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Oncogene activation and hepatocarcinogenesis.

S C Strom1, J B Faust

  • 1Department of Pathology, Medical College of Virginia, Virginia Commonwealth University, Richmond.

Pathobiology : Journal of Immunopathology, Molecular and Cellular Biology
|January 1, 1990
PubMed
Summary
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Oncogenes like c-myc are consistently found in rodent liver tumors, unlike ras family genes. Cell transformation by oncogenes leads to growth factor independence and decreased growth factor receptor expression in liver cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Hepatocarcinogenesis

Background:

  • Dominant-transforming oncogenes are common in mouse liver tumors but not consistently in rat liver tumors.
  • Ras family oncogenes are frequently identified, but c-myc gene expression increases in both rat and mouse hepatocellular tumors.

Purpose of the Study:

  • To investigate the role of oncogenes in liver tumor development in rodents.
  • To understand the cellular and molecular changes associated with oncogene-induced liver cancer.

Main Methods:

  • Immortalization and transformation of hepatocytes and liver epithelial cells using viral or cellular oncogenes.
  • Analysis of gene expression patterns, including oncogenes and growth factor receptors, in transformed cells and tumors.

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Main Results:

  • Oncogene-induced cell transformation results in growth factor independence or reduced requirements.
  • Transformation is linked to a significant decrease in exogenous growth factor receptor expression in hepatocellular tumors.
  • Increased c-myc expression is a consistent finding in both rat and mouse liver tumors.

Conclusions:

  • c-myc upregulation is a common event in rodent liver carcinogenesis.
  • Oncogene transformation alters cellular behavior, promoting uncontrolled growth and affecting growth factor signaling pathways relevant to liver cancer.