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1.
大多数少突胶质细胞肿瘤存在1号染色体短臂(1p)和19号染色体长臂(19q)的杂合性缺失,且具有这一分子遗传学改变的病人,其放化疗敏感性较高,预后较好。此外,还有一些分子遗传学的变化,如MGMT基因启动子甲基化、p53基因突变、Ki-67基因高表达、IDH1基因突变等,可能对少突胶质细胞肿瘤的诊断、治疗以及预后判断有一定的提示作用。本文就少突胶质细胞肿瘤最新的分子遗传学研究进展作一综述。  相似文献   

2.
少支胶质细胞肿瘤最重要的分子遗传学特征是1p/19q等位基因的杂合性缺失,近年来已初步证实了其基因表型变化与生物学行为之间的联系,即分子遗传学特征与其发生发展、放化疗敏感性、治疗方式选择以及预后之间存在着相关性,大大促进了以形态学为基础的诊疗模式向以分子发生机制为基础的新的诊疗模式的转变。  相似文献   

3.
目的 研究胶质瘤中1p/19q联合缺失与患者临床特征及O6-甲基鸟嘌呤-DNA甲基转移酶(O6-methylguanine-DNA methyltransferase,MGMT)表达的关系.方法 使用荧光原位杂交技术,对中山大学附属肿瘤医院2009年3月至2011年3月的63例手术确诊胶质瘤标本进行1p/19q联合缺失检测,利用统计学方法分析1p/19q联合缺失患者与无联合缺失患者在性别、年龄、部位、病理类型及MGMT表达状态是否有差异.结果 全组63例患者,男38例,女25例,年龄(41.7 ± 15.3)岁.其中,16例(25.4%)存在1p/19q联合缺失.1p/19q联合缺失患者与无联合缺失患者在性别、年龄及肿瘤部位间的差异无统计学意义.各病理类型1p/19q联合缺失的比例从高到低依次为少突胶质细胞瘤(9/16)、间变性少突胶质细胞瘤(3/8)、星形细胞瘤(2/10)、间变性星形细胞瘤(1/6)及胶质母细胞瘤(1/21),其差异有统计学意义(P < 0.01).在全组63例胶质瘤及25例含少突成分胶质瘤中,MGMT阳性肿瘤1p/19q联合缺失比例与MGMT阴性组间的差异皆无统计学意义.结论 1p/19q联合缺失主要与胶质瘤的病理类型有关,含少突成分胶质瘤中1p/19q联合缺失比例较高.1p/19q联合缺失可作为少突胶质细胞瘤病理诊断的重要参考指标.  相似文献   

4.
原发性和继发性GBM分子遗传水平研究进展   总被引:1,自引:0,他引:1  
胶质母细胞瘤Glioblastoma(GBM)可以分为原发性和继发性两种。这两种肿瘤的病理组织学改变在光学显微镜下很难区分,但在发生、发展、临床表现及预后均有显著差异。原发性GBM特征性分子遗传学改变是EGFR基因的扩增、10号染色体杂合性的缺失,多数伴有PTEN的突变、P16INK4a杂合性的缺失及MDM2的扩增。继发性GBM特征性的分子遗传学改变为P53基因突变和染色体17p杂合性的缺失,大多数也存在10q、19q杂合性丢失。  相似文献   

5.
目的根据2016年WHO中枢神经系统肿瘤分类第4版修订方案(2016年WHO指南),探讨分子标志物对病理诊断和预后的指导意义。方法对既往诊断为少突-星形细胞瘤或间变少突-星形细胞瘤的病例回顾病理检查结果参照2016年WHO指南重新进行整合性诊断。收集2014至2016年,45例经手术切除后组织病理诊断为少突-星形细胞瘤及间变少突-星形细胞瘤的病例。采用直接测序法检测IDH1/2基因突变及TERT启动子区突变,采用荧光原位杂交(FISH)检测1p/19q的共缺失状态,采用甲基化特异性PCR(MSP)方法检测O6-甲基鸟嘌呤-DNA甲基转移酶(MGMT)甲基化水平。分析TERT启动子突变及MGMT甲基化与患者总生存期和无复发生存期的关系。结果依据2016年WHO指南,结合IDH基因突变、1p/19q共缺失等分子标志物特征,45例整合诊断为:少突胶质细胞瘤(IDH突变型和1p/19q共缺失)22例;弥漫性胶质瘤[IDH野生型(IDH野生型和1p/19q共缺失)]2例;弥漫星形细胞瘤(IDH突变型8例,IDH野生型3例)11例;间变少突胶质细胞瘤(IDH突变型和1p/19q共缺失)2例;间变弥漫星形细胞瘤(IDH突变型3例,IDH野生型1例)4例;少突-星形细胞瘤(未知类型)4例。TERT启动子突变及MGMT甲基化的患者总生存期较短,但差异无统计学意义。结论依据2016年WHO指南和更新的修改建议,并不能把既往诊断为少突-星形细胞瘤的患者进行完全分类;此类混合性胶质瘤的生物学和遗传学特征还需进行深入研究。  相似文献   

6.
目的分析对比幕上异柠檬酸脱氢酶(IDH)突变型及野生型低级别胶质瘤的影像学特征,并与病理相关指标进行统计及相关性分析。方法手术及病理证实82例低级别胶质瘤(WHOⅡ级),其中IDH突变型39例,IDH1野生型43例,术前行核磁共振影像(MRI)增强扫描61例,按照无强化、轻度强化、中度强化、重度强化分别进行统计,并与增殖细胞核抗原Ki-67(Ki-67)标记指数、钙黏蛋白(CD34)CD34及1号染色体短臂/19号染色体长臂(1p/19q)杂合性联合缺失(co-deleiton)情况进行统计及相关性分析。结果 IDH突变低级别胶质瘤好发于右侧额叶,其次为右侧颞叶和左侧颞叶,IDH野生型低级别胶质瘤好发于左侧额叶,其次为左侧颞叶和右侧颞叶,经Fisher's Exact Test检验,二者间有统计学差异(P0.05)。肿瘤IDH是否突变导致的肿瘤强化程度、Ki-67、CD34及1p/19q联合缺失差异均无统计学意义(P0.05)。肿瘤强化程度与Ki-67指标呈正相关性(Spearman秩相关分析),与CD34和1p/19q联合缺失,无统计学意义的相关性。结论 IDH1突变低级别胶质瘤具有显著的好发部位,以右侧额叶为主,右侧颞叶其次,低级别胶质瘤无论IDH是否突变其常规增强MRI表现无明显差异。  相似文献   

7.
正2016年世界卫生组织()中枢神经系统肿瘤分类定义一种罕见的胶质神经元肿瘤,以弥漫性软脑膜病变为特征,肿瘤细胞形态类似少突胶质细胞,部分病例可见神经元分化;存在BRAF基因融合及染色体1p缺失或1p/19q-共缺失,不存在异柠檬酸脱氢酶(IDH)基因突变。弥漫性软脑膜胶质神经元肿瘤好发于儿童和青少年,组织学形态观察,肿瘤组织由低至中等密  相似文献   

8.
正2016年世界卫生组织(WHO)中枢神经系统肿瘤分类将"少突胶质细胞瘤,异柠檬酸脱氢酶(IDH)-突变和1p/19q-共缺失"定义为弥漫性浸润、生长缓慢、IDH1/2-突变、染色体1p/19q-共缺失的胶质瘤。组织学形态,肿瘤组织由形态类似少突胶质细胞的肿瘤细胞组成,胞核圆形、大小较一致,胞质肿胀、透亮;典型病例常可见微钙化、分支状毛细血管,亦可见星形细胞瘤样成分(图1)。免疫组织化学染色,多数肿瘤细胞胞质强阳性表达R132H-突变的IDH1(图2a),较少细胞胞核表达P53,由于肿瘤缺乏ATRX突变,常可见胞核表达ATRX(图2b),小肥胖细胞和神经胶质纤维性少突胶质细胞胞质表达胶质纤维酸性蛋白  相似文献   

9.
目的 探讨少突胶质细胞起源肿瘤基因组DNA失衡及其与病理分级的关系.方法 用比较基因组杂交技术检测了33例少突胶质细胞起源肿瘤石蜡包埋组织,分析其全基因组DNA失衡状况.结果 少突胶质细胞瘤(ODG)及间变性少突胶质细胞瘤(AODG)的基因组DNA失衡检出率分别为100%(16/16)和88%(15/17),共发现24个有DNA获得和24个有DNA丢失的染色体区带.其中,-19q、-1p/-19q联合性缺失检出率在ODG组明显高于AODG组(P<0.05),+7p检出率在AODG组明显高于ODG组(P<0.05).在22对常染色体及X染色体中,+1q、+7P、+8P、+8q、+9q、+18p、+18q、+20p及-1p、-19q、-Xq出现频率较高.+2q、+4p、+4q、+6p、+10p、+15q、+20q、+22q仅见ODG组,+11q、+12p、+Xp仅见于AODG组.而-3p、-5q、-8p、-12p、-12q、-15q、-19p、-20q、-XP仅见ODG组,-2q、-4p、-4q、-5p、-6q、-7p、-11q、-14q仅见于AODG组.结论 ODG和AODG均有各自特征性的染色体基因组DNA失衡谱;-1p/-19q是评价国人该类肿瘤生物学行为的重要参考指标,对治疗敏感性及患者预后判断有重要的指导意义;+7p和-19q对评估国人该类肿瘤的生物学行为和患者预后有一定参考价值.
Abstract:
Objective To investigate the relationship between genomic DNA imbalance in oligodendroglial tumors and its different classification.Method 16 oligodendrogliomas and 17 anaplastic oligodendrogliomas were investigated by comparative genomic hybridization on Paraffin-Embedded tissue samples, and the chromosomal genomic DNA imbalances were analyzed.Results Chromosome DNA imbalance rates in oligodendrogliomas and anaplastic oligodendrogliomas are 100% and 88% respectively,and chromosomal regions of 24 gains and 24 losses were found in these tumors.19q loss and 1p/19q loss are frequent in oligodendroglioma.The gain of 7p happened predominantly in anaplastic oligodendroglioma, and their differences were significant(P < 0.05 ).+ 1q, + 7p, + 8p, + 8q, + 9q, + 18p, + 18q, + 20p and-1p,-19q,-Xq are frequently occurred in oligodendroglial tumors.+2q, +4p, +4q, +6p, + 10p,+ 15q, + 20q and + 22q are only identified in oligodendroglioma, + 11q, + 12p and + Xp are only identified in anaplastic oligodendroglioma.-3p,-5q,-8p,-12p,-12q,-15q,-19p,-20q and-Xp are only identified in oligodendroglioma, and-2q,-4p,-4q,-5p,-6q,-7p,-11q and-14q are only identified in anaplastic oligodendroglioma.Conclusions The characteristic imbalance spectrum of oligodendroglial tumors is the molecular genetic base to determine their histological phenotype and grade.-1p/-19q are also the important molecular genetic markers to estimate biological behavior,chemotherapy sensitivity of these tumors and patients' prognosis.+7p and-19q may be useful to evaluate the biological behavior of these tumors and patients' prognosis.  相似文献   

10.
目的探讨弥漫性软脑膜胶质神经元肿瘤的临床病理学和分子遗传学特征。方法与结果男性患儿,5岁9个月,临床表现为严重脑积水伴抽搐发作2次;头部MRI显示,双侧侧脑室明显增宽,提示脑积水,并出现双侧小脑上沟散在斑片样异常略高信号影;脊椎MRI显示,T5~7水平脊髓增粗,可见髓内异常略高信号影;增强扫描可见脑干表面、双侧小脑半球表面脑膜、全脊膜和部分硬脊膜、马尾神经增厚并强化征象。遂行胸髓病变探查切除术+椎管重建术,术中可见蛛网膜与软脊膜之间半透明胶冻样异常组织增生,堵塞蛛网膜下隙。组织学形态,低或中等密度的形态单一的少突胶质细胞样肿瘤细胞,在软脑膜内呈弥漫性或巢团样生长,未见坏死和核分裂象。免疫组织化学染色,肿瘤细胞胞核表达少突胶质细胞转录因子2,胞质表达突触素、微管相关蛋白-2和S-100蛋白,Ki-67抗原标记指数为4%~10%。荧光原位杂交显示单独1p杂合性缺失。最终诊断为弥漫性软脑膜胶质神经元肿瘤。患者共住院22 d,出院后3个月死亡。结论 2016年世界卫生组织中枢神经系统肿瘤分类第4版修订版新增弥漫性软脑膜胶质神经元肿瘤的诊断,但未予明确分级,目前国内尚无报道。由于该病较为少见且极易与其他中枢神经系统肿瘤和炎症性病变相混淆,因此组织学形态、免疫组织化学染色和分子遗传学特征显得尤为重要。  相似文献   

11.
OBJECTIVE: To investigate possible correlations between molecular alterations and tumor location in Chinese patients with oligodendroglial tumors. METHODS: A series of 105 gliomas, including 42 oligoastrocytomas, and two control groups of 28 oligodendrogliomas and 35 astrocytomas, were retrospectively reviewed. In each case, the radiologic picture and loss of heterozygosity (LOH) on chromosome 1p and 19q detected by denaturing high-performance liquid chromatography (DHPLC) were analyzed. Correlations between molecular profile and tumor location were made by chi-square and Fisher's exact tests. RESULTS: Oligodendroglial tumors located in the nontemporal lobes were significantly more likely to have combination of LOH 1p and LOH 19q than tumors arising in the insula, temporal lobe, and temporal with another lobe (p=0.001). Subgroup analysis confirmed this finding in oligodendrogliomas (p=0.006), but the difference did not reach significance in the oligoastrocytoma group, although the trend was similar (p=0.067). In contrast to the oligodendroglial tumors, we detected no association between molecular alterations and location for diffuse astrocytomas. CONCLUSION: We conclude that molecular subsets of oligodendroglial tumors may arise preferentially in certain lobes of the brain, with tumors having LOH 1p and LOH 19q occurring most frequently in the nontemporal lobes. These findings suggest that molecular subsets of oligodendroglial tumors may arise from site-specific precursor cells, which has provided some information for the current management of these neoplasms in China.  相似文献   

12.
Aims: The objective of the present study was to verify the correlation of chromosomes 1p and 19q status and expressions of O6-methylguanine DNA methyltransferase (MGMT), p53 and Ki-67 in diffuse gliomas of World Health Organization grades II and III. Methods: A series of 146 diffuse gliomas, including 45 oligodendrogliomas, 42 oligoastrocytomas and 59 astrocytomas, were analysed by denaturing high-performance liquid chromatography for 1p and 19q status and by immunohistochemistry for MGMT, p53 and Ki-67 expression patterns. The molecular alterations were then correlated with clinicopathological characteristics and with each other. Results: Loss of heterozygosity (LOH) on 1p, combined LOH on 1p and 19q, low MGMT expression and high Ki-67 expression were associated with oligodendroglial tumours, whereas high p53 expression was associated with astrocytic and mixed tumours. LOH on 1p and low MGMT expression were associated with grade II oligodendroglial tumours, whereas high expressions of p53 and Ki-67 were associated with grade III oligodendroglial tumours. In addition, high Ki-67 expression was associated with grade III astrocytomas. LOH on 1p and LOH on 19q were associated with nontemporal oligodendroglial tumours. Nonrandom associations were found between LOH on 1p and LOH on 19q, MGMT expression and p53 expression, and MGMT expression and Ki-67 expression, whereas mutual exclusions were found between LOH on 1p and 19q and p53 expression, and LOH on 1p and Ki-67 expression. Conclusions: The present study revealed significant interrelationships of the investigated molecular alterations and clinicopathological characteristics in diffuse gliomas of World Health Organization grades II and III, which support a promising role of molecular markers in the diagnostic assessment of these neoplasms.  相似文献   

13.
Glioblastoma multiforme is the most malignant astrocytic glioma and usually resistant to chemotherapy. A small fraction of glioblastomas may contain areas with histological features of oligodendroglial differentiation. To determine the molecular genetic alterations in such "glioblastomas with oligodendroglial component", we investigated 13 of these tumors for genetic alterations and/or expression of the TP53, CDKN2A, PTEN, and EGFR genes. In addition, we performed microsatellite analyses for loss of heterozygosity (LOH) on chromosome arms 1p, 19q and 10q. None of tumors showed evidence for LOH on 10q. LOH on 1p was detected in 3 tumors, 1 of which additionally showed LOH on 19q. The 3 tumors with LOH on 1p showed neither TP53 mutations nor nuclear p53 accumulation. In contrast, 9 of 10 tumors without demonstrated losses on 1p showed nuclear p53 accumulation. TP53 mutations were identified in 3 of these cases. Further aberrations detected were epidermal growth factor receptor (EGFR) overexpression (3 of 13 tumors), homozygous CDKN2A deletion (2 of 11 tumors), and PTEN mutation (1 of 13 tumors). Taken together, our results indicate that "glioblastomas with oligodendroglial component" carry heterogeneous genetic alterations. LOH on 10q, PTEN mutation, and homozygous CDKN2A deletion appear to be less common in these tumors as compared to ordinary glioblastomas. Furthermore, a subset of these tumors demonstrates LOH on 1p, i.e., an alteration that has recently been linked to chemosensitivity and good prognosis in anaplastic oligodendrogliomas.  相似文献   

14.
BACKGROUND: Loss of heterozygosity (LOH) on 1p and 19q is observed in most oligodendroglial tumors. LOH on 10q appears to be less common in these tumors as compared to other gliomas. PATIENTS AND METHODS: We reviewed 14 patients with oligodendroglial tumors (10 low-grade and 4 anaplastic oligodendroglioma) to evaluate the frequency of LOH on 1p, 10q and 19q and correlate it with tumor grade and patients' age and gender; 5 loci on 1p and 5 on 19q as well as 4 on 10q were analyzed for LOH using PCR techniques. RESULTS: LOH on 1p together with 19q was detected in 6 tumors, 1 tumor showed deletion of 19q accompanied with deletion on 10q. Deletion on 1p was associated with deletion of 19q (p < 0.005) and mutual associations among deletions at loci on 19q (p < 0.05) were found. Patients with LOH on 1p were younger on average than patients with retained heterozygosity (p = 0.05). Grade II oligodendrogliomas predominated among younger patients (p < 0.01) while grade III oligodendrogliomas predominated among women (p < 0.005). No association between LOH on 1p nor 19q and tumor grade or patients' gender was found. CONCLUSION: Our study provides several clinically interesting findings and further supports the hypothesis of chromosome 1p and 19q involvement in the oligodendroglial cancerogenesis.  相似文献   

15.
To identify a better diagnostic criteria for oligodendroglial tumors, we investigated the clinical, histological, and immunohistochemical features that would be able to predict a 1p/19q loss of heterozygosity (LOH) in these tumors. We performed a PCR-based LOH test with the 1p and 19q microsatellite markers by microdissecting tumor in 56 samples (44 oligodendrogliomas and 12 mixed oligoastrocytomas) of paraffin-embedded tissue. Patients with oligodendroglial tumors with 1p/19q LOH had a statistically significant better prognosis for overall survival. Comparative analysis of several features indicated that the 1p/19q LOH tumors were associated with two histological features, tumor cellularity and perinuclear halo, and low O6-methylguanine-DNA-methyltransferase (MGMT) expression and high cytoplasmic glutathione S-transferase pi (GST-) expression. In addition, the incidence of 1p/19q LOH was infrequent in the youngest age category (less than 20 years old) studied. Using the new features, we could predict the 1p/19q status of oligodendroglial tumors with greater than 90% accuracy. Therefore, applying these features in clinical practice, would be helpful in clarifying oligodendroglial tumor diagnosis.  相似文献   

16.
Glioblastoma (GBM) is considered by the WHO classification to represent the most malignant grade of the astrocytic tumors. However, a subset of GBM includes recognizable areas with oligodendroglial features, suggesting that some GBM may also have an oligodendroglial origin. The aim of this study was to analyze the molecular profile of GBM associated with an oligodendroglial component (GBMO). We analyzed a series of 25 GBMO. Loss of heterozygosity (LOH) on 1p and 19q, known as common markers of oligodendroglial tumors, were observed in 40% and 60% of cases, respectively; 72% of the tumors displayed one or both of these markers. All but 4 tumors (84%) showed alterations known to be preferentially involved in the progression of astrocytic tumors to GBM, such as EGFR amplification (44%), P16 deletion (48%), LOH on 10q (64%), PTEN (20%), and TP53 (24%) mutations. Therefore, GBMO displayed all the genetic aberrations found in "standard" GBM with a comparable incidence, but differed from GBM by having a higher rate of LOH on 1p and 19q. These results suggest that GBMO might represent a subgroup of tumors of oligodendroglial origin that is distinct from the "standard" GBM in terms of tumorigenesis pathway.  相似文献   

17.
A polymorphous variant of oligodendroglioma was described by K.J. Zülch half a century ago, and is only very sporadically referred to in the subsequent literature. In particular, no comprehensive analysis with respect to clinical or genetic features of these tumors is available. From a current perspective, the term polymorphous oligodendroglioma (pO) may appear as contradictory in terms, as nuclear monotony is a histomorphological hallmark of oligodendrogliomas. For the purpose of this study, we defined pO as diffusely infiltrating gliomas felt to be of oligodendroglial rather than astrocytic differentiation and characterized by the presence of multinucleate tumor giant cells and/or nuclear pleomorphism. In a total of nine patients, we identified tumors consistent with this working definition. All tumors were high‐grade. We characterized these with respect to clinical, histomorphological and genetic features. Despite clinical and genetic heterogeneity, we identified a subset of tumors of bona fide oligodendroglial differentiation as characterized by combined loss of heterozygosity of chromosome arms 1p and 19q (LOH 1p19q). Those tumors that lacked LOH 1p19q showed a high frequency of IDH1 mutations and loss of alpha thalassemia/mental retardation syndrome X‐linked gene (ATRX) immunoreactivity, indicating a possible phenotypic convergence of true oligodendrogliomas and gliomas of the alternative lengthening of telomeres (ALT) pathway. p53 alterations were common irrespective of the 1p19q status. Histomorphologically, the tumors featured interspersed bizarre multinucleate giant tumor cells, while the background population varied from monotonous to significantly pleomorphic. Our findings indicate, that a rare polymorphous – or “giant cell” – variant of oligodendroglioma does indeed exist.  相似文献   

18.
To evaluate the role of molecular genetics in the routine clinic, we investigated allelic imbalance at 1p36, 19q13, 17p13, 10p12-15, and 10q22-26 and p53 mutation in 100 oligodendroglial neoplasms diagnosed at a single treatment center between 2000 and 2003. The -1p/-19q genotype, seen in 64, 34, 77, and 30% of OII, OAII, OIII, and OAIII respectively, was inversely related to p53 mutation and 17p13 loss. Genotype was unrelated to tumor location and could not distinguish high-grade tumors that presented de novo from those that progressed from a previous lower grade malignancy. Presentation with seizures was more common in cases with the -1p/-19q genotype, and these remained stable for longer before treatment. In longitudinal samples, 74% retained their initial histological differentiation, whereas 29% showed new genetic alterations, the -1p/-19q genotype being acquired in three cases. Loss of 1p36 and 19q13, 17p13, chromosome 10, and p53 mutation were significantly associated with survival from presentation in Kaplan-Meier analysis (p < 0.01), and loss of 1p36 and 19q13 and loss of 17p13 retained significance in multivariate analysis. In this recently diagnosed unselected series, clinical differences in tumors with and without the -1p/-19q genotype support a genetic approach to aid diagnosis and prognostication for oligodendroglial neoplasms.  相似文献   

19.
OBJECTIVE AND IMPORTANCE: Oligodendroglial tumors rarely occur after radiation therapy. Here, we report a rare case of anaplastic oligodendroglioma arising after radiation therapy, in which genetic analysis was performed. CLINICAL PRESENTATION AND INTERVENTION: A 41-year-old man who had received radiation therapy for a tumor of the suprasellar and pineal regions 31 years previously, presented with headache and progressive right hemiparesis. Magnetic resonance (MR) images revealed a ring-enhanced mass lesion in the left frontal lobe. Total removal of the tumor was performed through left frontoparietal craniotomy, and the histologic diagnosis was anaplastic oligodendroglioma. Using 23 microsatellite markers, the allelic status of chromosomes 1p, 10, 17p and 19q was evaluated by a PCR-based loss of heterozygosity (LOH) assay. Markers on chromosomes 1p, 17p and 19q revealed LOH, but none of the markers on chromosome 10 showed LOH. Based on the genetic analysis, this tumor was considered to be sensitive to chemotherapy. Two courses of chemotherapy, with procarbazine, ACNU and vincristine, were performed. However, tumor recurrence was detected only 3 months after the surgery. Despite additional radiochemotherapy, the tumor aggressively increased in size and the patient died with multiple recurrent tumors 1 year after surgery. CONCLUSION: The anaplastic oligodendroglioma presented in this report showed a more aggressive clinical course than was expected from the genetic analysis. The significance of 1p and 19q LOH in radiation-induced oligodendroglial tumors might differ from that in spontaneous counterparts.  相似文献   

20.
Tumor-related seizures are a well-known presenting symptom of primary brain tumors, particularly low-grade gliomas (LGGs). The objective of the present study was to investigate the possible correlation between tumor-related seizures and molecular genetic profile in Chinese patients with LGGs. A series of 103 LGGs, including 27 oligodendrogliomas, 41 oligoastrocytomas and 35 astrocytomas, was analyzed by denaturing high-performance liquid chromatography (DHPLC) for 1p and 19q status, with particular emphasis on correlations with tumor-related seizures. Most oligodendrogliomas and oligoastrocytomas had LOH 1p and LOH 19q, which were rarely seen in combination in astrocytomas (p<0.001). LOH 1p and LOH 19q were also closely associated (p=0.022). The majority of patients with LGGs presented with seizures at disease onset (68.9% of all patients). The most common seizure type was secondary generalized seizures (81.7% of patients with seizures). Patients without LOH 19q were more likely to present with seizures (p=0.033), particularly secondary generalized seizures (p=0.005), than those with this alteration. The current study presented an update on studies on tumor-related seizures and molecular genetic profile, and brought forward putative candidate genes for secondary generalized seizures on chromosome 19q, based on the assumption that common molecular genetic pathways may exist for glioma development and tumor-related seizures.  相似文献   

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