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Related Experiment Video

Updated: Jun 27, 2026

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis

Published on: September 12, 2019

Experimental agents which inhibit hepatocarcinogenesis.

Jung-Hwan Yoon¹, Hyo-Suk Lee

¹Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul, Korea. yoonjh@snu.ac.kr

|December 19, 2008

Summary

This summary is machine-generated.

Hepatocellular carcinoma (HCC) therapies targeting blood vessel growth show limited success. Blocking these signals alongside hypoxia-induced pathways may improve treatment effectiveness for liver cancer.

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An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis

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Generation of Subcutaneous and Intrahepatic Human Hepatocellular Carcinoma Xenografts in Immunodeficient Mice

Generation of Subcutaneous and Intrahepatic Human Hepatocellular Carcinoma Xenografts in Immunodeficient Mice

Published on: September 25, 2013

Area of Science:

Oncology
Vascular Biology
Cancer Therapeutics

Background:

Hepatocellular carcinoma (HCC) is highly vascular, leading to investigation of antiangiogenic therapies.
Current antiangiogenic therapies for HCC have limited therapeutic efficacy.
Tumor hypoxia resulting from angiogenesis inhibition can activate pro-survival signals, potentially driving HCC progression.

Purpose of the Study:

To explore the potential of simultaneously blocking angiogenesis and hypoxia-induced signaling pathways in HCC.
To present experimental agents targeting these critical HCC survival signals.

Main Methods:

Review of experimental agents and their mechanisms of action.
Analysis of signaling pathways involved in HCC angiogenesis and hypoxia response.

Main Results:

Limited efficacy of solely antiangiogenic therapies in HCC.
Identification of hypoxia-induced pathways that counteract antiangiogenic effects.
Potential for combination therapies targeting both angiogenesis and hypoxia-induced signals.

Conclusions:

Simultaneous blockade of angiogenesis and hypoxia-induced signals is crucial for enhancing HCC treatment efficacy.
Experimental agents targeting these dual pathways offer a promising therapeutic strategy for liver cancer.