Retinoblastoma in transgenic mice

Article Abstract:

Retinoblastoma, a malignant tumor of the eye which occurs in children, is the result of an inherited defect in the Rb gene. Any mutations which inactivate or eliminate the product of both Rb genes will cause the tumor. Research in mice has now revealed that the introduction of a viral protein into mice can cause retinoblastoma. The protein, called T antigen, is a product of simian virus 40, an animal virus which causes tumors. When the gene for T antigen was injected into fertilized mouse eggs, it was possible to obtain 15 strains of mice which had been transfected, and now carry the T antigen gene among their own. These mice had tumors in a number of different tissues, but one male developed eye cancer at the age of five months. The cancer was completely heritable, and 50 percent of his offspring developed eye cancer, as would be expected from a Mendelian dominant gene. Histological examination of the tumors revealed that they were retinoblastomas. Since the development of retinoblastoma in humans involves a mutation in the Rb gene, it is not clear why the presence of T antigen or its gene should cause retinoblastoma in these mice. One intriguing possibility is that the T antigen specifically binds to and inactivates the Rb gene product, which is necessary to inhibit carcinogenesis. Binding between T antigen and the Rb gene product has been demonstrated in vitro. In the transgenic mice, the retinoblastoma cells express both the Rb gene product and T antigen; it is tempting to speculate that the inhibition of the Rb product is occurring in vivo as well, and is responsible for producing the highly characteristic retinoblastoma observed in these mice. (Consumer Summary produced by Reliance Medical Information, Inc.)

Models

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Inactivation of the p53 pathway in retinoblastoma

Article Abstract:

Earlier studies suggest that retinoblastomas that initiate with mutations in the gene retinoblastoma 1 (RB1) bypass the p53 pathway because they arise from intrinsically death-resistant cells during retinal development. It is shown, in contrast to this theory that the tumor surveillance pathway mediated by Arf, MDM2, MDMX and p53 is activated after loss of RB1 during retinogenesis providing evidence that the p53 pathway is inactivated in retinoblastoma and does not originate from intrinsically death resistant cells.

Science & research, Research, Diagnosis, Risk factors, Gene mutations, Gene mutation, Genetic aspects

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Ras signalling linked to the cell-cycle machinery by the retinoblastoma protein

Article Abstract:

The Ras proto-oncogene which is the major component needed by the cells to pass through the G1/S transition of the cell-cycle is functionally linked to retinoblastoma tumour-suppressor protein (Rb). Any disruption of Rb can cause failure of the cells to arrest in G1 following the inactivation of Ras. Rb is an important G1-specific mediator that connects Ras to cell-cycle regulation.

Analysis, Proto-oncogenes, Tumor proteins

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