Modulation of oncogenic potential by alternative gene use in human prostate cancer

Shrihari S. Kadkol, Jonathan R. Brody, Jonathan Pevsner, Jining Bai, Gary R. Pasternack

Research output: Contribution to journalArticlepeer-review

50 Scopus citations


Only a small percentage of primary prostate cancers have genetic changes. In contrast, nearly 90% of clinically significant human prostate cancers seems to express high levels of the nuclear phosphoprotein pp32 by in situ hybridization. Because pp32 inhibits oncogene-mediated transformation, we investigated its paradoxical expression in cancer by comparing the sequence and function of pp32 species from paired benign prostate tissue and adjacent prostatic carcinoma from three patients. Here we demonstrate that pp32 is expressed in benign prostatic tissue, but pp32r1 and pp32r2, closely- related genes located on different chromosomes, are expressed in prostate cancer. Although pp32 is a tumor suppressor, pp32r1 and pp32r2 are tumorigenic. Alternative use of the pp32, pp32r1 and pp32r2 genes may modulate the oncogenic potential of human prostate cancer.

Original languageEnglish (US)
Pages (from-to)275-279
Number of pages5
JournalNature medicine
Issue number3
StatePublished - 1999
Externally publishedYes

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology


Dive into the research topics of 'Modulation of oncogenic potential by alternative gene use in human prostate cancer'. Together they form a unique fingerprint.

Cite this