POSSIBLE INTERACTION OF CELL MEMBRANE- BOUND N-ras PATHWAYS WITH NF2-RELATED CYTOSKELETON FACTORS IN ONCOGENESIS OF MENINGIOMAS
Yapijakis C1, Mamali I1, Papapetrou KP2, Stranjalis GS2, Protopapa DP3, Vassilopoulos D1, Sakas DE2
*Corresponding Author: Christos Yapijakis, D.M.D., M.S., Ph.D., Department of Neurology, University of Athens Medical School, Eginition Hospital, Vas Sofias 74, Athens 11528, Greece; Tel: +30-10-7289-125; Fax: +30-10-8811-243; E-mail: cyapijakis_ua_gr@yahoo.com
page: 17

Abstract

Meningiomas are the most common tumors of the central nervous system, accounting for about 15% of all primary brain tumors. The most frequent genetic alteration detected in these tumors is in the neurofibromatosis 2 (NF2) tumor suppressor gene. In order to assess the possi­ble role of the N-ras oncogene in meningiomas, we studied 10 frozen biopsies and four paraffin-embedded tissue samples obtained from 14 unrelated Greek patients who had been operated on for meningioma grades I-III. Normal expression of N-ras was detected immunohistochemically in 28.6%, while over-expression was detected in 64.3% of the samples (all grades II or III). In addition, mutation analysis of hot spot codons in two exons of the NF2 gene revealed an ArgStop nonsense mutation in four samples that contained mutant N-ras. The interaction between the N-ras and merlin pathways was suggested by the observation that absence of N-ras was detected in a grade I meningioma with an NF2 mutation. Thus, absence of N-ras may decrease the effect of NF2 loss towards advancement of malignancy. These findings provide preliminary evidence for an interaction of the N-ras and the NF2 pathways of cell growth control, and for an important role of N-ras in tumorigenic steps towards malignancy of meningiomas.

Key words: meningioma, neurofibromatosis 2 (NF2), N-ras, oncogenesis




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