Expression of the RB gene under the control of MuLV-LTR suppresses tumorigenicity of WERI-Rb-27 retinoblastoma cells in immunodefective mice.

J. Sumegi; E. Uzvolgyi; G. Klein

Expression of the RB gene under the control of MuLV-LTR suppresses tumorigenicity of WERI-Rb-27 retinoblastoma cells in immunodefective mice.

J. Sumegi, E. Uzvolgyi, G. Klein

Research output: Contribution to journal › Article › peer-review

Abstract

Retinoblastomas arise by the loss of the retinoblastoma (RB) gene. The isolation of the RB gene and its expression in RB protein defective tumor cells permits direct tests of the ability of the protein to act as a tumor suppressor. We demonstrate that a functional RB gene introduced into WERI-Rb-27 retinoblastoma cells by retrovirally mediated gene transfer can suppress their tumorigenicity in immunodefective mice.

Original language	English (US)
Pages (from-to)	247-250
Number of pages	4
Journal	Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research
Volume	1
Issue number	5
State	Published - May 1990
Externally published	Yes

ASJC Scopus subject areas

Molecular Biology
Cell Biology

Cite this

Expression of the RB gene under the control of MuLV-LTR suppresses tumorigenicity of WERI-Rb-27 retinoblastoma cells in immunodefective mice. / Sumegi, J.; Uzvolgyi, E.; Klein, G.

In: Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research, Vol. 1, No. 5, 05.1990, p. 247-250.

Research output: Contribution to journal › Article › peer-review

@article{9856996341f04eb1a368dc97d7095e47,

title = "Expression of the RB gene under the control of MuLV-LTR suppresses tumorigenicity of WERI-Rb-27 retinoblastoma cells in immunodefective mice.",

abstract = "Retinoblastomas arise by the loss of the retinoblastoma (RB) gene. The isolation of the RB gene and its expression in RB protein defective tumor cells permits direct tests of the ability of the protein to act as a tumor suppressor. We demonstrate that a functional RB gene introduced into WERI-Rb-27 retinoblastoma cells by retrovirally mediated gene transfer can suppress their tumorigenicity in immunodefective mice.",

author = "J. Sumegi and E. Uzvolgyi and G. Klein",

year = "1990",

month = may,

language = "English (US)",

volume = "1",

pages = "247--250",

journal = "Cell Growth and Differentiation",

issn = "1541-7786",

publisher = "American Association for Cancer Research Inc.",

number = "5",

}

TY - JOUR

T1 - Expression of the RB gene under the control of MuLV-LTR suppresses tumorigenicity of WERI-Rb-27 retinoblastoma cells in immunodefective mice.

AU - Sumegi, J.

AU - Uzvolgyi, E.

AU - Klein, G.

PY - 1990/5

Y1 - 1990/5

N2 - Retinoblastomas arise by the loss of the retinoblastoma (RB) gene. The isolation of the RB gene and its expression in RB protein defective tumor cells permits direct tests of the ability of the protein to act as a tumor suppressor. We demonstrate that a functional RB gene introduced into WERI-Rb-27 retinoblastoma cells by retrovirally mediated gene transfer can suppress their tumorigenicity in immunodefective mice.

AB - Retinoblastomas arise by the loss of the retinoblastoma (RB) gene. The isolation of the RB gene and its expression in RB protein defective tumor cells permits direct tests of the ability of the protein to act as a tumor suppressor. We demonstrate that a functional RB gene introduced into WERI-Rb-27 retinoblastoma cells by retrovirally mediated gene transfer can suppress their tumorigenicity in immunodefective mice.

UR - http://www.scopus.com/inward/record.url?scp=0025431208&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025431208&partnerID=8YFLogxK

M3 - Article

C2 - 1964797

AN - SCOPUS:0025431208

SN - 1541-7786

VL - 1

SP - 247

EP - 250

JO - Cell Growth and Differentiation

JF - Cell Growth and Differentiation

IS - 5

ER -

Expression of the RB gene under the control of MuLV-LTR suppresses tumorigenicity of WERI-Rb-27 retinoblastoma cells in immunodefective mice.

Abstract

ASJC Scopus subject areas

Other files and links

Fingerprint

Cite this