Results of a study published in the British Journal of Cancer state that researchers have discovered a unique drug combination that can slow the growth of non-small cell lung cancer in a “controlled” laboratory setting. This breakthrough offers hope for developing treatments based on this research to treat non-small cell lung cancer.
They do so by targeting the KRAS gene. KRAS acts as a molecular on/off switch, with the protein product of a healthy (normal) KRAS gene taking on the crucial role of “normal tissue cell signaling,” and a mutation of the KRAS gene is a precursor to many types of cancer. In terms of non-small cell lung adenocarcinomas KRAS mutation estimates range from 15% to 20% and afflicting over 10,000 people in the UK each year.
The study explored blocking the roles of two proteins known as MEK and M-TOR and in doing so they hoped to inhibit entirely or reduce the growth of non-small cell lung adenocarcinoma cells in a controlled setting. These two proteins, MEK & M-TOR, are “switched on” by KRAS. When this happens with a mutated KRAS gene, the cells can divide rapidly and turn into cancer.
Researchers tested a drug called Trametinib, whose trade name is “Mekinsit” and whose role list strictly that of a specific MEK Blocker. They also used drugs called AZD2014 whose specific function is to block M-TOR. Researchers discovered cancer cell growth was slowed at a great rate by blocking M-TOR as opposed to blocking MEK. But by using Trametinib and AZD2014 together, they were able to halt cell growth at a rate higher than that of either drug alone.
This is important because current trials explore the blocking of MEK in KRAS associated lung cancer, this new information shows results might be vast improved by adding an M-TOR blocker to the MEK blocker. As of yet, there are no drugs to specifically treat cancers with the KRAS mutation. This research lays the groundwork for such drugs to be developed.