P53 Immunohistochemistry and direct sequencing of codon 72 exon 4, in intracranial meningioma among sudanese patients

Introduction: Meningiomas are predominantly benign tumors, which arise from the arachnoids’ cap cells. They account for 20% of all primary intracranial neoplasms. The p53 tumor suppressor is a key regulator of cell cycle progression, such that its inactivation promotes increased cell growth and tumorigenesis. Inactivation of p53 as a consequence of p14 ARF loss and MDM2-mediated degradation may contribute to meningioma progression. Material and Methods: This is a cross-sectional study that had been performed at the National Center for Neurological Sciences during February 2011 to December 2013. All meningioma tumors at Elhassan Medical Laboratory for histopathology and cytology during the above mentioned period were processed for P53 protein immunohistochemistry. Data were analyzed using SPSS 13 software with reference P.value of 0.05 was considered statistically significant Results: The sequencing results showed heterozygosity of T>G in exon 4 at protein position ( Ala 70Ala) in 16 samples (10 fibrous, 5 atypical and one anaplastic). Within the afore-mentioned 16 samples, 6 samples showed heterozygosity of C>T in exon 4 at position Ala 69 Val, (this polymorphism had 5 features). Positive immmuno-staining for p53 was identified in 76% of the patients . Labelling indexes of 11-20% were reported in 32.8% of the p 53 group, mostly in fibrous and atypical subtypes of meningioma.