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ID 118862
Title Alternative
メタボリックシンドローム関連脂肪性肝炎発症モデルであるTSODマウスの肝臓には種々の亜型の肝細胞腺腫が自然発生する
Author
Jargalsaikhan, Orgil Tokushima University
Cai, Qinyi Tokushima University
Miyakami, Yuko Tokushima University
Atsumi, Kengo Tokushima University
Tomita, Mitsuru Tokushima University
Sutoh, Mitsuko Institute for Animal Reproduction
Toyohara, Shunji Institute for Animal Reproduction
Hokao, Ryoji Institute for Animal Reproduction
Keywords
glutamine synthetase
liver fatty acid-binding protein
serum amyloid A
beta-catenin
malignant transformation
focal nodular hyperplasia
immunostaining
diabetes
hyperlipidemia
HCA-like tumor
Content Type
Thesis or Dissertation
Description
Male Tsumura-Suzuki Obese Diabetes (TSOD) mice, a spontaneous metabolic syndrome model, develop non-alcoholic steatohepatitis and liver tumors by feeding on a standard mouse diet. Nearly 70% of liver tumors express glutamine synthetase (GS), a marker of hepatocellular carcinoma. In contrast, approximately 30% are GS-negative without prominent nuclear or structural atypia. In this study, we examined the characteristics of the GS-negative tumors of TSOD mice. Twenty male TSOD mice were sacrificed at 40 weeks and a total of 21 tumors were analyzed by HE staining and immunostaining of GS, liver fatty acid-binding protein (L FABP), serum amyloid A (SAA), and beta-catenin. With immunostaining for GS, six (29%) tumors were negative. Based on the histological and immunohistological characteristics, six GS-negative tumors were classified into several subtypes of human hepatocellular adenoma (HCA). One large tumor showed generally similar findings to inflammatory HCA, but contained small atypical foci with GS staining and partial nuclear beta-catenin expression suggesting malignant transformation. GS-negative tumors of TSOD mice contained features similar to various subtypes of HCA. Different HCA subtypes occurring in the same liver have been reported in humans; however, the diversity of patient backgrounds limits the ability to conduct a detailed, multifaceted analysis. TSOD mice may share similar mechanisms of HCA development as in humans. It is timely to review the pathogenesis of HCA from both genetic and environmental perspectives, and it is expected that TSOD mice will make further contributions in this regard.
Journal Title
International Journal of Molecular Sciences
ISSN
14220067
Publisher
MDPI
Volume
23
Issue
19
Start Page
11923
Published Date
2022-10-07
Remark
内容要旨・審査要旨・論文本文の公開
本論文は,著者Wenhua Shaoの学位論文として提出され,学位審査・授与の対象となっている。
Rights
This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
ETD
MEXT report number
乙第2132号
Diploma Number
乙医第1766号
Granted Date
2024-02-22
Degree Name
Doctor of Medical Science
Grantor
Tokushima University
departments
Medical Sciences
Oral Sciences
University Hospital