p53 mutations are absent from carcinogen-induced mouse liver tumors but occur in cell lines established from these tumors

1992 ◽  
Vol 6 (2) ◽  
pp. 148-158 ◽  
Author(s):  
Stefan Kress ◽  
Jorg König ◽  
Jürgen Schweizer ◽  
Heinz Löhrke ◽  
Richard Bauer-Hofmann ◽  
...  
Keyword(s):  
Cell Lines ◽  
Mouse Liver ◽  
Liver Tumors ◽  
P53 Mutations

p53 mutations in lungcancer cell lines and their correlation to radiosensitivity

Lung Cancer ◽  
2000 ◽  
Vol 29 (1) ◽  
pp. 168
Author(s):  
G Wagenius ◽  
M Bergqvist ◽  
D Brattström ◽  
O Brodin
Keyword(s):  
Cell Lines ◽  
P53 Mutations

IARC p53 mutation database: A relational database to compile and analyze p53 mutations in human tumors and cell lines

1999 ◽  
Vol 14 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Tina Hernandez-Boussard ◽  
Patricia Rodriguez-Tome ◽  
Ruggero Montesano ◽  
Pierre Hainaut
Keyword(s):  
Cell Lines ◽  
Relational Database ◽  
P53 Mutation ◽  
Human Tumors ◽  
P53 Mutations ◽  
Mutation Database

scholarly journals Growth hormone upregulates the pro-tumorigenic galectin 1 in mouse liver

2019 ◽  
Vol 8 (8) ◽  
pp. 1108-1117 ◽  
Author(s):  
María L Bacigalupo ◽  
Verónica G Piazza ◽  
Nadia S Cicconi ◽  
Pablo Carabias ◽  
Andrzej Bartke ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Transgenic Mice ◽  
Mouse Liver ◽  
Liver Tumors ◽  
Tumor Development ◽  
Hepatic Cancer ◽  
Liver Pathology ◽  
Liver Carcinogenesis ◽  
Short Period ◽  
Hcc Cells

Transgenic mice overexpressing growth hormone (GH) spontaneously develop liver tumors, including hepatocellular carcinoma (HCC), within a year. The preneoplastic liver pathology in these mice recapitulates that observed in humans at high risk of developing hepatic cancer. Although increased expression of galectin 1 (GAL1) in liver tissue is associated with HCC aggressiveness, a link between this glycan-binding protein and hormone-related tumor development has not yet been explored. In this study, we investigated GAL1 expression during liver tumor progression in mice continuously exposed to high levels of GH. GAL1 expression was determined by Western blotting, RT-qPCR and immunohistochemistry in the liver of transgenic mice overexpressing GH. Animals of representative ages at different stages of liver pathology were studied. GAL1 expression was upregulated in the liver of GH-transgenic mice. This effect was observed at early ages, when animals displayed no signs of liver disease or minimal histopathological alterations and was also detected in young adults with preneoplastic liver pathology. Remarkably, GAL1 upregulation was sustained during aging and its expression was particularly enhanced in liver tumors. GH also induced hepatic GAL1 expression in mice that were treated with this hormone for a short period. Moreover, GH triggered a rapid increment in GAL1 protein expression in human HCC cells, denoting a direct effect of the hormone on hepatocytes. Therefore, our results indicate that GH upregulates GAL1 expression in mouse liver, which may have critical implications in tumorigenesis. These findings suggest that this lectin could be implicated in hormone-driven liver carcinogenesis.

scholarly journals Oncogenic Determination of a Broad Spectrum of Phenotypes of Hepatocyte-Derived Mouse Liver Tumors

2017 ◽  
Vol 187 (12) ◽  
pp. 2711-2725 ◽  
Author(s):  
Masahiro Yamamoto ◽  
Bing Xin ◽  
Kenji Watanabe ◽  
Takako Ooshio ◽  
Kiyonaga Fujii ◽  
...  
Keyword(s):  
Broad Spectrum ◽  
Mouse Liver ◽  
Liver Tumors

scholarly journals Hepatoblastomas exhibit marked NNMT downregulation driven by promoter DNA hypermethylation

Tumor Biology ◽  
2020 ◽  
Vol 42 (12) ◽  
pp. 101042832097712
Author(s):  
Maria Prates Rivas ◽  
Talita Ferreira Marques Aguiar ◽  
Mariana Maschietto ◽  
Renan B Lemes ◽  
Luiz Carlos Caires-Júnior ◽  
...  
Keyword(s):  
Cell Lines ◽  
Liver Tumors ◽  
Quantitative Polymerase Chain Reaction ◽  
Magic Angle Spinning ◽  
Clinical Variable ◽  
Resonance Spectroscopy ◽  
Magic Angle ◽  
Dna Hypermethylation ◽  
Gene And Protein Expression

Hepatoblastomas exhibit the lowest mutational burden among pediatric tumors. We previously showed that epigenetic disruption is crucial for hepatoblastoma carcinogenesis. Our data revealed hypermethylation of nicotinamide N-methyltransferase, a highly expressed gene in adipocytes and hepatocytes. The expression pattern and the role of nicotinamide N-methyltransferase in pediatric liver tumors have not yet been explored, and this study aimed to evaluate the effect of nicotinamide N-methyltransferase hypermethylation in hepatoblastomas. We evaluated 45 hepatoblastomas and 26 non-tumoral liver samples. We examined in hepatoblastomas if the observed nicotinamide N-methyltransferase promoter hypermethylation could lead to dysregulation of expression by measuring mRNA and protein levels by real-time quantitative polymerase chain reaction, immunohistochemistry, and Western blot assays. The potential impact of nicotinamide N-methyltransferase changes was evaluated on the metabolic profile by high-resolution magic angle spinning nuclear magnetic resonance spectroscopy. Significant nicotinamide N-methyltransferase downregulation was revealed in hepatoblastomas, with two orders of magnitude lower nicotinamide N-methyltransferase expression in tumor samples and hepatoblastoma cell lines than in hepatocellular carcinoma cell lines. A specific TSS1500 CpG site (cg02094283) of nicotinamide N-methyltransferase was hypermethylated in tumors, with an inverse correlation between its methylation level and nicotinamide N-methyltransferase expression. A marked global reduction of the nicotinamide N-methyltransferase protein was validated in tumors, with strong correlation between gene and protein expression. Of note, higher nicotinamide N-methyltransferase expression was statistically associated with late hepatoblastoma diagnosis, a known clinical variable of worse prognosis. In addition, untargeted metabolomics analysis detected aberrant lipid metabolism in hepatoblastomas. Data presented here showed the first evidence that nicotinamide N-methyltransferase reduction occurs in hepatoblastomas, providing further support that the nicotinamide N-methyltransferase downregulation is a wide phenomenon in liver cancer. Furthermore, this study unraveled the role of DNA methylation in the regulation of nicotinamide N-methyltransferase expression in hepatoblastomas, in addition to evaluate the potential effect of nicotinamide N-methyltransferase reduction in the metabolism of these tumors. These preliminary findings also suggested that nicotinamide N-methyltransferase level may be a potential prognostic biomarker for hepatoblastoma.

Flow-suppressed hyperpolarized 13 C chemical shift imaging using velocity-optimized bipolar gradient in mouse liver tumors at 9.4 T

2016 ◽  
Vol 78 (5) ◽  
pp. 1674-1682 ◽  
Author(s):  
Hansol Lee ◽  
Joonsung Lee ◽  
Eunhae Joe ◽  
Seungwook Yang ◽  
Jae Eun Song ◽  
...  
Keyword(s):  
Chemical Shift ◽  
Mouse Liver ◽  
Liver Tumors ◽  
Chemical Shift Imaging

Activated oncogenes in B6C3F1 mouse liver tumors: implications for risk assessment

Science ◽  
1987 ◽  
Vol 237 (4820) ◽  
pp. 1309-1316 ◽  
Author(s):  
S. Reynolds ◽  
S. Stowers ◽  
R. Patterson ◽  
R. Maronpot ◽  
S. Aaronson ◽  
...  
Keyword(s):  
Risk Assessment ◽  
Mouse Liver ◽  
Liver Tumors ◽  
B6c3f1 Mouse

A constitutive deficiency in the monooxygenase system of spontaneous mouse liver tumors

1984 ◽  
Vol 5 (6) ◽  
pp. 785-788 ◽  
Author(s):  
Frederick F. Becker ◽  
Daniel L. Stout
Keyword(s):  
Mouse Liver ◽  
Liver Tumors ◽  
Monooxygenase System

Aldehyde dehydrogenase as a marker for chemically initiated mouse liver tumors

1986 ◽  
Vol 31 (2) ◽  
pp. 205-211 ◽  
Author(s):  
Raymond E. Richmond ◽  
Michael A. Pereira
Keyword(s):  
Aldehyde Dehydrogenase ◽  
Mouse Liver ◽  
Liver Tumors
Sign in / Sign up

Export Citation Format

Share Document