p53: A Frequent Target for Genetic Abnormalities in Lung Cancer

DOI Web Site 被引用文献64件
  • Takashi Takahashi
    National Cancer Institute-Navy Medical Oncology Branch, and Uniformed Services University of the Health Sciences, Bethesda, MD 20814.
  • Marion M. Nau
    National Cancer Institute-Navy Medical Oncology Branch, and Uniformed Services University of the Health Sciences, Bethesda, MD 20814.
  • Itsuo Chiba
    National Cancer Institute-Navy Medical Oncology Branch, and Uniformed Services University of the Health Sciences, Bethesda, MD 20814.
  • Michael J. Birrer
    National Cancer Institute-Navy Medical Oncology Branch, and Uniformed Services University of the Health Sciences, Bethesda, MD 20814.
  • Richard K. Rosenberg
    National Cancer Institute-Navy Medical Oncology Branch, and Uniformed Services University of the Health Sciences, Bethesda, MD 20814.
  • Michelle Vinocour
    National Cancer Institute-Navy Medical Oncology Branch, and Uniformed Services University of the Health Sciences, Bethesda, MD 20814.
  • Mark Levitt
    Division of Medical Oncology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15240.
  • Harvey Pass
    Surgery Branch, National Cancer Institute, Bethesda, MD 20814.
  • Adi F. Gazdar
    National Cancer Institute-Navy Medical Oncology Branch, and Uniformed Services University of the Health Sciences, Bethesda, MD 20814.
  • John D. Minna
    National Cancer Institute-Navy Medical Oncology Branch, and Uniformed Services University of the Health Sciences, Bethesda, MD 20814.

抄録

<jats:p>Allele loss is a hallmark of chromosome regions harboring recessive oncogenes. Lung cancer frequently demonstrates loss of heterozygosity on 17p. Recent evidence suggests that the p53 gene located on 17p13 has many features of such an antioncogene. The p53 gene was frequently mutated or inactivated in all types of human lung cancer. The genetic abnormalities of p53 include gross changes such as homozygous deletions and abnormally sized messenger RNAs along with a variety of point or small mutations, which map to the p53 open reading frame and change amino acid sequence in a region highly conserved between mouse and man. In addition, very low or absent expression of p53 messenger RNA in lung cancer cell lines compared to normal lung was seen. These findings, coupled with the previous demonstration of 17p allele loss in lung cancer, strongly implicate p53 as an anti-oncogene whose disruption is involved in the pathogenesis of human lung cancer.</jats:p>

収録刊行物

  • Science

    Science 246 (4929), 491-494, 1989-10-27

    American Association for the Advancement of Science (AAAS)

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