Human retinoblastoma susceptibility gene.
It is clear that the RB-deficient tumor cells lost their tumorigenicity in nude mice after regaining the RB gene expression. However, the mechanism of tumor suppression by the RB gene is still unknown. More studies on the biological activities of RB protein, pp110RB, are necessary to answer this question. Recent studies have shown that several oncogenic viral proteins, such as SV40 large T antigen (47) and adenoviral E1A protein (48), bind to RB protein. The significance of these bindings remains unclear; nevertheless, they suggest that depletion of functional RB protein by viral proteins may provide another mechanism of RB inactivation. Continued study of naturally occurring as well as engineered RB mutants may give us some information on the biological activity of RB protein, and its roles in oncogenesis, differentiation, development and gene regulation. Additionally, direct detection of RB gene mutations would have great clinical utility. Probes for the RB gene and gene product will be useful for genetic diagnosis of cancer susceptibility in affected families. Therefore, antibodies to the RB protein will be excellent tools for diagnostic and/or prognostic application in clinical medicine.
Department of Pathology, University of California, San Diego, La Jolla 92093.
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D000818:Animals; D001483:Base Sequence; D002874:Chromosome Mapping; D002882:Chromosomes, Human, Pair 13; D004198:Disease Susceptibility; D016147:Genes, Tumor Suppressor; D006801:Humans; D051379:Mice; D009154:Mutation; D012175:Retinoblastoma / Q000235:genetics*; D016160:Retinoblastoma Protein / Q000235:genetics
D016160:Retinoblastoma Protein