Balkan Journal of Medical Genetics

APLASIA RAS HOMOLOGOUS MEMBER I GENE AND DEVELOPMENT OF GLIAL TUMORS
Yakut S1, Tuncer MR2,* Berker M3, Goksu E2, Gurer I4, Ozes ON1, Luleci G1, Karauzum SB1
*Corresponding Author: Sibel Berker Karauzum, Department of Medical Biology and Genetics, Faculty of Medicine, Akdeniz University Antalya, Turkey; Tel.: +90 242 2496971; Fax: +90 242 2274482; E-mail: sibelkarauzum@akdeniz.edu.tr
page: 37

INTRODUCTION

Glial tumors, take part in neuroepithelial tumors, are one of the most common primary human brain tumors originating from the astrocytes, oligodendrioglial, ependymal or mixed glial cells [1]. Their development is a multi-step process that involves the accumulation of several genetic events such as activation of proto-oncogenes, expression of growth factors and their receptors or loss of expression tumor suppressor genes. Alterations of chromosome 1 that include deletion, LOH, amplification and hypermethylation, also play a role in the development of brain tumors. The LOH of 1p has been observed in most oligodendroglial and in some of the glioblastoma multiforme tumors (GBM) that originate from astrocytes [1-6]. All of these lead to the development of unregulated cell growth and differentiation. Aplasia Ras homologue member I (ARHI), also known as DIRAS3, was the first tumor suppressor gene identified in the Ras superfamily [7]. Even though the maternally-imprinted ARHI gene shows 60.0% sequence homology to the Ras proto-oncogene, when it reexpessed, it inhibits proliferation and motility by blocking signal transducer and activator of transcription 3, up regulating p21WAF1/ CIP1 and inhibiting signal through Ras/Map [7-9]. The maternally-silenced ARHI gene is expressed only from the paternal allele and is constitutively expressed in normal ovary, breast, heart, liver, pancreas, thyroid and brain tissues. Expression is lost or markedly down regulated by LOH or hypermethylation in most cancers of ovary, breast, pancreas, thyroid, and brain [10-14]. We have evaluated the expression levels of the ARHI gene in 21 primary human glial tumor tissue and normal brain tissue samples with a real time reverse transcriptase polymerase chain reaction (RTPCR) technique. To elucidate the possible cause of loss of expression, we also studied LOH in 21 tumors and peripheral blood samples of the patients by using fragment analysis with five highly polymorphic microsatellite markers and methylation profiles of 21 tumors using a hypermetylated healthy volunteer as a positive control by COBRA (combined bisulfite restriction analysis) and RFLP (restriction fragment length polymorphism) techniques.

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