cancer

Journal Club: Potential role of intratumor bacteria in mediating tumor resistance to the chemotherapeutic drug gemcitabine

The biggest reason that I was struck by this paper was not the specific finding that they made (as important as that may be), but rather the general theme that it supports: that microbes impact human health via the specific genes that are encoded by individual strains. 

The (very) short summary I would give for this paper is that the presence of specific bacterial strains decreases the effectiveness of an anticancer drug (gemcitabine) because those bacterial strains encode an enzyme that chemically modifies and deactivates that drug. The authors did a lot of careful and intricate work demonstrating that these bacteria are present within tumors, and that the effect can be linked to one particular enzyme. The figure below presents some microscopy used to detect bacteria in human tumor samples.

Fig. 4. Characterization of bacteria in human pancreatic ductal adenocarcinomas.

Fig. 4. Characterization of bacteria in human pancreatic ductal adenocarcinomas.

After acknowledging the hard work done by the authors, and the significant contribution that this paper will undoubtedly have on the field, I'd like to point out a larger theme. The authors found that a particular enzyme was responsible for this phenotype, which was the decreased efficacy of an anticancer drug. However they absolutely did not find that this enzyme was encoded by a particular genus or species of bacteria. Instead, the enzyme was found to be present and active sporadically across the entire range of Proteobacteria, a phylum found commonly across the human microbiome. In other words, the name that we give to bacteria (their taxonomic identity) is not as important as the particular set of genes in their genome

The world of microbiome research is more exciting than ever because of findings just like this one. We know that microbes are important for our health, and studies like this are starting to show us exactly why that is.