Pressure-enabled delivery of gemcitabine in an orthotopic pancreatic cancer mouse model.


Journal

Surgery
ISSN: 1532-7361
Titre abrégé: Surgery
Pays: United States
ID NLM: 0417347

Informations de publication

Date de publication:
09 2020
Historique:
received: 03 02 2020
revised: 28 03 2020
accepted: 25 04 2020
pubmed: 6 7 2020
medline: 12 11 2020
entrez: 5 7 2020
Statut: ppublish

Résumé

We describe the use of pancreatic retrograde venous infusion in an orthotopic murine model of pancreatic ductal adenocarcinoma and hypothesize that pancreatic retrograde venous infusion delivery of gemcitabine will increase concentrations of gemcitabine in the tumor and the subsequent tumor response to treatment. Murine pancreatic ductal adenocarcinoma (KPC4580P) was transplanted onto the pancreatic tail of C57BL/6J mice. Groups (n = 15) of mice were assigned to sham laparotomy and 100 mg/kg intraperitoneal infusion of gemcitabine (systemic gemcitabine), pancreatic venous isolation with pancreatic retrograde venous infusion of 100 mg/kg gemcitabine, or pancreatic retrograde venous infusion with saline infusion. Tumor pressures were recorded during pancreatic retrograde venous infusion. Mice were killed at 1 hour or 7 days after infusion. Baseline tumor pressures were 45 ± 8 mm Hg, and pancreatic retrograde venous infusion increased tumor pressures by 29 ± 6 mm Hg (P < .01). Pancreatic retrograde venous infusion gemcitabine mice had greater tumor gemcitabine concentrations compared with systemic gemcitabine (127 vs 19 ng/mg; P < .01) and lesser tumor volumes compared with both systemic gem and pancreatic retrograde venous infusion with saline (274 vs 857 vs 629 mm Pancreatic retrograde venous infusion increased tumor pressures greater than baseline, improved gemcitabine delivery, and increased the treatment response. These findings suggest that pressurized, regional delivery overcomes the increased pressure barrier in pancreatic ductal adenocarcinoma. Additional preclinical studies with cytotoxic and immunotherapeutic agents and clinical trials using pressure-enabled drug delivery with pancreatic retrograde venous infusion devices are underway.

Sections du résumé

BACKGROUND
We describe the use of pancreatic retrograde venous infusion in an orthotopic murine model of pancreatic ductal adenocarcinoma and hypothesize that pancreatic retrograde venous infusion delivery of gemcitabine will increase concentrations of gemcitabine in the tumor and the subsequent tumor response to treatment.
METHODS
Murine pancreatic ductal adenocarcinoma (KPC4580P) was transplanted onto the pancreatic tail of C57BL/6J mice. Groups (n = 15) of mice were assigned to sham laparotomy and 100 mg/kg intraperitoneal infusion of gemcitabine (systemic gemcitabine), pancreatic venous isolation with pancreatic retrograde venous infusion of 100 mg/kg gemcitabine, or pancreatic retrograde venous infusion with saline infusion. Tumor pressures were recorded during pancreatic retrograde venous infusion. Mice were killed at 1 hour or 7 days after infusion.
RESULTS
Baseline tumor pressures were 45 ± 8 mm Hg, and pancreatic retrograde venous infusion increased tumor pressures by 29 ± 6 mm Hg (P < .01). Pancreatic retrograde venous infusion gemcitabine mice had greater tumor gemcitabine concentrations compared with systemic gemcitabine (127 vs 19 ng/mg; P < .01) and lesser tumor volumes compared with both systemic gem and pancreatic retrograde venous infusion with saline (274 vs 857 vs 629 mm
CONCLUSION
Pancreatic retrograde venous infusion increased tumor pressures greater than baseline, improved gemcitabine delivery, and increased the treatment response. These findings suggest that pressurized, regional delivery overcomes the increased pressure barrier in pancreatic ductal adenocarcinoma. Additional preclinical studies with cytotoxic and immunotherapeutic agents and clinical trials using pressure-enabled drug delivery with pancreatic retrograde venous infusion devices are underway.

Identifiants

pubmed: 32620306
pii: S0039-6060(20)30273-7
doi: 10.1016/j.surg.2020.04.059
pii:
doi:

Substances chimiques

Antimetabolites, Antineoplastic 0
Deoxycytidine 0W860991D6
Gemcitabine 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

448-456

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Auteurs

Jayanth S Shankara Narayanan (JS)

Moores Cancer Center, University of California San Diego, CA.

Diego A Vicente (DA)

Moores Cancer Center, University of California San Diego, CA.

Partha Ray (P)

Moores Cancer Center, University of California San Diego, CA.

Louis F Chai (LF)

Immuno-oncology Institute and Department of Medicine, Roger Williams Medical Center, Providence, RI; Department of Surgery, Boston University School of Medicine, Boston, MA.

Suna Erdem (S)

Moores Cancer Center, University of California San Diego, CA.

Matthew J Carr (MJ)

Moores Cancer Center, University of California San Diego, CA.

Benedict A Capacio (BA)

Moores Cancer Center, University of California San Diego, CA.

Bryan F Cox (BF)

TriSalus Life Sciences, Westminster, CO.

David B Jaroch (DB)

TriSalus Life Sciences, Westminster, CO.

Steven C Katz (SC)

Immuno-oncology Institute and Department of Medicine, Roger Williams Medical Center, Providence, RI; Department of Surgery, Boston University School of Medicine, Boston, MA.

Rebekah R White (RR)

Moores Cancer Center, University of California San Diego, CA. Electronic address: rewhite@health.ucsd.edu.

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Classifications MeSH