Today I want to tell you about a recently published paper that I was a part of because it’s one that I’m really excited about, both for the findings and the methods. I’m going to start with the findings and then go back and explain how we got there.
The paper: Pangenome analysis reveals both niche-specific “specialists” and microbial “side hustlers” in colorectal cancer microbiomes. doi: 10.1080/19490976.2026.2728331
The biological question we were interested in was, “What is different about the bacteria present in the intestine (gut microbiome) of people with colorectal cancer (CRC) compared to people without this disease?” The motivation for this question is that we are looking for clues that will help us improve the state-of-the-art methods for preventing, detecting, and/or treating this disease. Of course, there are lots of unhelpful reasons why the gut microbiome could be different, such as the altered physiology of CRC making it easier for certain bacteria to grow, and so we think of these surveys as an initial step that can feed into controlled lab-based experiments. This question has been asked by many groups in lots of different ways over the years, and so what we did in this study was to apply a new data analysis approach to public datasets published by a handful of groups from around the world. Each of these datasets took considerable time, expense, and expertise to collect. We are grateful for the willingness of study participants to support scientific progress by making this contribution to the research community.
Previous work in this field has found that there are particular species of bacteria which tend to be found more commonly or abundantly in the gut microbiome of people with CRC, and other species which are found less commonly or abundantly. Other groups have identified differences in the prevalence of metabolic pathways shared across diverse organisms, and still others have measured differences down to the level of specific molecules. If I were to distill my understanding of the field into a vastly oversimplified soundbite, I would say that each study does find some difference in the CRC microbiome, but it is very hard to figure out from these observational studies which of these bacterial differences play a causal role and would therefore be the highest priority for developing preventions and therapeutics. For that, the observations from survey data must be transformed into falsifiable hypotheses which can be tested directly.
There has been groundbreaking work in the last few years that has identified specific bacteria and mechanisms which can reproducibly cause CRC in controlled experimental settings (animal models). While I cannot do justice to that field in this space, I will call out the work of Dr. Susan Bullman (MD Anderson Cancer Center) who has pioneered discoveries on a specific bacterium, Fusobacterium animalis, and its role in CRC. My thinking in this field was influenced greatly by a project in the Bulllman Lab that I was able to contribute some analysis tools to. In this work, Dr. Bullman’s group found that there was a previously-unrecognized subspecies of F. animalis which was far more carcinogenic than the other closely-related bacteria from the same species. In other words, they found that there was a biologically meaningful grouping of bacteria that did not correspond to any previously-recognized species or subspecies, and that group played a distinct role in causing human cancer.
In our recent paper, we expanded on our previous work and went looking for more cases like this, namely previously-unrecognized groups of bacteria hidden within species that had previously been identified as being associated in some way with CRC. We did end up finding some new examples that fit this pattern, with the top example being a lineage of Fusobacterium defined by the presence of a particular grouping of genes (an ‘operon’) encoding genes related to nutrient acquisition in low-glucose environments. We observed that this group of genes was present in a higher proportion of Fusobacterium genomes in the gut microbiome of participants with CRC, and lower proportions from healthy controls. This pattern was consistent across three independent studies performed in different parts of the world. While we have no data suggesting that this has identified any new cause of CRC, it would be possible to test that hypothesis by comparing specific examples of this bacterium with and without that group of genes.
Instead of listing lots of specific bacteria, I’d like to draw your attention to the way in which we ended up identifying them. The key identifying feature we used was whether those bacterial genomes encoded a particular set of genes. Bacteria tend to pass around groups of genes (horizontal gene transfer), and so it’s nice to track those genetic elements explicitly. More importantly, all of the results that we report from this survey are tied to groups of genes which are encoded by particular strains of a known species. The causal hypothesis can be tested in a very straightforward way – compare strains with those genes against strains lacking them. The actual experimental testing isn’t straightforward at all, but the comparison (bacteria plus or minus certain genes) is the bedrock of molecular biology.
Lastly, let’s talk about how we analyzed the data. You’ll notice that there were multiple bacterial species and multiple microbiome surveys. The compute intensive steps (organizing the gene content for each species, aligning a single microbiome survey against a single species’ genes) are all completely isolated and modular. This is really nice because it means you can add a species or a survey to the analysis without having to redo any of the previous steps. All of the outputs only get pulled together in the final steps. The whole thing is performed using the gig-map suite of Nextflow workflows that I’ve been working on for a few years. Each step is configured to run within the Cirro Data Platform (which has now spun out of Fred Hutch, and is where I work), which makes it easy for non-computational scientists to kick off complex workflows. My hope is that others who want to use the same approach for their own projects will find this relatively easy to use.
If you’ve made it this far, I’ll leave you with a philosophical thought. Bacteria are incredibly diverse and constantly exchanging small pieces of their genomes. This gives us a huge opportunity to map associations of human disease down to individual genes and operons. Those genes and operons also happen to be the most experimentally tractable unit of information to work with. Getting that level of resolution in an animal model would require some immensely large number of generations on the scale of the Collaborative Cross, but we get it with bacteria for free. What this approach gives us is an incredibly efficient way of generating hypotheses that can be tested in the lab. If I had the funding and time to run a research lab, I would develop a meaningful model of an important disease (like CRC), fill up a few freezers with isolates of interesting bacteria, and then sequence all of their genomes. Every new microbiome survey that’s published would then just add more information to prioritize which genes to investigate, with the luxury of a complete inventory of which isolates contain the genes of interest. Of course, I’m not going to do that myself, but if you’d like to get started in your own lab I’d be more than happy to help!