Klin Onkol 2006; 19(4): 228-233.
Summary
Backgrounds: TP73 gives rise to two diametrically opposed protein classes: transactivation-competent p73 proteins (TAp73) and transactivation-deficient NH2-terminaly truncated TAp73 proteins. ΔTAp73 are generated by aberrant splicing (p73Δex2, p73Δex2/3) and alternative promoter usage of intronic promoter P2 (ΔNp73). TP73 is involved in neural, mesenchymal and epithelial morphogenesis. Oncogenic activity of TP73 has been well documented and frequent tumor specific up-regulation of ΔTAp73 forms was observed in some types of cancer. ΔNp73 overexpression was found to be an independent prognostic marker for aggressive clinical behavior in patients with carcinomas and neuroblastoma .
Design and subject: Real-time PCR and immunohistochemical detection of TP73 isoforms in medulloblastoma samples. Methods and results: TAp73, ΔNp73, p73Δex2 transcripts have been analyzed in medulloblastoma specimens and normal cerebellar tissue. ΔNp73 overexpression as well as a trend to increased TAp73 expression were found. No correlations between TP73 isoforms and TRKC, MYCC expression were documented. Immunohistochemical analysis of ΔNp73 and p73a confirmed molecular genetic data.
Conclusions: Our findings suggest the involvement of TP73 in medulloblastoma tumorigenesis, defining TP73 as potential prognostic and therapeutic target for medulloblastoma.
