This discovery is the principal result of her doctoral dissertation, entitled Lipo-Polymeric Vectors for the Transfer of DNA in Cancer Cells of the Colon, which was subsidized by the Basque Government. In order to carry out the study, this scientist of the Department of Pharmacy and Pharmaceutical Technology used genetic therapy with non-viral vectors for transferring genetic material to the cancerous cells. With this technique, we can assure the therapeutic function of the drug in a wide variety of tissues. In addition, we can apply the treatment repeatedly, since it does not generate immunity, as occurs with viral vectors.

With the objective of improving the effectiveness of this methodology, the specialist worked on designing non-viral systems which act directly upon the liver and the colon. In this manner, she prepared, optimized and evaluated, in vitro and in vivo, a new pharmaceutical format called lipopolyplex. This compound aids the genetic material in penetrating into the damaged cells, and allows drug release in tumorous organs. 500,000 deaths per year

Experimentation with the new drug in mice has shown that it slows tumor growth with respect to those animals subjected to other procedures. This diminishing of the cancerogenous area is possible, according to the scientist, thanks to the stimulation of the immune system, since the introduction of the correct gene in the diseased body can cause it to repair itself and destroy the tumor.

In addition, the researcher of the University of Navarra noted that colon cancer alone causes more than 500,000 deaths per year in the West, and currently the only effective treatment is surgery. Despite this treatment, noted the researcher, between 40 and 60% of colon cancer patients die, and for this reason it is important that we seek out treatment based on genetic therapy.

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"However, while TRIM5a may have served humans well millions of years ago, the antiviral protein does not seem to be good at defending against any of the retroviruses that currently infect humans, such as HIV-1," Emerman said. "In the end, this drove human evolution to be more susceptible to HIV."

For example, the researchers found that changes in TRIM5a that make it better at fighting HIV actually inhibit its ability to stop PtERV1 and vice versa, which indicates that this antiviral gene may only be good at fighting off one virus at a time.

Uncovering the story of TRIM5a's role in battling one ancient retrovirus while increasing human susceptibility to modern-day HIV "is a lot like doing archaeology ” figuring out how humans have become who we are today and why we are or are not susceptible to modern viruses that presently circulate," Emerman said.

In fact, this emerging area of research, which seeks to better understand modern infections by studying ancient viruses, is known as "paleovirology."

"Ultimately," said co-author Malik, "if we want to understand why our defenses are the way they are, the answers inevitably lie in these ancient viruses more so than the ones that have affected us only recently, such as HIV."

This work was supported by National Institutes of Health grants to Emerman, a Searle Scholar Award to Malik and a National Science Foundation graduate fellowship to Kaiser.