Balkan Journal of Medical Genetics

MOLECULAR CYTOGENETIC STUDY OF THE NF2 GENE DELETION IN MENINGIOMA IN SUDANESE PATIENTS
AbdElmontalab Farah Y1, Fadl Elmula I2, Abushama HM1, Kreskowski K3, Liehr T3,*
*Corresponding Author: Dr. Thomas Liehr, Institut für Humangenetik, Kollegiengasse 10, D-07740 Jena, Germany; Tel.: 49-3641-935533; Fax: ++49-3641-935582; E-mail: Thomas.Liehr@med.uni-jena.de
page: 29

INTRODUCTION

Meningiomas are benign tumors with a relativey small number of genetic aberrations, accounting for ~1/3 of all primary brain tumors, are the second most common adult central nervous system tumors and occur in up to 1.5% of the general population; they are most frequently observed in the sixth decade of life [1-2]. Early cytogenetic studies showed complete or partial monosomy 22 as the most common chromosomal abnormality [1,3]. Later studies revealed a tumor suppressor gene on chromosome 22, sub-band q12.2, to be involved in meningioma formation and progression. Loss of the neurofibromatosis type 2 (NF2) gene is important in early development of meningioma [4], and plays a major role in familial meningioma which account for only ~2.0% of the cases [1-2]. Small insertions, deletion or single base pair mutations of the NF2 gene are present in ~60.0% of sporadic meningiomas [5]. Such deletions or mutations of NF2 have been observed in >70.0% of grade II or III meningiomas, but in only 25.0% of grade I meningiomas [1]. We here report on the investigation of cytogenetic aberrations in meningioma among Sudanese patients using banding cytogenetics and molecular cytogenetics.

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