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. 2013 Sep 25;63(6):974–983. doi: 10.1136/gutjnl-2013-305559

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Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 3.0) 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/3.0/

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Pharmacokinetics and pharmacodynamics of m-nab-paclitaxel in the KPfC secreted protein acidic and rich in cysteine (SPARC) mouse model. (A) Cohorts of KPfC SPARC^+/+ (n=8) and KPC SPARC^−/− mice (n=11) were treated with 60 mg/kg m-nab-paclitaxel, and tumour samples were taken 2 h after dosing and analysed by liquid chromatography tandem mass spectrometry (LC-MS/MS). (B) Representative high-resolution ultrasound picture of typical KPfC murine pancreatic tumour. (C) Quantification of tumour volume growth using biweekly three-dimensional high-resolution ultrasound shows no significant decrease in tumour burden on day 7 in KPfC SPARC^+/+ versus KPfC SPARC^−/− pancreatic tumours following three injections of 60 mg/kg m-nab-paclitaxel over 7 days. (D) Computer-based quantification of apoptosis (cleaved caspase-3) in pancreatic tumours from KPfC SPARC^+/+ (n=6) and KPfC SPARC^−/− mice (n=5) treated with 60 mg/kg m-nab-paclitaxel. All animals were sacrificed 2 h after the last dose of m-nab-paclitaxel.