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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

PAkt, cyclin D1 and p27/Kip.1 in glioblastomas with and without EGFR amplification and PTEN mutation.

BACKGROUND: PIP3, generated by P13-K activates Akt which inactivates AFX/FKHR; with the consequent decrease in p27/Kip.1 expression and enhancement of cyclin D1 expression through FRAP/mTOR. PTEN lipid phosphatase degrades PIP3 and negatively regulates Akt, whereas this is activated by EGFR through PI3. In glioblastomas, PTEN is mutated in 27%-40% and EGFR amplified in 60%-65% of cases. MATERIALS AND METHODS: PTEN mutation and EGFR amplification by PCRP Akt, p27/Kip.1 and cyclin D1 by immunohistochemistry, apoptosis by TUNEL and MIB.1 LI were studied in a series of 65 operated glioblastomas. RESULTS: EGFR amplification and PTEN mutation were present in 50% and 30% of glioblastomas, respectively. No relationship between EGFR amplification and PTEN mutation, and p27/Kip. 1 and cyclin D1 was found. However, cyclin D1 was positive in 69% of Akt-expressing areas, whereas p27 was positive in 30% only. CONCLUSION: A direct relationship is more evident between cyclin D1 and p27/Kip.1 and Akt than with PTEN and EGFR.[1]


  1. PAkt, cyclin D1 and p27/Kip.1 in glioblastomas with and without EGFR amplification and PTEN mutation. Fiano, V., Ghimenti, C., Imarisio, S., Silengo, L., Schiffer, D. Anticancer Res. (2004) [Pubmed]
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