Tingle SJ, Moir JA, White SA. Role of anti-stromal polypharmacy in increasing survival after pancreaticoduodenectomy for pancreatic ductal adenocarcinoma. World J Gastrointest Pathophysiol 2015; 6(4): 235-242 [PMID: 26600982 DOI: 10.4291/wjgp.v6.i4.235]
Corresponding Author of This Article
Steven A White, Professor, HPB and Transplant Consultant, HPB Unit, Freeman Hospital, Freeman Road, Newcastle upon Tyne, Tyne and Wear NE7 7DN, United Kingdom. steven.white@nuth.nhs.uk
Research Domain of This Article
Surgery
Article-Type of This Article
Retrospective Cohort Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastrointest Pathophysiol. Nov 15, 2015; 6(4): 235-242 Published online Nov 15, 2015. doi: 10.4291/wjgp.v6.i4.235
Role of anti-stromal polypharmacy in increasing survival after pancreaticoduodenectomy for pancreatic ductal adenocarcinoma
Samuel J Tingle, John A Moir, Steven A White
Samuel J Tingle, Faculty of Medical Sciences, Newcastle Medical School, Newcastle, Tyne and Wear NE2 4HH, United Kingdom
John A Moir, Newcastle Medical School Fibrosis Lab, Tyne and Wear NE2 4HH, United Kingdom
Steven A White, HPB and Transplant Consultant, HPB Unit, Freeman Hospital, Newcastle upon Tyne, Tyne and Wear NE7 7DN, United Kingdom
Author contributions: Tingle SJ performed the research and wrote the paper; Moir JA and White SA supervised and designed the project.
Institutional review board statement: The study was reviewed and approved for publication by our institutional reviewer, NUTH trust.
Informed consent statement: All cases were anonymised during data collection therefore informed consent was not required.
Conflict-of-interest statement: No authors have any conflict of interest.
Data sharing statement: The original anonymised database is available for collaborative studies via the corresponding author, steven.white@nuth.nhs.uk.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Steven A White, Professor, HPB and Transplant Consultant, HPB Unit, Freeman Hospital, Freeman Road, Newcastle upon Tyne, Tyne and Wear NE7 7DN, United Kingdom. steven.white@nuth.nhs.uk
Telephone: +44-191-2137074
Received: June 2, 2015 Peer-review started: June 5, 2015 First decision: July 6, 2015 Revised: September 9, 2015 Accepted: October 16, 2015 Article in press: October 19, 2015 Published online: November 15, 2015 Processing time: 167 Days and 15.8 Hours
Core Tip
Core tip: Stromal interactions play a large part in the dismal prognosis of pancreatic cancer. Recent laboratory studies have examined the potential use of common pharmaceuticals, such as calcium channel blocker (CCB), aspirin, angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers and statins, in inhibiting these protumorigenic stromal interactions. We retrospectively collected data from 164 patients whom underwent a pancreaticoduodenectomy to remove a pancreatic ductal adenocarcinoma, to see if the potential benefits of these drugs translated into increased survival. Our finding that those taking a combination of aspirin and CCB survived over twice as long as those on neither drug, highlights the potential of novel drug combinations to increase survival in pancreatic cancer.
