Tumor growth-promoting cellular host response during liver atrophy after portal occlusion.
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Tumor growth-promoting cellular host response during liver atrophy after portal occlusion. / Mueller, Lars; Göttsche, Juliane; Abdulgawad, Awad; Vashist Yogesh, K; Meyer, Jannine; Wilms, Christian; Hillert, Christian; Rogiers, Xavier; Broering Dieter, C.
in: LIVER INT, Jahrgang 25, Nr. 5, 5, 2005, S. 994-1001.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Tumor growth-promoting cellular host response during liver atrophy after portal occlusion.
AU - Mueller, Lars
AU - Göttsche, Juliane
AU - Abdulgawad, Awad
AU - Vashist Yogesh, K
AU - Meyer, Jannine
AU - Wilms, Christian
AU - Hillert, Christian
AU - Rogiers, Xavier
AU - Broering Dieter, C
PY - 2005
Y1 - 2005
N2 - 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.
AB - 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.
M3 - SCORING: Zeitschriftenaufsatz
VL - 25
SP - 994
EP - 1001
JO - LIVER INT
JF - LIVER INT
SN - 1478-3223
IS - 5
M1 - 5
ER -
