• Register
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.


Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.


Suppression of human colorectal carcinoma cell growth by wild-type p53.

Mutations of the p53 gene occur commonly in colorectal carcinomas and the wild-type p53 allele is often concomitantly deleted. These findings suggest that the wild-type gene may act as a suppressor of colorectal carcinoma cell growth. To test this hypothesis, wild-type or mutant human p53 genes were transfected into human colorectal carcinoma cell lines. Cells transfected with the wild-type gene formed colonies five- to tenfold less efficiently than those transfected with a mutant p53 gene. In those colonies that did form after wild-type gene transfection, the p53 sequences were found to be deleted or rearranged, or both, and no exogenous p53 messenger RNA expression was observed. In contrast, transfection with the wild-type gene had no apparent effect on the growth of epithelial cells derived from a benign colorectal tumor that had only wild-type p53 alleles. Immunocytochemical techniques demonstrated that carcinoma cells expressing the wild-type gene did not progress through the cell cycle, as evidenced by their failure to incorporate thymidine into DNA. These studies show that the wild-type gene can specifically suppress the growth of human colorectal carcinoma cells in vitro and that an in vivo-derived mutation resulting in a single conservative amino acid substitution in the p53 gene product abrogates this suppressive ability.

Pubmed ID: 2144057


  • Baker SJ
  • Markowitz S
  • Fearon ER
  • Willson JK
  • Vogelstein B


Science (New York, N.Y.)

Publication Data

August 24, 1990

Associated Grants

  • Agency: NCI NIH HHS, Id: CA 43703
  • Agency: NIGMS NIH HHS, Id: GM 07184
  • Agency: NIGMS NIH HHS, Id: GM 07309

Mesh Terms

  • Cell Division
  • Cell Line
  • Colonic Neoplasms
  • DNA Replication
  • Humans
  • Nuclear Proteins
  • Oncogene Proteins
  • Phosphoproteins
  • Plasmids
  • RNA, Messenger
  • Rectal Neoplasms
  • Transfection
  • Tumor Cells, Cultured
  • Tumor Suppressor Protein p53