Expression of the RB gene under the control of MuLV-LTR suppresses tumorigenicity of WERI-Rb-27 retinoblastoma cells in immunodefective mice.
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.
Sumegi
J
J
Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.
Uzvolgyi
E
E
Klein
G
G
D000818:Animals; D005134:Eye Neoplasms / Q000235:genetics / Q000473:pathology*; D015972:Gene Expression Regulation, Neoplastic; D005814:Genes, Viral; D006801:Humans; D007153:Immunologic Deficiency Syndromes / Q000150:complications*; D009052:Leukemia Virus, Murine / Q000235:genetics; D051379:Mice; D008815:Mice, Inbred Strains; D009368:Neoplasm Transplantation; D010641:Phenotype; D011993:Recombinant Fusion Proteins / Q000096:biosynthesis / Q000502:physiology*; D012091:Repetitive Sequences, Nucleic Acid; D012175:Retinoblastoma / Q000235:genetics / Q000473:pathology*; D016160:Retinoblastoma Protein / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D014407:Tumor Cells, Cultured / Q000378:metabolism / Q000473:pathology / Q000637:transplantation
D011993:Recombinant Fusion Proteins; D016160:Retinoblastoma Protein