Chromosome 17 Deletions and p53 Gene Mutations in Colorectal Carcinomas

DOI Web Site 被引用文献87件
  • Suzanne J. Baker
    Oncology Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21231.
  • Eric R. Fearon
    Oncology Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21231.
  • Janice M. Nigro
    Oncology Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21231.
  • Stanley R. Hamilton
    Department of Pathology and the Oncology Center, The Johns Hopkins Medical Institutions, Baltimore, MD 21205.
  • Ann C. Preisinger
    Oncology Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21231.
  • J. Milburn Jessup
    Department of Surgery, M. D. Anderson Hospital, Houston, TX 77030.
  • Peter vanTuinen
    Institute for Molecular Genetics, Baylor College of Medicine, Houston, TX 77030.
  • David H. Ledbetter
    Institute for Molecular Genetics, Baylor College of Medicine, Houston, TX 77030.
  • David F. Barker
    Department of Medical Informatics, University of Utah Medical Center, Salt Lake City, UT 84108.
  • Yusuke Nakamura
    Department of Human Genetics and Howard Hughes Medical Institute, University of Utah Medical Center, Salt Lake City, UT 84132.
  • Ray White
    Department of Human Genetics and Howard Hughes Medical Institute, University of Utah Medical Center, Salt Lake City, UT 84132.
  • Bert Vogelstein
    Oncology Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21231.

抄録

<jats:p>Previous studies have demonstrated that allelic deletions of the short arm of chromosome 17 occur in over 75% of colorectal carcinomas. Twenty chromosome 17p markers were used to localize the common region of deletion in these tumors to a region contained within bands 17p12 to 17p13.3. This region contains the gene for the transformation-associated protein p53. Southern and Northern blot hybridization experiments provided no evidence for gross alterations of the p53 gene or surrounding sequences. As a more rigorous test of the possibility that p53 was a target of the deletions, the p53 coding regions from two tumors were analyzed; these two tumors, like most colorectal carcinomas, had allelic deletions of chromosome 17p and expressed considerable amounts of p53 messenger RNA from the remaining allele. The remaining p53 allele was mutated in both tumors, with an alanine substituted for valine at codon 143 of one tumor and a histidine substituted for arginine at codon 175 of the second tumor. Both mutations occurred in a highly conserved region of the p53 gene that was previously found to be mutated in murine p53 oncogenes. The data suggest that p53 gene mutations may be involved in colorectal neoplasia, perhaps through inactivation of a tumor suppressor function of the wild-type p53 gene.</jats:p>

収録刊行物

  • Science

    Science 244 (4901), 217-221, 1989-04-14

    American Association for the Advancement of Science (AAAS)

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