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Insights into gemcitabine resistance and the potential for therapeutic monitoring

Byline: Teklab Gebregiworgis (1), Fatema Bhinderwala (1,2), Vinee Purohit (3), Nina V. Chaika (3), Pankaj K. Singh (3,4,5,6), Robert Powers (1,2) Keywords: NMR metabolomics; Pancreatic cancer; Gemcitabine; Drug resistance Abstract: Introduction Gemcitabine is an important component of pancreatic can... Full description

Journal Title: Metabolomics 2018, Vol.14(12), pp.1-7
Main Author: Gebregiworgis, Teklab
Other Authors: Bhinderwala, Fatema , Purohit, Vinee , Chaika, Nina , Singh, Pankaj , Powers, Robert
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 1573-3882 ; E-ISSN: 1573-3890 ; DOI: 10.1007/s11306-018-1452-7
Link: http://dx.doi.org/10.1007/s11306-018-1452-7
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recordid: springer_jour10.1007/s11306-018-1452-7
title: Insights into gemcitabine resistance and the potential for therapeutic monitoring
format: Article
creator:
  • Gebregiworgis, Teklab
  • Bhinderwala, Fatema
  • Purohit, Vinee
  • Chaika, Nina
  • Singh, Pankaj
  • Powers, Robert
subjects:
  • NMR metabolomics
  • Pancreatic cancer
  • Gemcitabine
  • Drug resistance
ispartof: Metabolomics, 2018, Vol.14(12), pp.1-7
description: Byline: Teklab Gebregiworgis (1), Fatema Bhinderwala (1,2), Vinee Purohit (3), Nina V. Chaika (3), Pankaj K. Singh (3,4,5,6), Robert Powers (1,2) Keywords: NMR metabolomics; Pancreatic cancer; Gemcitabine; Drug resistance Abstract: Introduction Gemcitabine is an important component of pancreatic cancer clinical management. Unfortunately, acquired gemcitabine resistance is widespread and there are limitations to predicting and monitoring therapeutic outcomes. Objective To investigate the potential of metabolomics to differentiate pancreatic cancer cells that develops resistance or respond to gemcitabine treatment. Results We applied 1D 1.sup.H and 2D 1.sup.H-- 13.sup.C HSQC NMR methods to profile the metabolic signature of pancreatic cancer cells. 13.sup.C.sub.6-glucose labeling identified 30 key metabolites uniquely altered between wild-type and gemcitabine-resistant cells upon gemcitabine treatment. Gemcitabine resistance was observed to reprogram glucose metabolism and to enhance the pyrimidine synthesis pathway. Myo-inositol, taurine, glycerophosphocholine and creatinine phosphate exhibited a "binary switch" in response to gemcitabine treatment and acquired resistance. Conclusion Metabolic differences between naive and resistant pancreatic cancer cells and, accordingly, their unique responses to gemcitabine treatment were revealed, which may be useful in the clinical setting for monitoring a patient's therapeutic response. Author Affiliation: (1) 0000 0004 1937 0060, grid.24434.35, Department of Chemistry, University of Nebraska-Lincoln, Lincoln, NE, 68588, USA (2) 0000 0004 1937 0060, grid.24434.35, Nebraska Center for Integrated Biomolecular Communication, University of Nebraska-Lincoln, Lincoln, NE, 68588, USA (3) 0000 0001 0666 4105, grid.266813.8, The Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, 68198, USA (4) 0000 0001 0666 4105, grid.266813.8, Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, 68198, USA (5) 0000 0001 0666 4105, grid.266813.8, Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, 68198, USA (6) 0000 0001 0666 4105, grid.266813.8, Department of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, NE, 68198, USA Article History: Registration Date: 19/11/2018 Received Date: 26/07/2018 Accepted Date: 19/11/2018 Online Date: 27/11/2018 Article note: Teklab
language: eng
source:
identifier: ISSN: 1573-3882 ; E-ISSN: 1573-3890 ; DOI: 10.1007/s11306-018-1452-7
fulltext: fulltext
issn:
  • 1573-3890
  • 15733890
  • 1573-3882
  • 15733882
url: Link


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titleInsights into gemcitabine resistance and the potential for therapeutic monitoring
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descriptionByline: Teklab Gebregiworgis (1), Fatema Bhinderwala (1,2), Vinee Purohit (3), Nina V. Chaika (3), Pankaj K. Singh (3,4,5,6), Robert Powers (1,2) Keywords: NMR metabolomics; Pancreatic cancer; Gemcitabine; Drug resistance Abstract: Introduction Gemcitabine is an important component of pancreatic cancer clinical management. Unfortunately, acquired gemcitabine resistance is widespread and there are limitations to predicting and monitoring therapeutic outcomes. Objective To investigate the potential of metabolomics to differentiate pancreatic cancer cells that develops resistance or respond to gemcitabine treatment. Results We applied 1D 1.sup.H and 2D 1.sup.H-- 13.sup.C HSQC NMR methods to profile the metabolic signature of pancreatic cancer cells. 13.sup.C.sub.6-glucose labeling identified 30 key metabolites uniquely altered between wild-type and gemcitabine-resistant cells upon gemcitabine treatment. Gemcitabine resistance was observed to reprogram glucose metabolism and to enhance the pyrimidine synthesis pathway. Myo-inositol, taurine, glycerophosphocholine and creatinine phosphate exhibited a "binary switch" in response to gemcitabine treatment and acquired resistance. Conclusion Metabolic differences between naive and resistant pancreatic cancer cells and, accordingly, their unique responses to gemcitabine treatment were revealed, which may be useful in the clinical setting for monitoring a patient's therapeutic response. Author Affiliation: (1) 0000 0004 1937 0060, grid.24434.35, Department of Chemistry, University of Nebraska-Lincoln, Lincoln, NE, 68588, USA (2) 0000 0004 1937 0060, grid.24434.35, Nebraska Center for Integrated Biomolecular Communication, University of Nebraska-Lincoln, Lincoln, NE, 68588, USA (3) 0000 0001 0666 4105, grid.266813.8, The Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, 68198, USA (4) 0000 0001 0666 4105, grid.266813.8, Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, 68198, USA (5) 0000 0001 0666 4105, grid.266813.8, Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, 68198, USA (6) 0000 0001 0666 4105, grid.266813.8, Department of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, NE, 68198, USA Article History: Registration Date: 19/11/2018 Received Date: 26/07/2018 Accepted Date: 19/11/2018 Online Date: 27/11/2018 Article note: Teklab Gebregiworgis and Fatema Bhinderwala have contributed equally to this work. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11306-018-1452-7) contains supplementary material, which is available to authorized users.
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