Researchers at the Washington University School of Medicine recently completed the first study of a gene that is unique to humans and the primate family and that may have ties to cancer.

The two-year project confirmed past evidence that a protein within the gene TBC1D3 was oncogenic, or capable of producing tumors, and could be a cancer-producing agent.

“This is the first hominoid-specific gene for which a biochemical mechanism has been proposed,” Philip Stahl, the head of the department of Cell Biology and Physiology, and the senior author of the study, said.

The newly-analyzed TBC1D3 is one of several hundred genes out of approximately 23,000 that can be traced back only to primates, or hominoids.

“These are genes that account for the things that are human specific,” Stahl said. Attributes such as speech, cognition, development and sensitivity to disease are all determined by this set of genetic material.

As significant as these genes may be regarding research and patient treatment, the medical field has produced few analyses on the matter, according to Priya Srikanth, a senior and a co-author of the paper.

Srikanth, a biochemistry and women’s studies double major, has been studying the gene since her freshman year.

“I think it’s a huge step in showing the affect these proteins can have and why it may be important to study [them],” Srikanth said. “Obviously there’s something different in primates and humans than there is in other animals, and this is one way to identify what it is.”

After finding that the gene was present in human tissues, researchers studied TBC1D3 in culture, allowing them to examine the affect on the cell when the gene was overproduced versus when it was absent.

“When we overproduced it in cells, the cell grew much faster, and when we deleted it from cells, it grew much more slowly,” Stahl said of the gene.

While observing the speed with which the cell grew, Stahl and his colleagues found that the presence of the gene triggered a receptor that is associated with certain types of cancer.

“Somehow the expression of this gene was regulating the sensitivity to growth hormone receptors,” Stahl said.

The study may help to prove the connection between TBC1D3 and cancer, but Stahl said that the research team still needs to do scientific work with human DNA to be sure of the gene’s presence in humans.

“We haven’t done any work in patients,” Stahl said, “so we don’t know if this is operative in cancer patients.”

The newly-completed study should be the first of a series of explorations into the significance of the gene.

“We [have] got a lot more to do, but that’s what’s exciting about this particular paper,” Stahl said. “We haven’t pinpointed the molecular mechanisms by which this occurs, and that will be a major focus of our work going forward.”

Srikanth, who plans to continue studying the effects of TBC1D3 over the next year while she applies to graduate doctoral programs, said that the research project has to continue in order for the team to attain tangible results and gain real knowledge of the gene’s effect.

“We really need to look into that if we really want to treat people as well as we can, and we really want to understand what’s going on,” she said.

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