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Tumor growth-promoting cellular host response during liver atrophy after portal occlusion

Authors

  • Lars Mueller,

    1. Department of Hepatobiliary Surgery and Visceral Transplantation, University Hospital Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany
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  • Juliane Goettsche,

    1. Department of Hepatobiliary Surgery and Visceral Transplantation, University Hospital Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany
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  • Awad Abdulgawad,

    1. Department of Hepatobiliary Surgery and Visceral Transplantation, University Hospital Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany
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  • Yogesh K. Vashist,

    1. Department of Hepatobiliary Surgery and Visceral Transplantation, University Hospital Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany
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  • Jannine Meyer,

    1. Department of Hepatobiliary Surgery and Visceral Transplantation, University Hospital Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany
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  • Christian Wilms,

    1. Department of Hepatobiliary Surgery and Visceral Transplantation, University Hospital Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany
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  • Christian Hillert,

    1. Department of Hepatobiliary Surgery and Visceral Transplantation, University Hospital Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany
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  • Xavier Rogiers,

    1. Department of Hepatobiliary Surgery and Visceral Transplantation, University Hospital Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany
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  • Dieter C. Broering

    1. Department of Hepatobiliary Surgery and Visceral Transplantation, University Hospital Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany
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Lars Mueller, MD, Department of Hepatobiliary Surgery and Visceral Transplantation, University Hospital Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany.
Tel:+49-40-42803-6136
Fax:+49-40-42803-3431
e-mail: l.mueller@uke.uni-hamburg.de

Abstract

Abstract: Background/Aims: Clinical observations suggest cancer progression after preoperative segmental portal vein occlusion, a procedure to prevent liver failure after major hepatic resections. The aim of this study was to determine whether portal occlusion induces host reactions which promote cancer invasion and angiogenesis.

Methods: The rat model of portal branch ligation (PBL) was compared with partial hepatectomy (PH) and sham operation (SO) and evaluated for the expression of heat shock protein-70 (hsp70), heme oxygenase-1 (hmox1), early growth response gene-1 (Egr-1) and urokinase-type plasminogen activator (uPA), its inhibitor (PAI-1) and receptor (uPAR).

Results:  Portal deprivation after PBL was associated with a regression of liver tissue to 25% of its original mass within 8 days with only modest fibrotic changes. During the progression of atrophy, there were significant inductions of hsp70-, hmox1- and Egr-1-mRNA in comparison with regenerating liver tissue. PAI-1-specific mRNA was transiently elevated at 3 – 48 h after PBL in the atrophying lobes, whereas uPA and uPAR were unaffected in comparison with PH or SO.

Conclusion:  Hepatic atrophy caused by PBL is associated with increased expression of genes known to promote tumor growth. These host events represent a possible explanation for the tumor progression after portal occlusion and require further evaluation.

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