We recently reported that bacteria can be found within pancreatic ductal adenocarcinoma (PDAC) tumors. Some of these bacteria can metabolize and thereby inactivate the nucleoside analog gemcitabine. We demonstrated that the long isoform of the bacterial enzyme cytidine deaminase (CDD) mediates the metabolism of gemcitabine. The clinical effect of overcoming this potential mechanism of drug resistance has yet to be studied.
Keywords: PDAC; chemoresistance; drug metabolism; gemcitabine; mechanisms of resistance to therapy; mycoplasma; novel therapeutic targets; pancreatic ductal adenocarcinoma; tumor microbiome.