Yakut Tahsin, Bekar Ahmet, Doygun Muammer, Acar Hasan, Egeli Unal, Ogul Erhan
Department of Medical Biology and Genetics, Faculty of Medicine, University of Uludag, Bursa, Turkey.
Teratog Carcinog Mutagen. 2002;22(3):217-25. doi: 10.1002/tcm.10013.
In this study, we investigated the relationship between genetic alterations such as chromosome 22 aneuploidy and p53 gene deletion, and the pathological types of meningioma of typical and aggressive forms. Thirty-four meningiomas (23 typical and 11 aggressive) were examined by application of fluorescence in situ hybridization (FISH) with chromosome 22 specific alpha satellite probe and a combination of p53 locus specific and chromosome 17 centromere specific alpha satellite probes, to evaluate the chromosome 22 aneuploidy and gain or loss of p53 gene along with chromosome 17. The results showed that, although chromosome 22 aneuploidy was seen in 7 out of 23 typical (30.4%) and 4 out of 11 aggressive meningiomas (36.3%), no p53 deletion was detected in typical meningiomas, and p53 deletion was detected in 3 out of 11 aggressive meningiomas (1 atypical and 2 malignant), which had recurrence. There were no simultaneous occurrences of p53 gene deletions between typical and aggressive meningiomas. The present findings indicate that the loss of chromosome 22 may be involved with tumorogenesis of typical and aggressive meningiomas, while p53 gene deletions may be involved with malignant progression and recurrence in the aggressive meningiomas.
在本研究中,我们调查了诸如22号染色体非整倍体和p53基因缺失等基因改变与典型和侵袭性脑膜瘤病理类型之间的关系。应用针对22号染色体的特异性α卫星探针以及p53基因座特异性和17号染色体着丝粒特异性α卫星探针组合的荧光原位杂交(FISH)技术,对34例脑膜瘤(23例典型脑膜瘤和11例侵袭性脑膜瘤)进行检测,以评估22号染色体非整倍体以及p53基因伴随17号染色体的增减情况。结果显示,虽然在23例典型脑膜瘤中有7例(30.4%)以及11例侵袭性脑膜瘤中有4例(36.3%)出现了22号染色体非整倍体,但在典型脑膜瘤中未检测到p53基因缺失,而在11例侵袭性脑膜瘤中有3例(1例非典型和2例恶性)检测到p53基因缺失,且这3例均有复发情况。典型脑膜瘤和侵袭性脑膜瘤之间未同时出现p53基因缺失。目前的研究结果表明,22号染色体缺失可能与典型和侵袭性脑膜瘤的肿瘤发生有关,而p53基因缺失可能与侵袭性脑膜瘤的恶性进展和复发有关。