@entity4910 - and XXXX -gene deregulation and @entity983 mutation analyses in @entity1137 of the breast.

@entity1 @entity1137 @entity0 @entity16262 @entity5 @entity4910 @entity513 @entity983 @entity1722
Because of the relatively low incidence of @entity0 , there are very few studies on the molecular characteristics of this @entity0 . In an attempt to improve its characterization, we investigated in a large collection of invasive @entity1137 (ILCs) the status of markers known to be involved in the better-studied @entity513 ( @entity513 ). In the current study we disposed of 80 well-characterized ILC cases. Gene amplification of @entity4910 ( @entity4910 ) and @entity1722 ( @entity1722 ) and expression of their gene products were studied by differential polymerase chain reaction (PCR) and immunohistochemistry, respectively. A comprehensive point mutation study of the phosphatase and tensin homolog @entity5 suppressor gene ( @entity983 ) was pursued by single strand conformation polymorphism (SSCP)/sequencing analysis. The @entity4910 gene was rarely amplified in ILC in spite of showing overexpression of the protein in 41% of @entity5 . Hence, unlike @entity513 , increase in gene dosage did not account for the protein excess. @entity983 mutations were detected in ILC (truncating mutations) in around 2% of the @entity5 . Unlike @entity513 , ILC did not display @entity1722 overexpression and expression of the transcription factor @entity16262 correlated inversely with @entity5 grade. The observed discrepancy in the pattern of the @entity1 oncogenes @entity4910 and @entity1722 , which are involved in the process of @entity5 , appears to suggest a different molecular basis for development and progression of ILC.
