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Using the mouse models, the researchers treated the cancerous mice with C93, a FAS inhibitor. When given the carcinogens in conjunction with C93, the mice had a reduced number of tumors compared to untreated mice by 75 percent, a marked reduction. Also, the size of those tumors that remained decreased substantially, making this chemopreventative compound highly effective.

Although these results are promising, the researchers did not know the mechanism of action in the cells and what C93 does inside tumors to prevent their growth. Extending their analysis, the researchers found that a protein known to be upregulated in cancers was also activated in their lung tumor models in mice.

This protein is called Akt, which is a protein involved in the cellular pathways of apoptosis, or programmed cell death, and also protein synthesis. Akt is phosphorylated in its active state, and it was shown by the research group to be active in lung tumors.

Interestingly, upon treatment of the lung tumors with C93, the levels of activated Akt dropped to a remarkably low level, suggesting a strong link between FAS and Akt pathways in lung cancer.

The researchers hope to bring this drug to the clinic to prevent lung cancer before it begins. An interesting side result from the analysis of C93 is that it is non-toxic at levels used to prevent lung cancer formation.

With these results in hand, the team from Hopkins has promising results in the fight against cancer.

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