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I've been reading a little about the "two-hit" hypothesis for tumor suppressor genes here, which mentions that some genes exhibiting haploinsufficiency are exceptions to the hypothesis. I've read elsewhere on this site (namely the answer to this question) that suggests haplosufficiency as a means of "silencing" the mutation of the tumor suppressor gene such that the expression of the wild-type allele compensates for the mutant allele.

Are there any other mechanisms that contribute to incomplete penetrance of tumor suppressor mutations?

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This is more of a comment


Mutation in tumour suppressor is a recessive trait and there is no active "silencing" of the mutation. If a tumour suppressor is a TF then a mutation in the DNA binding domain can have no effect if there is a complementary mutation in its binding site. This is just a theoretical possibility and I have not heard of any examples as such. I don't think any other mechanisms exist for "silencing" any loss of function mutation.

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