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A Three-Dimensional Spheroid Model to Investigate the Tumor-Stromal Interaction in Hepatocellular Carcinoma

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Adventures in hepatocarcinogenesis.

Henry C Pitot¹

¹McArdle Laboratory for Cancer Research, Department of Oncology and Pathology, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA. pitot@oncology.wisc.edu

Annual Review of Pathology

|November 28, 2007

Summary

Neoplasia, or abnormal tissue growth, progresses through initiation, promotion, and progression stages in liver cancer. These stages involve genetic and epigenetic alterations driving cell replication and genomic instability.

Area of Science:

Hepatocarcinogenesis research
Cancer biology
Molecular oncology

Background:

Neoplasia is defined as heritably altered, autonomous tissue growth.
Hepatocarcinogenesis, or liver cancer development, is modeled in rats.
This process involves three distinct stages: initiation, promotion, and progression.

Purpose of the Study:

To describe the quantifiable stages of hepatocarcinogenesis.
To elucidate the molecular mechanisms driving each stage.
To understand the transition from promotion to progression.

Main Methods:

Utilizing a rat model for hepatocarcinogenesis.
Analyzing genetic and epigenetic alterations.
Quantifying cellular replication and apoptosis.

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Main Results:

Initiation involves irreversible mutations and/or epigenetic changes.
Promotion enhances initiated cell replication and inhibits apoptosis.
Progression is characterized by karyotypic alterations and genomic instability.

Conclusions:

Hepatocarcinogenesis progresses through distinct, quantifiable stages.
Genetic and epigenetic alterations are key drivers throughout the process.
The transition to progression may be driven by epigenetic mechanisms acting on alterations fixed during promotion.