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Comparative mutational analysis of DPC4 (Smad4) in prostatic and colorectal carcinomas.

Authors
  • MacGrogan, D
  • Pegram, M
  • Slamon, D
  • Bookstein, R
Type
Published Article
Journal
Oncogene
Publisher
Springer Nature
Publication Date
Aug 28, 1997
Volume
15
Issue
9
Pages
1111–1114
Identifiers
PMID: 9285566
Source
Medline
License
Unknown

Abstract

Allelic deletions of chromosome 18q are reported to be common in prostate and colorectal cancers, suggesting that one or more tumor suppressor genes on 18q are involved in the genesis of these neoplasms. The DPC4 gene, a recently identified candidate tumor suppressor in 18q21, was examined for evidence of inactivation in prostatic carcinomas, and results compared to those of a parallel analysis of colorectal carcinomas, for which DPC4 mutation has been reported in approximately 10% of cases. In this study, only three (10%) of 29 informative primary prostate cancers showed allelic loss of chromosome 18q21 markers, and no point mutations or deletions of DPC4 were detected in the complete set of 45 primary or metastatic cases. In contrast, five (56%) of nine primary colorectal tumors displayed allelic loss of 18q markers and in one of these a somatically acquired G-->T missense mutation was found in exon 1. Of twelve colorectal tumor cell lines, one showed a G-->C missense mutation in exon 8 and two had partial homozygous deletions that would likely abrogate gene function. These data suggest that DPC4 is rarely if ever mutated during prostatic oncogenesis, whereas inactivation of this gene may contribute to the genesis of a subset of colorectal carcinomas.

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