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

doi:10.1038/6488

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 journal › Article › peer-review

50 Scopus citations

Abstract

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 language	English (US)
Pages (from-to)	275-279
Number of pages	5
Journal	Nature medicine
Volume	5
Issue number	3
DOIs	https://doi.org/10.1038/6488
State	Published - 1999
Externally published	Yes

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology

Access to Document

10.1038/6488

Cite this

@article{b0769c9948e34dfb8f0576b533e9140f,

title = "Modulation of oncogenic potential by alternative gene use in human prostate cancer",

abstract = "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.",

author = "Kadkol, {Shrihari S.} and Brody, {Jonathan R.} and Jonathan Pevsner and Jining Bai and Pasternack, {Gary R.}",

note = "Funding Information: Acknowledgments We thank D. Coffey, C.V. Dang, T.J. Kelly Jr., S. Kern, A. Owens Jr., D. Pardoll, H. Shin and S. Sisodia for reading the manuscript, G.S. Bova for providing the paired tissue samples from human prostate cancer patients, and R. Ashworth of The Johns Hopkins DNA Analysis Facility for automated sequencing. This work was supported by USPHS Grant RO1 CA 54404. In accordance with institutional policies, we wish to disclose the following information. G.R.P. is an inventor on US Patents 5756676, 5734022, and 5726018, which encompass the antecedent and present technology described in this manuscript. G.R.P., S.S.K. and J.R.B. are inventors on a pending US Patent application related to the present technology. There is no current licensee or other financial interest for the aforementioned technology.",

year = "1999",

doi = "10.1038/6488",

language = "English (US)",

volume = "5",

pages = "275--279",

journal = "Nature medicine",

issn = "1078-8956",

publisher = "Nature Publishing Group",

number = "3",

}

TY - JOUR

T1 - Modulation of oncogenic potential by alternative gene use in human prostate cancer

AU - Kadkol, Shrihari S.

AU - Brody, Jonathan R.

AU - Pevsner, Jonathan

AU - Bai, Jining

AU - Pasternack, Gary R.

N1 - Funding Information: Acknowledgments We thank D. Coffey, C.V. Dang, T.J. Kelly Jr., S. Kern, A. Owens Jr., D. Pardoll, H. Shin and S. Sisodia for reading the manuscript, G.S. Bova for providing the paired tissue samples from human prostate cancer patients, and R. Ashworth of The Johns Hopkins DNA Analysis Facility for automated sequencing. This work was supported by USPHS Grant RO1 CA 54404. In accordance with institutional policies, we wish to disclose the following information. G.R.P. is an inventor on US Patents 5756676, 5734022, and 5726018, which encompass the antecedent and present technology described in this manuscript. G.R.P., S.S.K. and J.R.B. are inventors on a pending US Patent application related to the present technology. There is no current licensee or other financial interest for the aforementioned technology.

PY - 1999

Y1 - 1999

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0033054167&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033054167&partnerID=8YFLogxK

U2 - 10.1038/6488

DO - 10.1038/6488

M3 - Article

C2 - 10086381

AN - SCOPUS:0033054167

SN - 1078-8956

VL - 5

SP - 275

EP - 279

JO - Nature medicine

JF - Nature medicine

IS - 3

ER -

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

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this