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Infrequent CDKN2 mutation in human differentiated thyroid cancers

W S Tung1, D W Shevlin, D Bartsch

  • 1Department of Surgery, Washington University School of Medicine, St. Louis, Missouri, USA.

Molecular Carcinogenesis
|January 1, 1996
PubMed
Summary
This summary is machine-generated.

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Alterations in the CDKN2 gene, a cell-cycle regulator, were investigated in thyroid cancers. CDKN2 gene alterations were found in a small subset of thyroid tumors, suggesting a role in specific cancer types.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The cyclin-dependent kinase inhibitor 2 (CDKN2) gene encodes the p16 cell-cycle regulator.
  • CDKN2 alterations (mutations, deletions) are observed in various tumor cell lines.
  • Its role in primary thyroid tumor development remains unclear.

Purpose of the Study:

  • To investigate the frequency of CDKN2 alterations in differentiated and anaplastic thyroid cancers.
  • To assess the involvement of CDKN2 in thyroid cancer genesis.

Main Methods:

  • Analysis of tumor and normal DNA from 35 thyroid carcinomas (papillary, follicular, anaplastic).
  • Screening of the CDKN2 coding region using single-strand conformational variant analysis and direct sequencing.
  • Evaluation of homozygous deletions via multiplex polymerase chain reaction (PCR).

Related Experiment Videos

  • Assessment of loss of heterozygosity (LOH) using polymorphic markers.

    • Main Results:

    • Two somatic missense mutations in CDKN2 were identified (one follicular, one anaplastic).
    • Homozygous or hemizygous deletions were suggested in five anaplastic tumors.
    • Loss of heterozygosity (LOH) in the 9p region (near CDKN2) was observed in 27% of follicular and 50% of anaplastic thyroid cancers.
    • No CDKN2 alterations were noted in papillary thyroid cancers.

    Conclusions:

    • CDKN2 alterations play a role in a minority of thyroid cancers.
    • LOH in the CDKN2 region is frequent in follicular and anaplastic thyroid cancers, but not papillary.
    • Loss of 9p sequences suggests a tumor suppressor gene's involvement in follicular and anaplastic thyroid cancer development.