Frequent inactivation of the retinoblastoma anti-oncogene is restricted to a subset of human tumor cells

Jonathan M. Horowitz, Sang Ho Park, Emil Bogenmann, Jeng Chung Cheng, David W. Yandell, Frederick J. Kaye, John D. Minna, Thaddeus P. Dryja, Robert A. Weinberg

Research output: Contribution to journalArticle

472 Scopus citations

Abstract

We have used polyclonal anti-synthetic peptide serum to study the role of retinoblastoma gene (RB) inactivation in a variety of human tumor cell lines. Our analysis indicates that inactivation of the RB protein, p105-Rb, is universal in retinoblastoma cells, vindicating the predictions of the Knudson 'two-hit' hypothesis. In addition, our analysis has shown that inactivations of the RB gene are nearly as frequent in a more common human tumor, small cell lung carcinoma. One-third of bladder carcinomas surveyed also carry altered or absent p105-Rb. Other human tumors by contrast demonstrate only infrequent inactivation of the RB gene. These results suggest that inactivation of the RB gene is a critical step in the pathogenesis of a subset of human tumors.

Original languageEnglish (US)
Pages (from-to)2775-2779
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume87
Issue number7
DOIs
StatePublished - 1990

Keywords

  • recessive oncogene
  • retinoblastoma protein
  • splicing

ASJC Scopus subject areas

  • General

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