The role of @entity876 mutations in bilateral XXXX .

@entity1 @entity0 @entity1885 @entity5 @entity876
Mutations of the @entity5 suppressor gene @entity876 have been implicated in certain familial cases of @entity0 . We examined a series of 38 cases of nonfamilial bilateral @entity0 using antibodies CM1 and DO7 to @entity876 wild-type and mutant protein (Novocastra Laboratories) by the avidin- @entity1885 -peroxidase complex method. The two antibodies reacted similarly. Mutant @entity876 protein was detected in 17 of 76 (22%) @entity5 but in only 3 of 38 (8%) paired @entity5 . There were no significant differences in @entity876 expression between synchronous (< 12 mos) and @entity5 (29% vs 17%, P = 0.09) or between first and second @entity5 (14% vs 26%, P = 0.29). Mutant @entity876 was detected bilaterally in one metachronous and two synchronous cases, which were amplified and sequenced and two synchronous cases, which were amplified and sequenced by polymerase chain reaction and single strand confirmation polymorphism. One synchronous case showed a bilateral mutation in exon 2-3; the other had a bilateral mutation in exon 8-9. In the metachronous case, a mutation could be demonstrated in only one breast. Analysis of all @entity5 demonstrated that when @entity876 protein is overexpressed in the first @entity5 , there is a 60% probability of overexpression in the second, whereas if absent from the first, it is unlikely to be present in the second. These data suggest that @entity876 mutations do not play a major role in the pathogenesis of bilateral disease in most @entity1 .
