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Keratin 18-deficiency results in steatohepatitis and liver tumors in old mice: A model of steatohepatitis-associated liver carcinogenesis

Backround: Steatohepatitis (SH)-associated liver carcinogenesis is an increasingly important issue in clinical medicine. SH is morphologically characterized by steatosis, hepatocyte injury, ballooning, hepatocytic cytoplasmic inclusions termed Mallory-Denk bodies (MDBs), inflammation and fibrosis. 1... Full description

Journal Title: Oncotarget 08 November 2016, Vol.7(45), pp.73309-73322
Main Author: Bettermann, Kira
Other Authors: Mehta, Anita Kuldeep , Hofer, Eva M , Wohlrab, Christina , Golob-Schwarzl, Nicole , Svendova, Vendula , Schimek, Michael G , Stumptner, Cornelia , Thüringer, Andrea , Speicher, Michael R , Lackner, Carolin , Zatloukal, Kurt , Denk, Helmut , Haybaeck, Johannes
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1949-2553 ; PMID: 27689336 Version:1 ; DOI: 10.18632/oncotarget.12325
Link: http://pubmed.gov/27689336
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recordid: medline27689336
title: Keratin 18-deficiency results in steatohepatitis and liver tumors in old mice: A model of steatohepatitis-associated liver carcinogenesis
format: Article
creator:
  • Bettermann, Kira
  • Mehta, Anita Kuldeep
  • Hofer, Eva M
  • Wohlrab, Christina
  • Golob-Schwarzl, Nicole
  • Svendova, Vendula
  • Schimek, Michael G
  • Stumptner, Cornelia
  • Thüringer, Andrea
  • Speicher, Michael R
  • Lackner, Carolin
  • Zatloukal, Kurt
  • Denk, Helmut
  • Haybaeck, Johannes
subjects:
  • Mallory-Denk Bodies
  • Keratin 18 Deficiency
  • Liver Tumors
  • Steatohepatitis
  • Fatty Liver -- Complications
  • Keratin-18 -- Genetics
  • Liver Neoplasms -- Etiology
ispartof: Oncotarget, 08 November 2016, Vol.7(45), pp.73309-73322
description: Backround: Steatohepatitis (SH)-associated liver carcinogenesis is an increasingly important issue in clinical medicine. SH is morphologically characterized by steatosis, hepatocyte injury, ballooning, hepatocytic cytoplasmic inclusions termed Mallory-Denk bodies (MDBs), inflammation and fibrosis. 17-20-months-old Krt18-/- and Krt18+/- mice in contrast to wt mice spontaneously developed liver lesions closely resembling the morphological spectrum of human SH as well as liver tumors. The pathologic alterations were more pronounced in Krt18-/- than in Krt18+/- mice. The frequency of liver tumors with male predominance was significantly higher in Krt18-/- compared to age-matched Krt18+/- and wt mice. Krt18-deficient tumors in contrast to wt animals displayed SH features and often pleomorphic morphology. aCGH analysis of tumors revealed chromosomal aberrations in Krt18-/- liver tumors, affecting loci of oncogenes and tumor suppressor genes. Livers of 3-, 6-, 12- and 17-20-months-old aged wild type (wt), Krt18+/- and Krt18-/- (129P2/OlaHsd background) mice were analyzed by light and immunofluorescence microscopy as well as immunohistochemistry. Liver tumors arising in aged mice were analyzed by array comparative genomic hybridization (aCGH). Our findings show that K18 deficiency of hepatocytes leads to steatosis, increasing with age, and finally to SH. K18 deficiency and age promote liver tumor development in mice, frequently on the basis of chromosomal instability, resembling human HCC with stemness features.
language: eng
source:
identifier: E-ISSN: 1949-2553 ; PMID: 27689336 Version:1 ; DOI: 10.18632/oncotarget.12325
fulltext: fulltext
issn:
  • 19492553
  • 1949-2553
url: Link


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titleKeratin 18-deficiency results in steatohepatitis and liver tumors in old mice: A model of steatohepatitis-associated liver carcinogenesis
creatorBettermann, Kira ; Mehta, Anita Kuldeep ; Hofer, Eva M ; Wohlrab, Christina ; Golob-Schwarzl, Nicole ; Svendova, Vendula ; Schimek, Michael G ; Stumptner, Cornelia ; Thüringer, Andrea ; Speicher, Michael R ; Lackner, Carolin ; Zatloukal, Kurt ; Denk, Helmut ; Haybaeck, Johannes
ispartofOncotarget, 08 November 2016, Vol.7(45), pp.73309-73322
identifier
subjectMallory-Denk Bodies ; Keratin 18 Deficiency ; Liver Tumors ; Steatohepatitis ; Fatty Liver -- Complications ; Keratin-18 -- Genetics ; Liver Neoplasms -- Etiology
descriptionBackround: Steatohepatitis (SH)-associated liver carcinogenesis is an increasingly important issue in clinical medicine. SH is morphologically characterized by steatosis, hepatocyte injury, ballooning, hepatocytic cytoplasmic inclusions termed Mallory-Denk bodies (MDBs), inflammation and fibrosis. 17-20-months-old Krt18-/- and Krt18+/- mice in contrast to wt mice spontaneously developed liver lesions closely resembling the morphological spectrum of human SH as well as liver tumors. The pathologic alterations were more pronounced in Krt18-/- than in Krt18+/- mice. The frequency of liver tumors with male predominance was significantly higher in Krt18-/- compared to age-matched Krt18+/- and wt mice. Krt18-deficient tumors in contrast to wt animals displayed SH features and often pleomorphic morphology. aCGH analysis of tumors revealed chromosomal aberrations in Krt18-/- liver tumors, affecting loci of oncogenes and tumor suppressor genes. Livers of 3-, 6-, 12- and 17-20-months-old aged wild type (wt), Krt18+/- and Krt18-/- (129P2/OlaHsd background) mice were analyzed by light and immunofluorescence microscopy as well as immunohistochemistry. Liver tumors arising in aged mice were analyzed by array comparative genomic hybridization (aCGH). Our findings show that K18 deficiency of hepatocytes leads to steatosis, increasing with age, and finally to SH. K18 deficiency and age promote liver tumor development in mice, frequently on the basis of chromosomal instability, resembling human HCC with stemness features.
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titleKeratin 18-deficiency results in steatohepatitis and liver tumors in old mice: A model of steatohepatitis-associated liver carcinogenesis
description
0Backround: Steatohepatitis (SH)-associated liver carcinogenesis is an increasingly important issue in clinical medicine. SH is morphologically characterized by steatosis, hepatocyte injury, ballooning, hepatocytic cytoplasmic inclusions termed Mallory-Denk bodies (MDBs), inflammation and fibrosis.
117-20-months-old Krt18-/- and Krt18+/- mice in contrast to wt mice spontaneously developed liver lesions closely resembling the morphological spectrum of human SH as well as liver tumors. The pathologic alterations were more pronounced in Krt18-/- than in Krt18+/- mice. The frequency of liver tumors with male predominance was significantly higher in Krt18-/- compared to age-matched Krt18+/- and wt mice. Krt18-deficient tumors in contrast to wt animals displayed SH features and often pleomorphic morphology. aCGH analysis of tumors revealed chromosomal aberrations in Krt18-/- liver tumors, affecting loci of oncogenes and tumor suppressor genes.
2Livers of 3-, 6-, 12- and 17-20-months-old aged wild type (wt), Krt18+/- and Krt18-/- (129P2/OlaHsd background) mice were analyzed by light and immunofluorescence microscopy as well as immunohistochemistry. Liver tumors arising in aged mice were analyzed by array comparative genomic hybridization (aCGH).
3Our findings show that K18 deficiency of hepatocytes leads to steatosis, increasing with age, and finally to SH. K18 deficiency and age promote liver tumor development in mice, frequently on the basis of chromosomal instability, resembling human HCC with stemness features.
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titleKeratin 18-deficiency results in steatohepatitis and liver tumors in old mice: A model of steatohepatitis-associated liver carcinogenesis
authorBettermann, Kira ; Mehta, Anita Kuldeep ; Hofer, Eva M ; Wohlrab, Christina ; Golob-Schwarzl, Nicole ; Svendova, Vendula ; Schimek, Michael G ; Stumptner, Cornelia ; Thüringer, Andrea ; Speicher, Michael R ; Lackner, Carolin ; Zatloukal, Kurt ; Denk, Helmut ; Haybaeck, Johannes
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abstractBackround: Steatohepatitis (SH)-associated liver carcinogenesis is an increasingly important issue in clinical medicine. SH is morphologically characterized by steatosis, hepatocyte injury, ballooning, hepatocytic cytoplasmic inclusions termed Mallory-Denk bodies (MDBs), inflammation and fibrosis.
doi10.18632/oncotarget.12325
pmid27689336
date2016-11-08