When colon cancer forms, the mucosal and lumen microbiomas change to support the metabolic requirements of the tumor. Therefore, bacteria could be targeted in order to reduce or prevent cancer formation or to treat it more effectively. However, so far the data on this are quite complex and constantly evolving. The result is that there is not yet a model that fully explains the correlation between microbiota and cancer.
The reason, in part, is the complexity of the system: every time we study the intestinal microbiome in relation to cancer we must consider different variables that confound the results, in addition to clinical and cancer heterogeneity. There is a lack of long and solid studies in which to investigate the evolution of cancer, from pre-adenoma formation into adenoma and then into cancer and these studies are very difficult to carry out. On the positive side, the amount of data collected increases every day and the complexity of the system becomes increasingly clearer.
One of the most interesting findings is the fact that this may not be related to bacteria alone. Phages and viruses, in fact, would be just as important and they could even have direct oncogenic functions. It is no coincidence that, for example, we see an increase in the overall incidence of HPV-associated tumors, although this is still a completely unexplored territory.
So the challenge in colorectal cancer is to link all these complex issues to try and achieve a unifying theory so that we can reduce the incidence of the disease which is the second biggest killer among all cancers. This is especially important in light of a worrying change in the epidemiology of this disease: in young people, the millennials, the risk of rectal cancer is 4 times that of a person born in the 1960s.
As James Kinross (Imperial College London) tells us, there is an urgent need to understand the role of the intestinal microbiome in the etiology of cancer.