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

  title={Potential role of intratumor bacteria in mediating tumor resistance to the chemotherapeutic drug gemcitabine},
  author={Leore T Geller and Michal Barzily-Rokni and Tal Danino and Oliver H Jonas and Noam Shental and Deborah Nejman and Nancy Gavert and Yaara Zwang and Zachary A Cooper and Kevin Shee and Christoph A. Thaiss and Alexandre Reuben and Jonathan Livny and Roi Avraham and Dennie Tompers Frederick and Matteo Ligorio and Kelly Chatman and Stephen E Johnston and Carrie M Mosher and Alexander S. Brandis and Garold Fuks and Candice Gurbatri and Vancheswaran Gopalakrishnan and Michael Kim and Mark W Hurd and Matthew H. G. Katz and Jason Fleming and Anirban Maitra and David A Smith and Matt Skalak and Jeffrey Bu and Monia Michaud and Sunia A. Trauger and Iris Barshack and Talia Golan and Judith Sandbank and Keith T. Flaherty and Anna Mandinova and Wendy S. Garrett and Sarah P. Thayer and Cristina R Ferrone and Curtis Huttenhower and Sangeeta N. Bhatia and Dirk Gevers and Jennifer A Wargo and Todd R. Golub and Ravid Straussman},
Growing evidence suggests that microbes can influence the efficacy of cancer therapies. By studying colon cancer models, we found that bacteria can metabolize the chemotherapeutic drug gemcitabine (2′,2′-difluorodeoxycytidine) into its inactive form, 2′,2′-difluorodeoxyuridine. Metabolism was dependent on the expression of a long isoform of the bacterial enzyme cytidine deaminase (CDDL), seen primarily in Gammaproteobacteria. In a colon cancer mouse model, gemcitabine resistance was induced by… CONTINUE READING
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