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Involvement of mutations in the DPC4 promoter in endometrial carcinoma development

Y Zhou1, H Kato, D Shan

  • 1Department of Reproductive Physiology and Endocrinology, Medical Institute of Bioregulation, Kyushu Univeristy, Beppu, Oita, Japan.

Molecular Carcinogenesis
|May 20, 1999
PubMed

Insights

Loss of heterozygosity on chromosome 18q is common in endometrial cancer. Researchers found that deletions in the 18q21.1 region, affecting the DPC4 gene, disrupt its transcription, suggesting DPC4

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Endometrial carcinomas frequently exhibit loss of heterozygosity on chromosome 18q.
  • Identifying the specific gene targeted by these deletions is crucial for understanding endometrial cancer development.

Purpose of the Study:

  • To map deletions on chromosome 18q in endometrial tumors.
  • To investigate the role of the DPC4 gene in endometrial carcinogenesis.

Main Methods:

  • Deletion mapping of chromosome 18q in 64 endometrial tumors.
  • Analysis of DPC4 gene transcription and coding region sequences.
  • DPC4 promoter analysis using chloramphenicol acetyltransferase assays.

Main Results:

  • Loss of heterozygosity at 18q was observed in 20 tumors, with 14 showing deletions at 18q21.1, the location of the DPC4 gene.
  • DPC4 transcription was disturbed in all examined tumors with 18q21.1 deletions.
  • Mutations in the DPC4 promoter, not the coding region, were identified in tumors with silenced DPC4 transcription.

Conclusions:

  • The DPC4 gene is implicated in endometrial carcinoma development.
  • Disturbed DPC4 transcription, potentially due to promoter mutations, contributes to endometrial tumorigenesis.

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