One of the best ways to save lives from cancer is preventing tumors from developing in the first place.

But like any new treatment, ways to prevent cancer also have to be tested in clinical trials to make sure they work. Even something as widely used as aspirin, for example, is no exception and is currently being scrutinized in large-scale cancer prevention studies across the world, to make sure its potential benefits as well as harms are understood.

Clinical trials are still tests though, and there’s no guarantee that they will have a positive outcome. While we need trials to be certain that a new way to prevent cancer saves lives, a failure can be costly and potentially harm people.

But there’s an exciting new area of research that may help to better predict if a clinical trial is likely to succeed or not. And researchers can do this by simply looking at the natural variety in our genes.

In a study published yesterday in the Journal of the National Cancer Institute, led by Professor Richard Martin from the University of Bristol, a team of researchers looked at genetic data from tens of thousands of people and compared it to a clinical trial that wasn’t successful. They wanted to see if their new method—called Mendelian randomization—could have predicted the trial’s outcome.

The results were almost bang on the mark.

A trial with unintended consequences

Let’s hop back in time to 2001 and take a look at the newly launched Selenium and Vitamin E Cancer Prevention Trial (SELECT). Based on results from population and lab research, doctors set up the trial with the aim of finding out whether taking vitamin E or the chemical selenium as daily diet supplements could lower the risk of prostate cancer.

It was a large trial; more than 35,000 healthy men from the US, Puerto Rico, and Canada signed up to take part.

The men were split into 4 groups and given a dummy pill, a vitamin E supplement, a selenium supplement, or both vitamin E and selenium together. Doctors measured levels of vitamin E and selenium in blood samples taken from the men, then kept records of what happened to the men over the next 5 years.

The first results from the trial were released in 2008, and the figures were concerning.

Although it was early days, the results suggested that men taking vitamin E by itself were at increased risk of developing prostate cancer, and suggested those taking selenium were at a higher risk of developing type 2 diabetes. Men taking part were told to stop taking their supplements.

Follow-up results in 2011 confirmed the early findings—men taking vitamin E were at 17% increased risk of developing prostate cancer.

There was weaker evidence that while selenium didn’t affect the overall risk of prostate cancer and so didn’t prevent the disease as predicted, men were more likely to develop an aggressive form of the disease. And more men taking selenium developed diabetes, although again this link was less certain.

The trial was abandoned at a cost of $114m (£84.5m) and had led to more cases of prostate cancer. But that’s just science, right?

Was the answer in our genes all along?

According to Martin and his newly published research, there may have been a way to predict this result in advance.

The basis of ‘Mendelian randomization’ is natural variation in our genes, says James Yarmolinsky, a PhD student in Martin’s lab and one of the study authors.

“We’re interested in genetic variation at certain locations in our DNA that we’re born with—called SNPs—that subtly affect differences that exist between individuals in many of their characteristics, like hair color, body weight, and blood pressure,” Yarmolinsky says.

Even though as individuals we look quite different to each other, our DNA is remarkably similar: 99.5% identical. But SNPs can change the instructions of our DNA code, resulting in slightly different protein molecules being made. Such genetic differences give us variation as a species and are the backbone of evolution.

“We are studying these SNPs because of the way that we randomly inherit them from each of our parents,” Yarmolinsky says.

“This random process mimics how researchers carry out clinical trials to test out potential treatments for diseases, where people are randomly assigned to which treatment group they’re in. That’s why Mendelian randomization is sometimes called ‘Nature’s randomized controlled trial.’”

The researchers think in some cases, SNPs could give us better information than traditional studies of large groups of people, helping us understand things we could do to lower cancer risk, such as behaviour and lifestyle changes.