CML cells when they have ceased responding to imatinib or Glivec.
During the research, the team found that drugs known as MEK inhibitors, when used in combination with nilotinib appeared to eliminate CML cells after they stopped showing responsiveness to Glivec. Medications such as Imatinib and nilotinib possibly killed the CML cells by locking a protein called BCR-ABL which is responsible for instigating the survival signal crucial for the metastasis of CML cells.
Lead author, Professor Richard Marais from the ICR, stated “We are learning more about the molecular locks which have ‘seized up’, keeping survival signals turned on in CML cells. This important research shows that drugs currently in development can free these locks to switch off survival signals and destroy cancer cells.”
However, since the aforementioned protein sometimes changes its structure, the drugs may not be able to deactivate the protein, thereby resulting in spreading of the cancer. Thus, the team disclosed a second group of molecular keys such as the MEK inhibitors which deactivate the MEK protein which is a class of substances regulating the survival signals.
Nilotinib supposedly made the resistant cancer cells more reactive to the influences of MEK inhibitors and therefore the cumulative effects resulted in the death of the resistant cells. This analysis essentially implied that MEK inhibitors, when used along with nilotinib may combat CML resistance to imatinib and nilotinib.
The findings could pave the path to better CML treatment in cases where resistance against a targeted drug crops up.