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Mutational study of p16CDKN2/MTS1/INK4A and p57KIP2 genes in hepatocellular carcinoma

F Bonilla1, I Orlow, C Cordón-Cardó

  • 1Molecular Genetics Unit, Clinica del Trabajo, Avd. de la Reina Victoria, 21, Madrid, 28003, Spain.

International Journal of Oncology
|April 18, 1998
PubMed

Insights

Alterations in p16 and p57KIP2 genes are uncommon in hepatocellular carcinoma (HCC). However, microsatellite alterations in the 9p21-24 region were observed in 24% of HCC cases studied.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • p16 and p15 are key cyclin-dependent kinase inhibitors.
  • p57KIP2 exhibits selective expression in the liver.
  • p16CDKN2/MTS1/INK4A alterations are frequent in various primary tumors.

Purpose of the Study:

  • To investigate alterations in p16 and p57KIP2 genes in hepatocellular carcinoma (HCC).
  • To determine the frequency of genetic changes in these tumor suppressor genes within HCC.

Main Methods:

  • Analysis of 17 tumor and normal DNA pairs from HCC patients.
  • Utilized Southern blot, PCR-SSCP, and DNA sequencing.
  • Employed microsatellite markers for the p16 gene region (9p21-24).

Main Results:

  • Southern blot analysis revealed no allelic losses for p16 or p57KIP2.
  • An additional band was detected with p16 cDNA in 4 out of 17 cases.
  • Microsatellite alterations in the 9p21-24 region were found in 4/17 (24%) of HCC cases.

Conclusions:

  • Deletions or point mutations in p16 and p57KIP2 are infrequent in HCC.
  • The study identified microsatellite alterations in the 9p21-24 region in a subset of HCC.
  • Further research may clarify the role of these microsatellite alterations in HCC pathogenesis.

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