A new target has been found for a novel new drug in the fight against lung cancer. The research was carried out at the Salk Institute of Biological Science.
The drug is designed to deactivate an enzyme known for causing inflammation in cancer.
Lung cancer covers a variety of conditions: small cell carcinoma, non-small cell carcinoma, carcinoid, sarcoma and then various unspecified cancers such as mesothelioma.
The diseases have a variety of causes, some that are preventable and some that are not. The preventable causes include: smoking and inhaling carcinogens. The non-preventable causes are: exposure to cosmic radiation, radon gas, asbestos, viruses and various particles.
You could argue that radon gas and asbestos exposure are preventable, however, it isn’t a personal choice to be around them if you are unaware that they’re in your immediate environment.
As previously discussed in this post, the reason why cancer causes the vast amount of inflammation that it does is in order to provide itself with a constant stream of lactate. It uses lactate as it’s primary energy substrate in order to feed it’s proliferative habits as well as it’s large protein synthesis requirement.
This new research has found that a drug is able to target a specific enzyme known for causing inflammation – IKK2. The study showed that when IKK2 was blocked in mice, their life span increased and their tumors stopped growing.
For the research, non-small cell lung cancer (the same type as roughly 80% of all lung cancer) was induced in mice using a modified virus. The viral DNA spliced itself into the cell’s own DNA causing a massive mutation which eventually lead to cancer. Initially their research led them toward a protein complex known as NF-KB; a chief complex involved in initiating inflammation in the body. However, disrupting NF-KB’s activity can have serious side effects for the rest of the body systems.
Inflammation is sometimes needed – be it for correct immune response, the break down of old, worn out cell organelles etc.
This is what lead researchers to IKK2, the enzyme responsible for NF-KBs activation. Through inhibition of IKK2 in specific cells (tumor cells), inflammation can be decreased specifically at a local site rather than system wide.
Additional research is also being carried out regarding the gene Timp-1. Timp-1 is activated by NF-KB and is responsible for telling tumor cells to rapidly divide (or proliferate). Suppression of this gene yielded the same results as blocking IKK2, perhaps slightly better results. This means that the next step in research and treatment is to develop antibodies that target Timp-1 in the cell and deactivate it thus preventing proliferation from occuring.