Is it possible that diet and gut bacteria promote early-stage colorectal cancer?

This transcript has been edited for clarity.

Hello. I'm David Kerr, Professor of Cancer Medicine at the University of Oxford. I would like to take a moment to think about the ever-increasing number of infectious diseases. Early-onset colorectal cancer. On Friday, I saw two Stage IV patients at the clinic. Both were in their early 30s. They both had young families and it was a disaster.

I think this is an issue that needs to be addressed epidemiologically. we know early onset colorectal cancer It is defined as a disease that occurs in people under the age of 50. very rapid increase Such cases have been occurring all over the world over the past 20-30 years, and currently approximately 200,000 people are diagnosed with such cases each year, although the number is definitely increasing.

I think epidemiologists have correctly identified that this sudden rapid increase suggests that there are new environmental changes that support or accentuate the increase in early-onset disease.

There is great team The study was compiled by a collaborative group of epidemiologists, geneticists and bioinformaticians, including Paul Brennan and Mike Stratton, who sought to understand the basis of early-onset colorectal cancer. For this purpose, we are considering a worldwide study. Their approach combines traditional epidemiology, genomics, and impressive computational support to try to uncover the signatures of the mutations involved.

A leading hypothesis is that over the past 20 to 25 years, changes in dietary habits have changed the intestinal microbiota, and in some cases, there are now more bacteria capable of producing and synthesizing intestinal bacteria. That is. and release mutagenic chemicals. There are subtypes of Escherichia coli The company makes one such mutagen called colibactin.

Again, through some of the painstaking and extraordinary research that Mike Stratton and colleagues conducted at the Sanger Institute, they used a variety of different techniques (in vitro, observational, etc.) to Characterizing exposure to colibactin and specific mutations.

They conducted a large global study (one of their strengths) involving different countries around the world, collected material from older and younger colorectal cancer patients, and found that suddenly They plan to conduct a surprisingly large mutation study to see if the mutation signature exists. Colibactin-related symptoms are more common in these early-onset cases. The hypothesis is that exposure to this mutagen during childhood increases the mutational burden of tumors, thereby increasing the likelihood of early cancer development.

We all believe that it takes five, six, or seven separate mutational events, usually occurring randomly, to transform a normal cell into a tumor cell. The earlier these occur, the larger the tumor and the greater the burden of normal single-cell mutations, the more likely it is to develop cancer sooner or later.

Some would say this is very interesting research and advances modern genetic epidemiology. We wish them all the best. This will be a truly international effort over 3-5 years, bringing together a truly international research team of excellence. We hope that we can shed further light on the epidemiology of this early-onset disease. Because only through understanding can this disease be deflected and addressed.

As we have said many times before, knowledge is power. If we understand the underlying epidemiology, we can intervene, as I did on Friday, with two young patients with extremely limited life expectancies and extended family members left behind by their loss. The disorganized disaster of the clinic can and will hopefully be avoided. parent.

Give your team more power. We wish them success with this study, but again, this is a promising guide to the future of modern computational genetic epidemiology.

Thank you for your attention. If you have any ideas or comments, we'd love to hear them. Are you in the field? Are the number of young patients increasing? Do you have any ideas or hypotheses about the microbiome and what bugs might be involved?

As always, thanks for listening, Medscapers.