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Comment
. 2001 Feb 19;193(4):F15-8.
doi: 10.1084/jem.193.4.f15.

Haploinsufficiency for tumor suppression: the hazards of being single and living a long time

D A Largaespada  1
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Comment

Haploinsufficiency for tumor suppression: the hazards of being single and living a long time

D A Largaespada. J Exp Med. .
No abstract available

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Figures

Figure 1
Figure 1
Mechanisms for loss of tumor suppression activity. A normal cell with one mutated TSG allele (TSG−) on the dark chromosome and one wild-type allele (TSG+) on the white chromosome is shown in the oval. Classical TSGs are somatically inactivated by one of the mechanisms shown in the bottom box, resulting in tumor formation. A class of TSG genes, such as PML, may be unable to fully suppress tumor cell growth in the presence of a factor, shown here as protein X, which can partially inhibit TSG protein function. In APL, factor X is the PML-RARα fusion oncoprotein itself. In this model, the order of events could be switched, they could occur simultaneously, and the inhibition of TSG function could be more indirect than shown here.
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