Peripheral neuropathies, hepatocellular carcinomas and islet cell adenomas in transgenic mice

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Abstract
The ability to introduce foreign DNA into the genome of mice offers unique opportunities to produce new models of disease processes. Recent experiments have shown that integration and expression of simian virus 40 (SV40) T antigen genes1 and the murine mammary tumour virus (MMTV)–myc genes2 in transgenic mice can lead to the development of neoplasia in a remarkably tissue-specific manner. In the case of SV40-bearing mice, tumours consistently develop in the choroid plexus1. In the accompanying paper, we show that the 72-base pair (bp) enhancer in the SV40 genome is instrumental in directing tumorigenesis to the choroid plexus3. However, when the enhancer is deleted from a construction also containing the metallothionein-human growth hormone fusion gene (SVΔe-MGH), an entirely new pattern of pathology results. The present report focuses on transgenic mice carrying this construct; they develop demyelinating peripheral neuropathies, hepatocellular carcinomas and islet cell adenomas.