The etiology and pathogenesis of tumors of the central nervous system are still inadequately explained. In the present study the expression patterns of a critical molecular component of wnt signaling Show more
The etiology and pathogenesis of tumors of the central nervous system are still inadequately explained. In the present study the expression patterns of a critical molecular component of wnt signaling pathway - axin I was investigated in 42 patients with glioblastoma, the most aggressive form of glial tumors. Immunostaining and image analysis revealed the quantity and localization of the protein. Downregulation of this tumor suppressor expression was observed in 31% of tumors when compared to the levels of axin in healthy brain tissues. Axin was observed in the cytoplasm in 69% of glioblastoma samples, in 21.4% in both the cytoplasm and nucleus and 9.5% had expression solely in the nucleus. Mean values of relative axin's expression obtained by image analysis showed that the highest relative quantity of axin was measured when the protein was in the nucleus and the lowest relative quantity of axin when the protein was localized in the cytoplasm. Investigation on axin's existence at the subcellular level in glioblastomas suggests that axin's expression and spatial regulation is a dynamic process. Despite increasing knowledge on glioma biology and genetics, the prognostic tools for glioblastoma still need improvement. Our findings on expression of axin 1 may contribute to better understanding of glioblastoma molecular profile. Show less
In the present study changes of components of Wnt signaling pathway--axin (AXIN1) and beta-catenin (CTNNB1) in a sample of 72 neuroepithelial brain tumors were investigated. AXIN-1 gene was tested by Show more
In the present study changes of components of Wnt signaling pathway--axin (AXIN1) and beta-catenin (CTNNB1) in a sample of 72 neuroepithelial brain tumors were investigated. AXIN-1 gene was tested by PCR/loss of heterozygosity (LOH). Immunostaining and image analysis revealed the quantity and localization of relevant proteins. Polymorphic marker for AXIN-1, showed LOH in 11.1% of tumors. LOH was distributed to 6.3% of glioblastomas, one was found in neuroepithelial dysembrioplastic tumor and one in medulloblastoma. Down regulation of axin expression and up regulation of beta-catenin were detected in the analyzed tumors. Axin was observed in the cytoplasm in 68.8% of samples, in 28.1% in both the cytoplasm and nucleus and 3.1% had no expression. Beta-catenin was observed mainly in the nucleus and cytoplasm (59.4%). Expression in 34.4% of samples was in the cytoplasm and 6.3% showed no expression. Comparison of mean values of relative increase of axin and beta-catenin showed that they are significantly reversely proportional (P = 0.014). Relative quantity of beta-catenin in patients with gross deletion of AXIN1 was significantly higher in comparison to patients without LOH (P = 0.040). Our results demonstrate that changes of key components of the Wnt signaling play a role in neuroepithelial brain tumors. Show less