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| • |
In these
tumors induced by the Friend
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virus, the
p53 gene found in the tumor
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cells is very
often rearranged, leading
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to an absence
of expression or the
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synthesis of a
truncated or mutant
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protein (Mowat
et al. 1985) The
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mutation often
affects one of the
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conserved
blocks of the protein
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(Munroe et al.
1988). In all cases
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studied, the
second allele is either lost
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through loss
of the chromosome, or
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inactived by
deletion. In this tumor
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model,
functional inactivation of the
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p53 gene
seems to confer a selective
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growth
advantage to erythroid cells
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during the
development of Friend
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leukemia in
vivo.
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