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Composition, diversity and potential utility of intervention-naïve pancreatic cancer intratumoral microbiome signature profiling via endoscopic ultrasound
  1. Ferga C Gleeson1,
  2. Patricio Jeraldo2,
  3. Michael J Levy1,
  4. Stephen J Murphy3,
  5. Helena Mendes-Soares2,
  6. Giannoula Karagouga3,
  7. Alexa F Mccune3,
  8. Ana Garcia Garcia Deparedes1,4,
  9. Benjamin R Kipp5,
  10. Stephanie D Song2,
  11. Sahil Khanna1,
  12. Darrell S Pardi1,
  13. Nicholas Chia2,6
  1. 1 Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA
  2. 2 Microbiome Program, Center for Individualized Medicine, Mayo Clinic, Rochester, Minnesota, USA
  3. 3 Biomarker Discovery Program, Center of Individualized Medicine, Mayo Clinic, Rochester, Minnesota, USA
  4. 4 Gastroenterology and Hepatology Department, Universidad de Alcala de Henares, Alcala de Henares, Comunidad de Madrid, Spain
  5. 5 Division of Anatomic Pathology and Center of Individualized Medicine, Mayo Clinic, Rochester, Minnesota, USA
  6. 6 Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA
  1. Correspondence to Dr Ferga C Gleeson, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55901, USA; gleeson.ferga{at}mayo.edu

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We read with great interest the recent article by Cheng et al that discussed the topic of gut microbiome modulation, which may promote sensitivity or resistance to chemotherapeutic agents or immune checkpoint inhibitors.1 Historically, the pancreas was considered to be a sterile organ; however, bacterial DNA has been detected in 76% of surgically resected pancreatic ductal adenocarcinoma (PDAC) samples, some of which had prior biliary instrumentation, and in 15% of normal pancreas controls.2 3 It is unknown how bacteria may colonise the pancreas, but some have postulated bacterial reflux into the pancreatic duct via the major/minor papilla as a possibility and by dysbiosis due to pancreatitis, obesity, smoking and diabetes, as it alters gut permeability.4 5 Intratumoral microbiome composition may also impact therapeutic drug sensitivity and disease survival.6 The presence of PDAC intratumoral Gammaproteobacteria has the potential to inactivate gemcitabine sensitivity via the bacterial enzyme cytidine deaminase.7 Conversely, Bifidobacterium is believed to promote beneficial effects …

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Footnotes

  • Twitter @FergaGleeson

  • Contributors FCG, guarantor for the article, was involved in planning, conducting the study and reporting. PJ and NC were involved in planning, conducting the study and reporting. MJL, AGGD, BK, SDS, SK and DSP were involved in reporting and final review. SJM, HM-S, GK and AFM were involved in planning and conducting the study.

  • Funding This study was funded by Mayo CCaTS grant number UL1TR000135.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.