作者: Annett Hölsken , Jürgen Kreutzer , Bernd M Hofmann , Volkmar Hans , Falk Oppel
DOI: 10.1111/J.1750-3639.2008.00180.X
关键词:
摘要: Activating beta-catenin (CTNNB1) mutations can be identified in the majority of adamantinomatous craniopharyngiomas (adaCP), suggesting an aberrant Wnt signaling pathway this histopathologically peculiar tumor entity. However, there is no proven evidence that nuclear translocation associated with CTNNB1 and target gene activation. We performed a laser-microdissection-based study comparing accumulating vs. non-accumulating cells. Mutational analysis expression profiling using real-time polymerase chain reaction were conducted papillary specimens. Target activation, is, over-expression Axin2 could detected adaCP, especially cells accumulation. In addition, increased BMP4 was cell population, which supports hypothesis oral ectodermal origin. Interestingly, populations carried within exon 3. extended analysis, therefore, towards genetic regions encoding for membrane linkage active/passive transport mechanisms (exon 4 8-13), but not detect any alteration. This first report demonstrating association between accumulation activation adaCP. The results confirm as molecular basis distinct challenging clinical morphological phenotype