Loss of p53 Expression in Myc-induced B Lineage Tumors
Transgenic mice carrying an activated oncogene have been used extensively to investigate the mutational requirements for tumorigenesis. Transgenic mice carrying the c-myc gene under the control of the Immunoglobulin heavy chain enhancer express the transgene exclusively in lymphoid tissues (Adams et al 1985; Harris et al 1988; Schmidt et al 1988; Scheuermann and Bauer 1990). At an early age these mice develop normally with only small effects on the normal lymphoid compartments. Invariably the mice develop lymphoid tumors after a latent period of about 10 weeks. The tumors are clonal, that is they derive from a single precursor cell, as judged by the rearrangement status of the antigen receptor genes. The fact that the tumors which arise in these mice are clonal and develop after a certain latent period suggests that inappropriate expression of c-myc is not sufficient for tumorigenesis, and that additional events, probably mutational, are necessary for transformation. Thus, these transgenic mice provide an excellent model system for the identification of genes which collaborate with activated myc in lymphoid tumorigenesis.
KeywordsTransgenic Mouse Lineage Tumor Endogenous mRNA Antigen Receptor Gene preB Cell
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- Scheuermann RH, Bauer SR (1992) PCR-based mRNA quantification using an internal standard: A method for the analysis of oncogene expression. Methods Enzymol. in press.Google Scholar