Introduction of a normal retinoblastoma (Rb) gene into Rb-deficient lymphoblastoid cells delays tumorigenicity in immunodefective mice

• Published in: Leukemia research 1998-10, Vol.22 (10), p.905-912
• Main Authors: Lefebvre, Donatienne, Gala, Jean-Luc, Heusterspreute, Michel, Delhez, Huguette, Philippe, Marianne
• Format: Article
• Language: English
• Subjects: Animal tumors. Experimental tumors; Animals; B-Lymphocytes; Biological and medical sciences; DNA, Neoplasm - genetics; Experimental tumors, general aspects; Gene therapy; Genes, Retinoblastoma; Genetic Therapy; Humans; IM9 cells; Medical sciences; Mice; Mice, SCID; Multiple Myeloma - immunology; Phenotype; Polymerase Chain Reaction - methods; Retinoblastoma gene; RNA, Neoplasm - genetics; SCID mice; Severe Combined Immunodeficiency - genetics; Severe Combined Immunodeficiency - therapy; Time Factors; Transfection; Tumor Cells, Cultured; Tumor-suppressor gene; Tumorigenicity; Tumors
• ISSN: 0145-2126; 1873-5835
• DOI: 10.1016/S0145-2126(98)00079-4

Inactivation of the Rb susceptibility gene occurs in various human cancers and has been associated with tumorigenicity. Rb gene is inactivated in 30% of acute leukaemias. The effect of Rb protein expression was assessed in the lymphoblastoid cell line IM-9 defective for Rb protein, after stable transfection with a wild-type Rb gene. The Rb transgene was under the control of the MoMuLv-LTR. Protein expression by the transduced cells was confirmed by Western blot and flow cytometry analyses. Compared to the parental cell line, growth rate remained unchanged in the Rb transfected clones. In SCID mice however, tumor formation originating from these clones was delayed. The current data suggest therefore that, in this Rb-defective haematopoietic cell line, Rb expression correlates with reduced tumorigenicity but not with reduced growth rate.