A simple ten-minute universal cancer test that can be detected by the human eye or an electronic device - published in Nature Communications (Dec 2018) by the Trau lab at the University of Queensland. Red indicates the presence of cancerous cells and blue doesn't.
Matt Trau, a professor of chemistry at the University of Queensland, stunned the science world back in December when the prestigious journal Nature Communications published his lab's discovery about a unique property of cancer DNA that could lead to a simple, cheap, and accurate test to detect any type of cancer in under 10 minutes.
No one believed it. I didn't believe it. I thought, "Gosh, okay, maybe it's a fluke."
Trau granted very few interviews in the wake of the news, but he recently opened up to leapsmag about the significance of this promising early research. Here is his story in his own words, as told to Editor-in-Chief Kira Peikoff.
There's been an incredible explosion of knowledge over the past 20 years, particularly since the genome was sequenced. The area of diagnostics has a tremendous amount of promise and has caught our lab's interest. If you catch cancer early, you can improve survival rates to as high as 98 percent, sometimes even now surpassing that.
My lab is interested in devices to improve the trajectory of cancer patients. So, once people get diagnosed, can we get really sophisticated information about the molecular origins of the disease, and can we measure it in real time? And then can we match that with the best treatment and monitor it in real time, too?
I think those approaches, also coupled with immunotherapy, where one dreams of monitoring the immune system simultaneously with the disease progress, will be the future.
But currently, the methodologies for cancer are still pretty old. So, for example, let's talk about biopsies in general. Liquid biopsy just means using a blood test or a urine test, rather than extracting out a piece of solid tissue. Now consider breast cancer. Still, the cutting-edge screening method is mammography or the physical interrogation for lumps. This has had a big impact in terms of early detection and awareness, but it's still primitive compared to interrogating, forensically, blood samples to look at traces of DNA.
Large machines like CAT scans, PET scans, MRIs, are very expensive and very subjective in terms of the operator. They don't look at the root causes of the cancer. Cancer is caused by changes in DNA. These can be changes in the hard drive of the DNA (the genomic changes) or changes in the apps that the DNA are running (the epigenetics and the transcriptomics).
We don't look at that now, even though we have, emerging, all of these technologies to do it, and those technologies are getting so much cheaper. I saw some statistics at a conference just a few months ago that, in the United States, less than 1 percent of cancer patients have their DNA interrogated. That's the current state-of-the-art in the modern medical system.
Professor Matt Trau, a cancer researcher at the University of Queensland in Australia.
(Courtesy)
Blood, as the highway of the body, is carrying all of this information. Cancer cells, if they are present in the body, are constantly getting turned over. When they die, they release their contents into the blood. Many of these cells end up in the urine and saliva. Having technologies that can forensically scan the highways looking for evidence of cancer is little bit like looking for explosives at the airport. That's very valuable as a security tool.
The trouble is that there are thousands of different types of cancer. Going back to breast cancer, there's at least a dozen different types, probably more, and each of them change the DNA (the hard drive of the disease) and the epigenetics (or the RAM memory). So one of the problems for diagnostics in cancer is to find something that is a signature of all cancers. That's been a really, really, really difficult problem.
Ours was a completely serendipitous discovery. What we found in the lab was this one marker that just kept coming up in all of the types of breast cancers we were studying.
No one believed it. I didn't believe it. I thought, "Gosh, okay, maybe it's a fluke, maybe it works just for breast cancer." So we went on to test it in prostate cancer, which is also many different types of diseases, and it seemed to be working in all of those. We then tested it further in lymphoma. Again, many different types of lymphoma. It worked across all of those. We tested it in gastrointestinal cancer. Again, many different types, and still, it worked, but we were skeptical.
Then we looked at cell lines, which are cells that have come from previous cancer patients, that we grow in the lab, but are used as model experimental systems. We have many of those cell lines, both ones that are cancerous, and ones that are healthy. It was quite remarkable that the marker worked in all of the cancer cell lines and didn't work in the healthy cell lines.
What could possibly be going on?
Well, imagine DNA as a piece of string, that's your hard drive. Epigenetics is like the beads that you put on that string. Those beads you can take on and off as you wish and they control which apps are run, meaning which genetic programs the cell runs. We hypothesized that for cancer, those beads cluster together, rather than being randomly distributed across the string.
Ultimately, I see this as something that would be like a pregnancy test you could take at your doctor's office.
The implications of this are profound. It means that DNA from cancer folds in water into three-dimensional structures that are very different from healthy cells' DNA. It's quite literally the needle in a haystack. Because when you do a liquid biopsy for early detection of cancer, most of the DNA from blood contains a vast abundance of healthy DNA. And that's not of interest. What's of interest is to find the cancerous DNA. That's there only in trace.
Once we figured out what was going on, we could easily set up a system to detect the trace cancerous DNA. It binds to gold nanoparticles in water and changes color. The test takes 10 minutes, and you can detect it by eye. Red indicates cancer and blue doesn't.
We're very, very excited about where we go from here. We're starting to test the test on a greater number of cancers, in thousands of patient samples. We're looking to the scientific community to engage with us, and we're getting a really good response from groups around the world who are supplying more samples to us so we can test this more broadly.
We also are very interested in testing how early can we go with this test. Can we detect cancer through a simple blood test even before there are any symptoms whatsoever? If so, we might be able to convert a cancer diagnosis to something almost as good as a vaccine.
Of course, we have to watch what are called false positives. We don't want to be detecting people as positives when they don't have cancer, and so the technology needs to improve there. We see this version as the iPhone 1. We're interested in the iPhone 2, 3, 4, getting better and better.
Ultimately, I see this as something that would be like a pregnancy test you could take at your doctor's office. If it came back positive, your doctor could say, "Look, there's some news here, but actually, it's not bad news, it's good news. We've caught this so early that we will be able to manage this, and this won't be a problem for you."
If this were to be in routine use in the medical system, countless lives could be saved. Cancer is now becoming one of the biggest killers in the world. We're talking millions upon millions upon millions of people who are affected. This really motivates our work. We might make a difference there.
Based on recent research, new therapies could promote a mix of viruses in the intestines to help prevent diseases of aging.
The microbiota and aging
In the early 1970s, scientists discovered that the composition of our gut microbiota changes as we age. Recent studies have found that the changes are remarkably predictable and follow a pattern: The microbiota undergoes rapid, dramatic changes as toddlers transition to solid foods; further changes become less dramatic during childhood as the microbiota strikes a balance between the host and the environment; and as that balance is achieved, the microbiota remains mostly stable during our adult years (ages 18-60). However, that stability is lost as we enter our elderly years, and the microbiome undergoes dramatic reorganization. This discovery led scientists to question what causes this change and what effect it has on health.
Centenarians have a distinct gut community enriched in microorganisms that synthesize potent antimicrobial molecules that can kill multidrug-resistant pathogens.
“We are always eager to find out why some people live extremely long lives. Previous research has shown that the intestinal bacteria of old Japanese citizens produce brand-new molecules that make them resistant to pathogenic — that is, disease-promoting — microorganisms. And if their intestines are better protected against infection, well, then that is probably one of the things that cause them to live longer than others,” said Joachim Johansen, a researcher at the University of Copenhagen.
In 2021, a team of Japanese scientists set out to characterize the effect of this change on older people’s health. They specifically wanted to determine if people who lived to be over 100 years old — that is, centenarians — underwent changes that provided them with unique benefits. They discovered centenarians have a distinct gut community enriched in microorganisms that synthesize potent antimicrobial molecules that can kill multidrug-resistant pathogens, including Clostridioides difficile and Enterococcus faecium. In other words, the late-life shift in microbiota reduces an older person’s susceptibility to common gut pathogens.
Viruses can change alter the genes of bacteria
Although the late-in-life microbiota change could be beneficial to health, it remained unclear what facilitated this shift. To solve this mystery, Johansen and his colleagues turned their attention to an often overlooked member of the microbiome: viruses. “Our intestines contain billions of viruses living inside bacteria, and they could not care less about human cells; instead, they infect the bacterial cells. And seeing as there are hundreds of different types of bacteria in our intestines, there are also lots of bacterial viruses,” said Simon Rasmussen, Johansen’s research advisor.
Centenarians had a more diverse virome, including previously undescribed viral genera.
For decades, scientists have explored the possibility of phage therapy — that is, using viruses that infect bacteria (called bacteriophages or simply phages) to kill pathogens. However, bacteriophages can also enhance the bacteria they infect. For example, they can provide genes that help their bacterial host attack other bacteria or provide new metabolic capabilities. Both of these can change which bacteria colonize the gut and, in turn, protect against certain disease states.
Intestinal viruses give bacteria new abilities
Johansen and his colleagues were interested in what types of viruses centenarians had in their gut and whether those viruses carried genes that altered metabolism. They compared fecal samples of healthy centenarians (100+ year-olds) with samples from younger patients (18-100 year-olds). They found that the centenarians had a more diverse virome, including previously undescribed viral genera.
They also revealed an enrichment of genes supporting key steps in the sulfate metabolic pathway. The authors speculate that this translates to increased levels of microbially derived sulfide, which may lead to health-promoting outcomes, such as supporting mucosal integrity and resistance to potential pathogens.
“We have learned that if a virus pays a bacterium a visit, it may actually strengthen the bacterium. The viruses we found in the healthy Japanese centenarians contained extra genes that could boost the bacteria,” said Johansen.
Simon Rasmussen added, “If you discover bacteria and viruses that have a positive effect on the human intestinal flora, the obvious next step is to find out whether only some or all of us have them. If we are able to get these bacteria and their viruses to move in with the people who do not have them, more people could benefit from them.”
This article originally appeared on Big Think, home of the brightest minds and biggest ideas of all time.
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