Drug Resistance in Cancer

The introduction of molecularly targeted therapies such as Bevacizumab and Gleevec (Imatinib) has transformed the treatment of cancer over the last two decades. Since then more than 250 targeted therapies have been approved for the treatment of forty different cancers.

Cancer is mostly caused by abnormal activation of a driver oncogene or inactivation of a tumor suppressor gene that encode a enzyme regulating key cellular processes. Molecularly targeted therapies work by specifically inhibiting the abnormally expressed protein or enzyme in cancer cells.

A major challenge faced by these drugs is the development of resistance. The most common mechanisms are mutations in the target enzyme, increased copies of the gene encoding the enzyme or developing bypass mechanisms to escape the effect of the drug. The consequence of development of resistance is treatment failure or relapse.

Analysis of the key mutations in drug targets and related pathways can help identify patients that are most likely to respond to a targeted therapy, and patients that are unlikely to respond to the therapy. This significantly increases the chances for high efficacy and reducing treatment failure for a given drug.

OncoDynamix has a novel platform OncembleX that analyses the mutations in driver and tumor suppressor genes in samples from cancer patients and recommends the appropriate drug for a cancer patient with a specific cancer.

Author:Ramesh Jayaraman-Chief Scientific Officer, OncoDynamiX Lifesciences.