Bcl-2/Bax蛋白表达与大鼠脑胶质瘤恶性程度的关系研究

目的:探讨大鼠脑胶质瘤中Bcl-2和Bax蛋白表达与其恶性程度的关系。方法:经病理和免疫组织化学染色证实的不同恶性程度的大鼠脑胶质瘤20例,用免疫组织化学法和原位缺口末端标记(TUNEL)法分别检测10例正常大鼠脑组织和20例不同恶性程度的大鼠脑胶质瘤中Bcl-2、Bax蛋白表达阳性率和凋亡细胞百分率。结果:正常大鼠脑组织中未见Bcl-2和Bax蛋白阳性表达,且凋亡细胞百分率仅为(0.5±0.1)％;不同恶性程度的大鼠脑胶质瘤间Bcl-2、Bax蛋白表达阳性率和凋亡细胞百分率的差异有显著性(P<0.05),且随着恶性程度的增高,Bcl-2蛋白表达阳性率有降低的趋势,而Bax蛋白表达阳性率和凋亡细胞百分率均有升高的趋势。相关分析显示,大鼠脑胶质瘤的恶性程度与Bax蛋白表达阳性率和凋亡细胞百分率呈正相关(r=0.891,P<0.05),而与Bcl-2蛋白表达阳性率呈负相关(r=-0.889,P<0.05)。结论:Bcl-2、Bax蛋白表达阳性率和凋亡细胞百分率可能与大鼠脑胶质瘤的恶性程度有关。     

NF-κBp65、Bcl-2、Bcl-xL蛋白在胰腺癌中的表达及其与P53和凋亡指数的关系

背景与目的:核因子κB通过调控下游bcl-2家族基因表达参入细胞凋亡调节过程,而p53除了参入细胞周期调节外也参入依赖bcl-2基因的细胞凋亡调控。在胰腺癌中NF-κBp65、Bcl-2和Bcl-xL蛋白表达与p53和凋亡的关系还不清楚。本研究系统地分析了核因子κBp65及其下游的bcl-2和bcl-xL抑凋亡基因在胰腺癌(PC)中的表达以及与P53蛋白表达和凋亡指数(AI)的关系。方法:免疫组化法检测25例胰腺导管腺癌(PC)和9例正常胰腺组织(NP)中P53蛋白表达;Western印迹法分析NF-κBp65蛋白表达;RT-PCR分析Bcl-2和Bcl-XL蛋白表达,TdT酶介导的原位缺口标记(TUNNEL)法了解胰腺癌细胞凋亡情况(AI)。结果:P53在PC组织阳性率(56%,14/25),高于NP组织阳性率(P<0.00);NF-κBp65、Bcl-2和Bcl-xL在PC组织表达相对值分别为:1.06±0.16、0.79±0.13、0.76±0.24,分别高于NP组织:0.23±0.016、0.23±0.074、0.18±0.026(分别P<0.05);14例p53阳性PC中,NF-κBp65、Bcl-2和Bcl-Xl表达相对值分别为:1.32±0.23、0.92±0.33、0.82±0.21;11例p53阴性PC中,NF-κBp65、Bcl-2和Bcl-xL表达相对值分别为:0.78±0.15、0.54±0.19、0.71±0.28(分别P<0.05,P<0.05,P>0.05);NF-κBp65和Bcl-2分别与P53表达有明显的正相关性(分别P<0.01,P<0.05),Bcl-xL与P53无相关性(P>0.05),NF-κBp65与Bcl-XL表达正相关(P<0.01),而NF-κBp65与Bcl-2表达无相关性(P>0.05);胰腺癌平均AI为(15.4±6.48)%,NF-κBp65表达与AI负相关(r=-0.297,P<0.05),而Bcl-2、Bcl-xL与AI无相关性(r=-0.203,P>0.05;r=-0.156,P>0.05)。结论:胰腺癌中抗凋亡因子表达上调,凋亡指数主要决定于NF-κBp65蛋白水平;NF-κBp65通过对下游bcl-xL基因表达的调控参与胰腺癌凋亡过程;p53在凋亡调节过程中起重要作用。     

宫颈癌化疗前后肿瘤细胞凋亡及相关基因Bcl-2、Bax表达的对比分析

目的 探讨宫颈癌化疗前后肿瘤细胞Bcl-2、Bax蛋白表达及凋亡的变化及其临床意义.方法 采用免疫组织化学S-P法及TUNEL法,检测55例宫颈癌单一拓扑替康化疗前后的110个肿瘤样本中Bcl-2、Bax蛋白水平及细胞凋亡水平.结果 子宫颈癌单一拓扑替康化疗后有效率为34.5%(19/55);化疗前后凋亡阳性率分别为41.8%、50.9%,无显著性差异(P＞0.05).Bcl-2蛋白在子宫颈癌化疗前后的表达阳性率分别为54.5%和49.1%,无显著性差异(P＞0.05);Bax蛋白在子宫颈癌化疗前后的表达阳性率分别为50.9%和74.5%,有显著性差异(P＜0.05);组织学有效的病例化疗前癌组织中Bcl-2的阳性率为52.6%(9/19),组织学无效病例的阳性率为55.6%(16/36),无显著性差异(P＞0.05);组织学有效的病例化疗前癌组织中Bax阳性率为63.2%(7/19),组织学无效病例的阳性率为44.4%(20/36),无显著性差异(P＞0.05).结论 拓扑替康具有诱导宫颈癌细胞凋亡的作用,其作用与上调Bax的表达相关.化疗前癌组织Bcl-2、Bax蛋白表达量与拓扑替康组织学疗效无相关性.     

胃癌组织中LMO1与Bcl-2、Bax、Survivin、Caspase-3蛋白表达的关系及意义

摘 要：［目的］ 检测LMO1、Bcl-2、Bax、Survivin、Caspase-3蛋白在胃癌组织中的表达,并对这些蛋白之间的关系和临床意义进行分析。 ［方法］ 对96例胃癌手术患者的肿瘤组织标本及50例癌旁组织标本进行免疫组化染色（SP法）,检测LMO1、Bcl-2、Bax、Survivin、Caspase-3蛋白的表达情况。同时收集患者的病理学情况,对与各指标的关系进行分析。 ［结果］ 胃癌组织中LMO1、Bcl-2、Survivin表达均比癌旁组织增强（均P<0.05）,Caspase-3蛋白在胃癌组织中表达低于癌旁组织（P<0.05）,Bax在两种组织中表达无明显差异（P>0.05）。胃癌组织中细胞凋亡率明显低于癌旁组织（P<0.01）。胃癌组织中LOM1蛋白强表达者细胞凋亡率明显低于弱表达者（P<0.01）。Spearman相关分析发现,胃癌组织中LMO1与Bcl-2表达存在正相关（r=0.3058,P=0.002）,LMO1与Caspase-3表达存在负相关（r=-0.2886,P=0.004）;Bcl-2与Survivin表达存在正相关关系（r=0.2986,P=0.0315）,Bcl-2与Bax表达呈负相关（r=-0.4062,P<0.001）,Survivin与Caspase-3也呈负相关（r=-0.3142,P=0.002）。［结论］ 胃癌组织中LMO1蛋白可能通过调节Bcl-2、Caspase-3的表达和活性而参与肿瘤凋亡。     

bcl-2、p53在皮肤肿瘤中的表达及意义

目的探讨bcl-2、p53在几种皮肤肿瘤中的表达及意义。方法采用流式细胞术(FCM)和免疫荧光技术对皮肤鳞状细胞癌(SCC)、恶性黑色素瘤(MM)、基底细胞癌(BCC)、色素痣(PN)bcl-2、p53蛋白的表达进行定量分析,以荧光指数(FI)作为定量表达指标。结果鳞状细胞癌、基底细胞癌的bcl-2、p53基因蛋白的FI值均显著性高于正常对照(P<0.05),基底细胞癌的bcl-2基因的FI值显著性高于鳞状细胞癌(P<0.05),而二者的p53基因蛋白的FI值无显著性差异(P>0.05);恶性黑色素瘤、色素痣的bcl-2、p53基因蛋白的FI值均显著性高于正常对照(P<0.05),恶性黑色素瘤的p53基因的FI值显著性高于色素痣(P<0.05),而二者的bcl-2基因蛋白的FI值无显著性差异(P>0.05)。结论鳞状细胞癌、恶性黑色素瘤、基底细胞癌、色素痣中均有bcl-2的表达,基底细胞癌bcl-2表达显著高于鳞状细胞癌,说明基底细胞癌的发生发展可能与细胞凋亡受抑密切相关;p53在恶性黑色素瘤的表达高于色素痣,说明p53为黑色素瘤的恶性标志,检测p53表达可以作为鉴别皮肤黑色素瘤恶性病变的辅助手段。     

脑膜瘤细胞凋亡与增殖活性的研究

 目的　通过对良性脑膜瘤组织细胞凋亡的原位观察和增殖性抗原 Ki- 67表达状态的研究 ,探讨不同级别脑膜瘤组织中细胞增殖和凋亡情况。方法　对 40例术前未经任何治疗的脑膜瘤手术标本 ,分别进行凋亡细胞的 DNA缺口原位末端标记 ( TUNEL)法和 Ki- 67抗原的免疫组化染色。结果　恶性及非典型脑膜瘤中 Ki- 67标记指数明显高于良性脑膜瘤 ( P<0 .0 1 ) ,恶性和非典型脑膜瘤之间也有显著性差异 ( P<0 .0 1 )。在恶性及非典型脑膜瘤中凋亡指数显著性高于良性脑膜瘤 ( P<0 .0 1 )。结论　恶性及非典型脑膜瘤中自发性细胞凋亡增多。 Ki- 67指数和病理分级有很好的一致性 ,能较好的反映脑膜瘤的增殖特性.     

甲状腺癌组织中凋亡相关蛋白Fas,FasL,Bcl-2和Bax的表达及意义

目的 研究凋亡相关蛋白Fas,FasL,Bcl-2和Bax在甲状腺癌组织中的表达及意义.方法应用免疫组织化学,采用TUMEL法,检测34例甲状腺癌及10例结节性甲状腺肿、9例甲状腺腺瘤组织病理标本中的细胞凋亡指数(Apoptosis Index, AI);并用通用型二步法对凋亡相关蛋白Fas,FasL,Bcl-2和Bax的表达进行检测.结果 (1)对照组细胞平均AI(%)为12.39±2.21,甲状腺癌细胞平均AI(%)为20.17±2.68,即肿瘤组的细胞凋亡指数高于对照组,二者有显著性差异(t＝4.138＞t(0.05),P＜0.05).(2)甲状腺癌组织中Fas,FasL,Bcl-2和Bax蛋白表达显著高于对照组.(3)Fas,FasL,Bcl-2和Bax蛋白表达的阳性率与其病理类型、临床分期无明显关系(P＞0.05).结论甲状腺癌组织中有较高水平细胞凋亡,Fas,FasL,Bcl-2和Bax的表达均明显增强,并且通过参与调节细胞凋亡而与甲状腺癌的发生有关,但与病理类型、临床分期无明显关系.     

Gab2基因在胃癌中的表达及对胃癌细胞增殖、凋亡、迁移及AKT、p-AKT、Bax、Bcl-2表达的影响研究

目的 探讨Gab2基因在胃癌中的表达及对胃癌细胞增殖、凋亡、迁移及对AKT、p-AKT、Bax、Bcl-2表达的影响.方法 采用RT-PCR及Western Blot检测胃癌组织和癌旁组织中Gab2的表达.培养人胃癌细胞株SGC-7901,分别用Gab2小干扰RNA(Gab2-siRNA)和阴性对照(siRNA-NC)转染细胞,以空脂质体转染的细胞作为对照组,各组细胞培养48 h.应用Western Blot检测细胞中Gab2、AKT、p-AKT、Bax、Bcl-2蛋白表达的变化,CCK-8检测细胞增殖情况,流式细胞仪检测细胞凋亡,Transwell小室检测细胞迁移能力.结果 胃癌组织中Gab2的mRNA及蛋白表达水平均明显高于癌旁组织(P﹤0.01);Gab2-siRNA组Gab2蛋白表达水平明显低于对照组(P﹤0.01);siRNA-NC组细胞的存活率、凋亡率、迁移数及AKT、p-AKT、Bax、Bcl-2蛋白表达与对照组比较,差异均无统计学意义(P﹥0.05);Gab2-siRNA组细胞的AKT蛋白表达与对照组比较,差异无统计学意义(P﹥0.05),细胞的存活率、迁移数及p-AKT、Bcl-2蛋白表达明显低于对照组(P﹤0.01),细胞凋亡率及Bax蛋白表达明显高于对照组(P﹤0.01).结论 Gab2在胃癌组织高表达,沉默Gab2的表达能显著抑制人胃癌细胞株SGC-7901的增殖和迁移,并通过调节Bax、Bcl-2蛋白表达促进细胞凋亡,其可能的机制与AKT信号通路的调控有关.     

rhu-TNF腔内治疗恶性胸腔积液的疗效与可能机制探讨

摘 要：［目的］ 研究注射用重组人改构肿瘤坏死因子(rhu-TNF)腔内注射治疗恶性胸腔积液的疗效并探讨其可能机制。［方法］ 将60例恶性胸腔积液患者随机分为对照组（29例）和观察组（31例）,对照组给予顺铂(DDP)治疗,观察组在对照组基础上给予rhu-TNF。收集并对比治疗前后各组胸水的Bcl-2 mRNA和Bax mRNA表达,以及治疗后的疗效(RR)、临床获益反应(CBR)、不良反应、疾病进展时间(TTP)。［结果］ 治疗前,两组Bcl-2 mRNA和Bax mRNA的表达无显著差异(P>0.05),治疗后,两组Bcl-2 mRNA均降低(P<0.05),Bax mRNA的表达增高(P<0.05);与对照组比,观察组的Bcl-2 mRNA明显降低(P<0.05),Bax mRNA的表达明显增高(P<0.05)。对照组RR、CBR分别为 41.38%和48.28%,观察组RR、CBR分别为70.97%和77.41%,两组间差异有统计学意义(P<0.05)。随访3~12个月,对照组TTP为5.1个月,观察组TTP为7.1个月,差异有统计学意义(P<0.05)。两组不良反应无显著差异。［结论］ rhu-TNF治疗恶性胸腔积液的机理之一在于降低胸腔脱落细胞Bcl-2表达,升高Bax表达,促进肿瘤细胞凋亡,且无明显的不良反应。     

化疗前后子宫颈癌细胞凋亡与Bcl-2、Bax基因表达的相关性研究

目的 探讨化疗诱导子宫颈癌细胞凋亡与癌组织Bcl-2、Bax基因表达的关系.方法 选择30例经单一拓扑替康化疗的子宫颈癌患者治疗前和治疗后癌组织标本60个样本,用原位分子杂交方法检测癌组织中Bcl-2 mRNA与Bax mRNA表达情况,TUNEL法检测细胞凋亡水平.结果 子宫颈癌单一拓扑替康化疗后组织疗效评定,有效率为36.7%(11/30);化疗前后凋亡阳性率分别为36.7%、66.7%,化疗后凋亡阳性率有所增高,但差异无统计学意义(P＞ 0.05).Bcl-2 mRNA在子宫颈癌化疗前后的表达阳性率分别为60.0%和36.7%,差异无统计学意义(P＞0.05);Bax mRNA在子宫颈癌化疗前后的表达阳性率分别为43.3%和80 .0%,差异有统计学意义(P＜0.05);组织学有效的病例化疗前癌组织中Bcl-2 mRNA 及Bax mRNA的阳性率分别为63.6%(7/11)、63.6%(7/11),组织学无效病例的阳性率分别为63.2%(12/19)、31.6%(6/19),差异均无统计学意义(P＞0.05). 结论拓扑替康具有诱导子宫颈癌细胞凋亡的作用,其作用与上调Bax的表达相关 .化疗前癌组织Bcl-2 mRNA及Bax mRNA表达量与拓扑替康组织学疗效无相关性.     

Expression of Bcl-2, bax and Bcl-X<Subscript>L</Subscript> in meningioma cells and its clinical significance

Objective To explore the relationship between expression of apoptosis-modulating proteins and histopathological grade and recurrence in meningioma. Methods Immunohistochemistry method (LSAB) was used to detect the expression of Bcl-2, Bax Bnd Bcl-X_L in 80 cases of meningioma including benign group (38 cases), atypical group (26 cases) and malignant group (16 cases). Results Expression of Bcl-2 oncoprotein positive in 88% cases in malignant group was significantly higher than that of benign group (37%,P<0.05). There was no significant difference in the expression positive rate of Bax, Bcl-X_L oncoprotein among benign, atypical and maligant groups (P>0.05), but Bcl-2+Bcl-X_L/Bax was associated statistically with meningioma grade (P<0.01). There was no significant difference in the compare expression of Bcl-2, Bax, Bcl-X_L oncoprotein positive in non-recurrent, initially resected recurrent and recurrent meningiomas (P>0.05). Conclusion Bcl-2, Bax and Bcl-X_L might play important roles in meningiomas and BCL-2+BCL-X_L/Bax is useful parameters for estimation of biological behavior of meningiomas.     

PCNA和Ki-67在脑膜瘤组织中的表达及其意义

目的：探讨增殖细胞抗原（PCNA）和Ki-67核抗原在脑膜瘤中的表达及其与肿瘤良、恶性及复发的关系。方法:采用LSAB法检测80例脑膜瘤组织中PCNA和Ki-67的表达。结果：恶性脑膜瘤PCNA标记指数（PCNALI）和Ki-67标记指数（Ki-67LI)明显高于良性脑膜瘤（P＜0．01）和非典型性脑膜瘤（P＜0．05），复发脑膜瘤PCNA LI显著高于未复发脑膜瘤（P＜0．01），复发脑膜瘤Ki-67LI也显著高于未复发脑膜瘤（P＜0．01），Ki-67表达与PCNA表达呈正相关。结论：脑膜瘤细胞标记指数可作为判断脑膜瘤良；恶性的客观指标之一，标记指数对预测脑膜瘤的复发有一定意义。     

脑膜瘤细胞凋亡及凋亡相关基因bcl—2、p53蛋白的表达

目的 探讨脑膜瘤自发性细胞凋亡相关基因bcl-2、p53蛋白在脑膜瘤中的表达及其意义。方法 采用TUNEL法和免疫组化S－P法检测40例脑膜瘤中细胞凋亡及凋亡相关基因bcl-2,p53蛋白的表达。结果 恶性和非典型脑膜瘤中的细胞凋亡指数（AI）明显高于良性脑膜瘤（P＜0．05）,良性脑膜瘤不同亚型之间bcl-2,p53表达无显著性差异（P＞0．05）;p53蛋白表达随脑膜瘤恶性程度增高而增强,具有显著性差异（P＜0．05）,p53阳性与阴性的脑膜瘤中的细胞凋亡指数无显著性差异;bcl-2蛋白表达与脑膜瘤细胞凋亡呈负相关。结论 恶性及非典型脑膜瘤中自发性细胞凋亡增多;凋亡是脑膜瘤恶性或不典型的1个重要的生物学行为;p53基因在脑膜瘤的恶变过程中发生重要作用,与脑膜瘤的恶性进展密切相关;bcl-2基因在脑膜瘤中可抑制细胞凋亡。     

Antigen expression on recurrent meningioma cells

Introduction

Meningiomas are intracranial brain tumours that frequently recur. Recurrence rates up to 20% in 20 years for benign meningiomas, up to 80% for atypical meningiomas and up to 100% for malignant meningiomas, have been reported. The most important prognostic factors for meningioma recurrence are meningioma grade, meningioma invasiveness and radicality of neurosurgical resection. The aim of our study was to evaluate the differences in antigenic expression on the surface of meningioma cells between recurrent and non-recurrent meningiomas.

Methods

19 recurrent meningiomas and 35 non-recurrent meningiomas were compared regarding the expression of MIB-1 antigen, progesterone receptors, cathepsin B and cathepsin L, using immunohistochemistry.

Results

MIB-1 antigen expression was higher in the recurrent meningioma group (p=0.001). No difference in progesterone receptor status between recurrent and non-recurrent meningiomas was confirmed. Immunohistochemical intensity scores for cathepsin B (p= 0.007) and cathepsin L (p<0.001) were both higher in the recurrent than in the non-recurrent meningioma group.

Conslusions

MIB-1 antigen expression is higher in recurrent compared to non-recurrent meningiomas. There is no difference in expression of progesterone receptors between recurrent and non-recurrent meningiomas. Cathepsins B and L are expressed more in recurrent meningiomas.     

Different distribution of c-myc and MIB-1 positive cells in malignant meningiomas with reference to TGFs, PDGF, and PgR expression

We investigated the expression of transforming growth factors (TGFs), platelet-derived growth factor (PDGF), progesterone receptor (PgR), and c-myc in 20 cases of meningioma of various grades: 17 benign, 2 atypical, and 1 anaplastic. All cases of atypical and anaplastic meningioma were positive for c-myc, whereas all 17 benign meningiomas were negative for c-myc immunostaining. Expression of TGF-α, TGF-β, and PDGF-BB proteins was seen in more than 80% of the meningioma cases and was not restricted to their histological grade of meningioma. PgR was expressed mainly in benign meningiomas. Moreover, the cells expressing c-myc protein were not usually stained by MIB-1. These results indicate that c-myc does not directly work on the proliferation of meningioma cells, and even in homogeneous meningioma cells, there may be many functional variations that lead the meningioma cells to their growth.     

AR、PCNA表达与脑膜瘤临床病理因素的相关性研究

目的探讨雄激素受体(AR)在脑膜瘤组织中的表达及其与肿瘤增殖潜力的关系.方法采用免疫组化SABC法,检测AR、增殖细胞核抗原(PCNA)在39例脑膜瘤组织中的表达.结果51.3%(20/39)的脑膜瘤组织中AR呈不同程度的表达.良性、非典型性、恶性脑膜瘤中AR表达率分别为31.6%(6/19)、58.3%(7/12)、87.5%(7/8).恶性脑膜瘤中AR阳性细胞数显著高于非典型性和良性脑膜瘤(P＜0.05).恶性脑膜瘤平均PCNA标记指数(PCNA U)明显高于非典型性(P＜0.05)和良性脑膜瘤(P＜0.05).AR阳性脑膜瘤的PCNA U高于AR阴性脑膜瘤(P＜0.05),AR表达与PCNA的表达呈正相关.结论脑膜瘤AR表达与其病理级别有关,AR参与了肿瘤的生长和血管生成;检测脑膜瘤中AR表达可间接反映肿瘤的增殖潜力.     

Different activation of mitogen-activated protein kinase and Akt signaling is associated with aggressive phenotype of human meningiomas.

PURPOSE: Activation of intracellular signaling cascades has been implicated in the growth control of benign meningiomas, but their role for meningioma progression and outcome is unknown. Here we determined the expression and function of proteins involved in mitogen-activated protein kinase (MAPK) and phosphinositol-3 kinase (PI3K)/Akt signaling in benign, atypical, and malignant meningiomas and studied their association with clinicopathologic data including meningioma recurrence. EXPERIMENTAL DESIGN: Expression of various MAPK and PI3K signaling proteins was determined in 70 primary meningiomas and, if present, in recurrent tumors by immunohistochemistry and Western blotting. The expression patterns in primary and recurrent tumors were related to clinical data. The effect of MAPK and PI3K pathway inhibition on cell proliferation and apoptosis was determined using a primary malignant meningioma cell culture. RESULTS: Atypical and malignant meningiomas showed higher levels of phospho-Akt compared with benign tumors, and their proliferation could be inhibited by PI3K blocking using wortmannin. PI3K inhibition did not induce apoptosis in malignant meningioma cells. In contrast, expression of phospho-Raf and phospho-MAPK was decreased in aggressive meningiomas compared with benign tumors, but MAPK inhibition by PD98059 resulted in tumor cell apoptosis and decreased proliferation. Reduced MAPK activation was associated with meningioma recurrence, and PI3K activation was associated with poor preclinical condition and brain invasion of malignant meningiomas. CONCLUSIONS: Both MAPK and PI3K/Akt pathways are activated at different levels in benign and malignant meningiomas. Activation of PI3K/Akt signaling contributes to the aggressive behavior of malignant meningiomas, whereas MAPK activation is involved in both proliferation and apoptosis of malignant meningiomas.     

Tumor grade-related <Emphasis Type="Italic">NDRG2</Emphasis> gene expression in primary and recurrent intracranial meningiomas

Approximately 30% of all primary CNS tumors are meningiomas. Depending on histological type, meningiomas can recur as follows: benign—with five-year recurrence of 5%, atypical—recurrence approximately 40%, and anaplastic with recurrence of 50–80%. In an attempt to understand the molecular mechanism of meningioma recurrence we investigated the N-Myc downstream-regulated gene 2 (NDRG2), which has recently been described as important in suppressing cellular carcinogenesis in different types of cancer. The objective of the study was to investigate NDRG2 gene expression at the mRNA level in primary and recurrent meningiomas as a potential marker of tumor aggressiveness, malignancy, and recurrence. Primary and recurrent meningiomas of WHO grades I, II, and III from 35 patients operated on between 2005 and 2008 year at the Department of Neurosurgery of Kaunas Medical University Hospital (Lithuania) were studied. Using the qRT-PCR method we measured NDRG2 gene expression at the mRNA level in primary (n = 24) and recurrent (n = 11) meningiomas. Statistically significant differences in NDRG2 gene expression level were observed between primary and recurrent meningioma groups (P < 0.05) and between benign (WHO grade I) and atypical (WHO grade II) meningiomas (P < 0.05). No statistically significant differences were observed (P > 0.05) among histological subtypes of benign (WHO grade I) meningiomas: fibrous, meningothelial, and transitional. In accordance with our results, reduction of NDRG2 gene expression at the mRNA level could help to explain malignant progression and predisposition to recurrence in meningiomas.