From the moment you walk into the doctor’s office, you’re being asked to take part in a test that could determine whether you’re genetically predisposed to developing a serious illness.
Your results are taken and sent to your family doctor, who can then make a final diagnosis and recommend treatment.
The tests have been around for years, but there’s only been one study that actually compared them.
But now a group of doctors at Columbia University in New York have used DNA from a chimpanzee to make a startling discovery: It turns out that the gene that determines how fast and how hard you can run is also what determines whether or not you’ll develop prostate cancer.
The results are published today in the Proceedings of the National Academy of Sciences.
“The findings are really exciting, especially for those who think they can’t live long enough to develop prostate,” said Dr. James McGovern, an assistant professor in the Department of Medicine at Columbia and a co-author of the paper.
“But we also knew there was a link between the two.
So it was really exciting to see this connection in the first place.”
The gene that affects the ability to run quickly has been known since the 1980s, but McGovern said the finding that it also affects how hard the human body works in response to stress was surprising.
“Our hypothesis was that there was some kind of stress response to running,” McGovern told ESPN.
“We thought that this would be a marker for how much stress was involved in the human response to exercise.
But what we found is that in a chimpanahuman, stress does not correlate with a response to run.
So we have this stress response and we do not have this run response.
That’s the key finding.”
In order to understand the relationship between running and prostate cancer, the researchers looked at the genomes of more than 1,000 people who had been tested for prostate cancer and used the results to create a human version of the gene.
They also analyzed the genes of 2,200 people from the general population, and compared them to their results.
The human version was found to have a mutation that resulted in an increased chance of developing prostate cancer in the future.
In contrast, the chimpanzee had no such mutation, suggesting that the mutation was present in the animal but was suppressed by human genes.
The researchers then examined the genes that control the immune system in humans, and found that the chimps’ mutation had been responsible for an increased risk of developing cancer in people who were healthy.
This was an unexpected finding, McGovern explained.
“You’d expect that you’d see some protection against cancer in humans if you had a normal immune system,” McDavid said.
“This finding suggests that our immune system is really protective against cancer.”
McGovern and his colleagues did the same for the genetic markers for the immune response to the stress test.
They found that both the genetic marker and the immune marker were associated with a decreased risk of cancer in individuals who were in good health.
“People who have a genetic predisposition for prostate and cancer are more likely to be diagnosed with prostate cancer than are those who don’t have a predisposition,” McGeorge said.
The findings suggest that in the general populace, people with a mutation in the immune-related gene may have a greater risk of having prostate cancer compared to those with a normal mutation.
“It doesn’t matter if you’re born or if you have a disease, whether you have inherited this or whether you don’t,” McGill said.
McGovern hopes the findings will help explain why many men are diagnosed with early prostate cancer as soon as they’re in their late 20s, 30s or 40s.
“There’s this idea that men who have been in their 40s or 50s are predispose to developing prostate tumors, but that’s not necessarily true,” McConchie said.
It also appears that the mutations are linked to prostate cancer risk in people with certain health conditions, such as obesity and smoking, McConcees said.
Other scientists have been interested in studying the connection between genetic predispositions and the risk of prostate cancer since the early 1980s.
For example, one of the earliest studies, in 1990, found that people with higher levels of a gene that helps regulate the immune responses in the body — called the Toll-like receptor 4 (TLR4) gene — were more likely than others to develop colon cancer.
But that study, conducted in the U.S., found no significant differences between those with and without this gene mutation.
The second study, in 2001, also found that mutations in the gene TLR4 could predict the risk for developing prostate, but those with the gene mutation were less likely to develop cancer.
McConces said it was the first time that the results were consistent with a link.
“I think there’s been a lot of work done on this gene and the TLR family,” McDon