According to a new study, researchers from the Salk Institute of Biological Studies, California, have discovered that medication used on an inflammation specific enzyme could create a new treatment scheme for certain pulmonary cancer subtypes.

Studies show that if the activity of the IKK2 enzyme (involved in inflammatory response) is blocked, tumor growth is slowed and the life span of lab rats is increased. Findings suggest that drugs that block the activity of this particular enzyme might prove effective in future pulmonary cancer treatment schemes.

Inder Verma, lead author of the study says that pulmonary cancer is one of the deadliest forms of cancer, whilst also having a very poor prognostic for patients. He also adds that they have developed a new method to induce pulmonary cancer to laboratory rats, having almost the same properties as human pulmonary cancer. The laboratory rats were then tested in order to discover the role of the IKK2 enzyme in cancer proliferation.

The correlation between inflammation and cancer has been known by scientists for a long time. Some biochemical structures that play an important role in the control of inflammation can also suffer genetic mutations that might be involved in cancerous proliferation. Researchers from the Salk Institute developed a method of inducing non-small-cell lung carcinoma (more than 80% of all pulmonary cancer types) in laboratory rats. In order to accomplish this, the cells of the rats were injected with a modified virus, action that could not be done with a human subject. This allowed them to study the molecular cause of non-small-cell lung carcinoma.

The next step was to study the protein complex NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells). This complex can be found in most mammal cells and has a key role in regulating the immune response. Incorrect regulation of the NF-kB complex has been linked to autoimmune diseases, viral infection and several types of cancer. Due to the many function the complex has, it is accepted that drugs that would interfere with the NF-kB regulation could cause major side effects.

In order to avoid this problem, scientists used the enzyme that stimulates the activity of the NF-kB complex, IKK2. Blocking the activity of the enzyme in the lab rats resulted in a less developed tumor and a longer life-span.

“Now that we understand IKK2 is required for NF-kB to promote tumor growth, we hope to find ways to target its activity with drugs,” says Yifeng Xia, first author on the paper and researcher in Verma’s laboratory.

Scientists also found out that the Timp-1 gene is involved in carrying out the regulations sent by the NF-kB complex towards the cancerous cells. These regulations induce the proliferation of the cells and the growth of the tumor. Suppressing these genes has also proven to be useful in reducing the growth of the tumor and increase the life-span of laboratory rats.

Futures studies from the Salk Institute may include the development of a small-cell pulmonary carcinoma model for laboratory rats. This type of pulmonary cancer is responsible for more than 16 percent of the cases and is believed to be greatly influenced by smoking.

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Doctor Tipster