Hepatic toxicity and compensatory hyperplasia in a rat model of aflatoxin bi-induced liver cancer

1996 ◽  
Author(s):  
Yulia Y. Maxuitenko
2020 ◽  
Vol 11 (24) ◽  
pp. 7302-7311
Author(s):  
Yang Cheng ◽  
Tianyang Chen ◽  
Jianjie Chen

Scanning ◽  
2012 ◽  
Vol 34 (4) ◽  
pp. 271-277 ◽  
Author(s):  
Jun Yan ◽  
Shuangmu Zhuo ◽  
Gang Chen ◽  
Changjun Tan ◽  
Weifeng Zhu ◽  
...  

2016 ◽  
Vol 218 ◽  
pp. 312-317 ◽  
Author(s):  
Masakazu Saitoh ◽  
Michiyoshi Hatanaka ◽  
Masaaki Konishi ◽  
Junichi Ishida ◽  
Sandra Palus ◽  
...  

2001 ◽  
Vol 39 (1) ◽  
pp. 96-101 ◽  
Author(s):  
Seishiro Watanabe ◽  
Yukihiro Kitade ◽  
Tsutomu Masaki ◽  
Mikio Nishioka ◽  
Kimihiko Satoh ◽  
...  
Keyword(s):  

2018 ◽  
Vol 14 (14) ◽  
pp. 2037-2050 ◽  
Author(s):  
Yanfeng Gao ◽  
Shuang Zhou ◽  
Fengfei Wang ◽  
Yue Zhou ◽  
Sen Sheng ◽  
...  

2012 ◽  
Vol 23 (12) ◽  
pp. 1685-1691 ◽  
Author(s):  
Manon Buijs ◽  
Jean-Francois H. Geschwind ◽  
Labiq H. Syed ◽  
Shanmugasundaram Ganapathy-Kanniappan ◽  
Rani Kunjithapatham ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Jinhua Wen ◽  
Menghua Zhao

Background. Sorafenib is an anticancer drug used in the treatment of unresectable hepatocellular carcinoma and advanced renal cell carcinoma. It is a substrate for the human OATP1B1. This study is aimed at assessing the role of OATP1B1 in transportation and uptake of sorafenib in hepatocellular carcinoma and how OATP1B1 affects the pharmacodynamics of sorafenib in vitro and in vivo. Methods. Sorafenib transport was measured in HepG2, HepG2-OATP1B1 ∗ 1a, HepG2-OATP1B1 ∗ 1b, HepG2-OATP1B1 ∗ 15, LO2, LO2-OATP1B1 ∗ 1a, LO2-OATP1B1 ∗ 1b, and LO2-OATP1B1 ∗ 15 cells, as well as in HepG2 cells transfected with miR-148a mimics. The viability and apoptosis rate of cells treated with sorafenib were evaluated. A liver cancer rat model was established to explore the pharmacokinetics and pharmacodynamics of sorafenib after overexpression of Oatp2. Results. Changes in expression and genetic mutations of OATP1B1 significantly affected the uptake of sorafenib in HepG2 and LO2 transgenic cells, and the uptake of sorafenib was higher in HepG2 than LO2. Genetic mutations of OATP1B1 significantly affected the cell viability and apoptosis rate of HepG2 cells after sorafenib treatment. Compared to control group, the uptake of sorafenib in miR-148a mimic-transfected HepG2 cells was decreased, and the cell viability was increased. PCN significantly increased the expression of Oatp2 and affected the pharmacokinetics of sorafenib. Vascular endothelial growth factor levels and microvascular density in tumor-adjacent tissues decreased significantly, suggesting that increased Oatp2 expression improves the treatment effect of sorafenib in a rat model of liver cancer. Conclusions. OATP1B1 plays an important role in the pharmacokinetics and pharmacodynamics of sorafenib in hepatocellular carcinoma.


Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3721
Author(s):  
Semon Wu ◽  
I-Chieh Tseng ◽  
Wen-Cheng Huang ◽  
Cheng-Wen Su ◽  
Yu-Heng Lai ◽  
...  

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer mortality. Cancer stem cells (CSCs) are responsible for the maintenance, metastasis, and relapse of various tumors. The effects of CSCs on the tumorigenesis of HCC are still not fully understood, however. We have recently established two new rat HCC cell lines HTC and TW-1, which we isolated from diethylnitrosamine-induced rat liver cancer. Results showed that TW-1 expressed the genetic markers of CSCs, including CD133, GSTP1, CD44, CD90, and EpCAM. Moreover, TW-1 showed higher tolerance to sorafenib than HTC did. In addition, tumorigenesis and metastasis were observed in nude mice and wild-type rats with TW-1 xenografts. Finally, we combined highly expressed genes in TW-1/HTC with well-known biomarkers from recent HCC studies to predict HCC-related biomarkers and able to identify HCC with AUCs > 0.9 after machine learning. These results indicated that TW-1 was a novel rat CSC line, and the mice or rat models we established with TW-1 has great potential on HCC studies in the future.


1987 ◽  
Vol 22 (2) ◽  
pp. 149-152 ◽  
Author(s):  
SANJAY SAINI ◽  
DAVID D. STARK ◽  
JACK WITTENBERG ◽  
LUIS-GASTON VICI ◽  
ALAN S. BROWN ◽  
...  

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