不同1p杂合缺失特性少枝胶质细胞瘤患者预后与差异蛋白相关性研究
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摘要
胶质瘤是中枢神经系统最常见的肿瘤,发病率高,但治愈率低。尽管外科新技术的发展以及化疗、放疗的广泛应用使得胶质瘤的预后有所改善,但是大多数胶质瘤的预后仍然较差。少枝胶质细胞瘤(Oligodendroglioma, OG)占胶质瘤的4-15%,占所有原发脑肿瘤的2-5%,是常见的成人神经系统恶性肿瘤之一,也是第一个经临床试验证实其预后与肿瘤的基因特征有关联的中枢神经系统肿瘤。研究发现这些对化疗敏感的少枝胶质瘤大都具有1p/19q的杂合性缺失(Loss of heterozygosity, LOH)。进一步的研究显示具有不同1p/19q LOH(或1p LOH)特征的这两类肿瘤在很多方面还有差异,如好发部位、肿瘤对放疗的敏感性及最终的预后等等。这些都说明在光镜下无法区分的这两种肿瘤可能是两类分子生物学特征不同的肿瘤,对它们的分型可能有助于临床的治疗和预后的判断。目前除了1p/19q染色体的差异以外,人们已经在两类肿瘤中找到了表达差异的蛋白,但是对差异蛋白与患者雨后的关联及最终的分子生物学机制仍然知之不多,所以有必要对此进一步的研究。
免疫组化是临床上常用的对病理进行辅助诊断的方法,操作简单,费用便宜,它可以通过对细胞内染色的有无进行定性,通过染色的位置进行蛋白的定位,并根据染色的深浅程度进行半定量的检测。我们此次使用免疫组化的方法对已确定1p19q分型的患者的肿瘤标本切片进行半定量的蛋白检测,并探讨差异蛋白与少枝胶质瘤患者预后情况的相关性。
胶质瘤病人的身体状况、活动能力及医疗需求等情况常用Karnofsky行为评分(KPS)来评估,将患者按照自己的身体状况分为11个等级,从100(无症状及体征)到0(死亡)依次递减。自从1948年问世以来,KPS已经成为应用最广泛的评估患者身体状况的方法。一般认为分值大于60分的患者方可以耐受常规的癌症治疗方案或者可纳入临床试验。我们对已进行少枝胶质细胞瘤切除的患者进行随访,通过KPS评分对患者的术后身体情况进行评估,并与差异蛋白进行相关性的探讨。
第一部分HMGB1、MAP2、UBA1、ATP6V1E1蛋白在
不同1p LOH特征的少枝胶质瘤中的表达差异性
目的：验证HMGB1、MAP2、UBA1、ATP6V1E1等差异蛋白在不同1pLOH特征的少枝胶质瘤中的表达并分析其意义。
方法：用免疫组化的方法验证HMGB1、MAP2、UBA1、ATP6V1E1等4种差异蛋白在23例1p杂合性缺失和21例1p正常的少枝胶质瘤标本中的表达的差异性
结果：免疫组化对44例少枝胶质细胞瘤标本的HMGB1、MAP2、ATP6V1E1的半定量分析结果显示在1pLOH组OG中的表达较1p正常组高,UBA1的表达在1p正常组OG中较1pLOH组高。
结论：HMGB1、MAP2、UBA1、ATP6V1E1在不同1p LOH特性的少枝胶质瘤中的表达具有差异性,这些特异蛋白都有望用于免疫组化诊断实现对OG的分子分型,并进一步用于OG的预后判断和指导治疗。
第二部分MAP2、ATP6V1E1蛋白与少枝胶质瘤患者预后的相关性
目的：探讨MAP2和ATP6V1E1两种差异蛋白与少枝胶质瘤患者预后情况的相关性
方法：随访33例少枝胶质细胞瘤患者术后2年的KPS评分,将评分变化与MAP2和ATP6V1E1两种差异蛋白的免疫组化评分进行比较,探讨其相关性
结果：MAP2及ATP6V1E1两种蛋白与少枝胶质瘤患者术后KPS评分进展有着显著地相关性,将两种蛋白的IHC评分整合后,这一相关性进一步加强。
结论：MAP2及ATP6V1E1与少枝胶质瘤的化疗敏感性及预后有关,有望用于临床对于胶质瘤的预后判断、分子分型和指导治疗,并进一步探讨少枝胶质瘤的发病机制。
Glioma is one of the most common central nervous system tumors. The incidence of glioma is high and the treatment efficacy has not been satisfactory. Better prognosis of glioma has been achieved with the improvement of surgical technique and the widespread application of chemotherapy and radiotherapy, however the overall prognosis of most gliomas is still poor. Oligodendroglioma(OG) is one major type of gliomas, which accounts for2-5%of primary brain neoplasms and4-15%of gliomas. Because these tumors respond well to chemotherapy and have good prognosis, the reason for this is becoming a hot topic in glioma research. It was reported that response to chemotherapy and good prognosis of OG patients were closely related to the presence of allelic losses on lp(or1p and19q) in the resected tumor tissue. Further research revealed that OGs with or without1p LOH had profound differences, such as tumor location, response to radiotherapy, prognosis. So the two types of OGs undistinguishable under optical microscopy may be tumors with different molecular biological character. The molecular classification of OGs may be helpful to their diagnosis and therapy. Except for the difference of lp/19q LOH, other features, such as expression of genes, proteins, and molecular biological mechanisms, are not clearly defined for the OGs. Further studies are needed to elucidate the molecular signatures, and thus possible mechanisms of OGs with1p LOH.
Immunohistochemistry is one of the most common pathology diagnosis method, which is easy to operate and cheap cost. It can achieve semi-quantitative detection depending on the situation of intracellular staining. We use immunohistochemistry to semi-quantitatively detect the proteins in OG with and without1p LOH, discuss the correlation between differential proteins and prognosis of patients.
The physical condition, activity ability and medical requirement of OG patients is usually estimate by Karnofsky Performance Scale (KPS). It is divided into11grades depending on the physical condition of the patient, from100(no symptom or clinical sign) to0(death). KPS is considered to be one of the most common used scale to estimate the condition of patient since inception in1948. It is generally acknowledged that the patients whose KPS is more than60can tolerant normaltherapeutic schedule and be included into clinical trials. We follow up the patients who has recepted OG resection, estimate the condition by KPS and discuss the correlation between differential proteins and prognosis of patients
Part I:The expression of HMGB1, MAP2, UBA1, ATP6V1E1in OGs with different1p LOH and its significance
Objective:To examine the expression of HMGB1, MAP2, UBA1, ATP6V1E1in OGs tissues with different1p LOH.
Methods:The expression of HMGB1, MAP2, UBA1, ATP6V1E1were validated in44independent OGs tissue samples with different1p LOH status using IHC method.
Results:The result of IHC validated that the expression of HMGB1, MAP2and ATP6V1E1was higher in OGs with1p LOH than in OGs without1p LOH, while the expression of UBA1was higher in OGs without1p LOH than in OGs with1p LOH.
Conclusion:The results of IHC show the difference in the expression of proteins in OGs tissues with different1p LOH.These specific proteins may be useful in diagnosis, prognosis and treatment selection for OG patients.
Part Ⅱ:Correlation analysis between MAP2, ATP6V1E1and prognosis of oligodendroglioma patients
Objective:To discuss the correlation between MAP2, ATP6V1E1and prognosis of patients.
Methods:33OG patients was followed-up with KPS score, compared the change of KPS score with IHC score of MAP2and ATP6V1E1, and discuss the correlation.
Results:The change of KPS score was significantly related to the IHC score of MAP2and ATP6V1E1. The correlation was further improve after we combined the IHC scores of these two proteins.
Conclusion:MAP2and ATP6V1E1may be related to sensitivity of chemotherapy and the prognosis. It can be used in judgment of prognosis, the direction of therapy, and further discussion of pathogenesis.
免疫组化是临床上常用的对病理进行辅助诊断的方法,操作简单,费用便宜,它可以通过对细胞内染色的有无进行定性,通过染色的位置进行蛋白的定位,并根据染色的深浅程度进行半定量的检测。我们此次使用免疫组化的方法对已确定1p19q分型的患者的肿瘤标本切片进行半定量的蛋白检测,并探讨差异蛋白与少枝胶质瘤患者预后情况的相关性。
胶质瘤病人的身体状况、活动能力及医疗需求等情况常用Karnofsky行为评分(KPS)来评估,将患者按照自己的身体状况分为11个等级,从100(无症状及体征)到0(死亡)依次递减。自从1948年问世以来,KPS已经成为应用最广泛的评估患者身体状况的方法。一般认为分值大于60分的患者方可以耐受常规的癌症治疗方案或者可纳入临床试验。我们对已进行少枝胶质细胞瘤切除的患者进行随访,通过KPS评分对患者的术后身体情况进行评估,并与差异蛋白进行相关性的探讨。
第一部分HMGB1、MAP2、UBA1、ATP6V1E1蛋白在
不同1p LOH特征的少枝胶质瘤中的表达差异性
目的：验证HMGB1、MAP2、UBA1、ATP6V1E1等差异蛋白在不同1pLOH特征的少枝胶质瘤中的表达并分析其意义。
方法：用免疫组化的方法验证HMGB1、MAP2、UBA1、ATP6V1E1等4种差异蛋白在23例1p杂合性缺失和21例1p正常的少枝胶质瘤标本中的表达的差异性
结果：免疫组化对44例少枝胶质细胞瘤标本的HMGB1、MAP2、ATP6V1E1的半定量分析结果显示在1pLOH组OG中的表达较1p正常组高,UBA1的表达在1p正常组OG中较1pLOH组高。
结论：HMGB1、MAP2、UBA1、ATP6V1E1在不同1p LOH特性的少枝胶质瘤中的表达具有差异性,这些特异蛋白都有望用于免疫组化诊断实现对OG的分子分型,并进一步用于OG的预后判断和指导治疗。
第二部分MAP2、ATP6V1E1蛋白与少枝胶质瘤患者预后的相关性
目的：探讨MAP2和ATP6V1E1两种差异蛋白与少枝胶质瘤患者预后情况的相关性
方法：随访33例少枝胶质细胞瘤患者术后2年的KPS评分,将评分变化与MAP2和ATP6V1E1两种差异蛋白的免疫组化评分进行比较,探讨其相关性
结果：MAP2及ATP6V1E1两种蛋白与少枝胶质瘤患者术后KPS评分进展有着显著地相关性,将两种蛋白的IHC评分整合后,这一相关性进一步加强。
结论：MAP2及ATP6V1E1与少枝胶质瘤的化疗敏感性及预后有关,有望用于临床对于胶质瘤的预后判断、分子分型和指导治疗,并进一步探讨少枝胶质瘤的发病机制。
Glioma is one of the most common central nervous system tumors. The incidence of glioma is high and the treatment efficacy has not been satisfactory. Better prognosis of glioma has been achieved with the improvement of surgical technique and the widespread application of chemotherapy and radiotherapy, however the overall prognosis of most gliomas is still poor. Oligodendroglioma(OG) is one major type of gliomas, which accounts for2-5%of primary brain neoplasms and4-15%of gliomas. Because these tumors respond well to chemotherapy and have good prognosis, the reason for this is becoming a hot topic in glioma research. It was reported that response to chemotherapy and good prognosis of OG patients were closely related to the presence of allelic losses on lp(or1p and19q) in the resected tumor tissue. Further research revealed that OGs with or without1p LOH had profound differences, such as tumor location, response to radiotherapy, prognosis. So the two types of OGs undistinguishable under optical microscopy may be tumors with different molecular biological character. The molecular classification of OGs may be helpful to their diagnosis and therapy. Except for the difference of lp/19q LOH, other features, such as expression of genes, proteins, and molecular biological mechanisms, are not clearly defined for the OGs. Further studies are needed to elucidate the molecular signatures, and thus possible mechanisms of OGs with1p LOH.
Immunohistochemistry is one of the most common pathology diagnosis method, which is easy to operate and cheap cost. It can achieve semi-quantitative detection depending on the situation of intracellular staining. We use immunohistochemistry to semi-quantitatively detect the proteins in OG with and without1p LOH, discuss the correlation between differential proteins and prognosis of patients.
The physical condition, activity ability and medical requirement of OG patients is usually estimate by Karnofsky Performance Scale (KPS). It is divided into11grades depending on the physical condition of the patient, from100(no symptom or clinical sign) to0(death). KPS is considered to be one of the most common used scale to estimate the condition of patient since inception in1948. It is generally acknowledged that the patients whose KPS is more than60can tolerant normaltherapeutic schedule and be included into clinical trials. We follow up the patients who has recepted OG resection, estimate the condition by KPS and discuss the correlation between differential proteins and prognosis of patients
Part I:The expression of HMGB1, MAP2, UBA1, ATP6V1E1in OGs with different1p LOH and its significance
Objective:To examine the expression of HMGB1, MAP2, UBA1, ATP6V1E1in OGs tissues with different1p LOH.
Methods:The expression of HMGB1, MAP2, UBA1, ATP6V1E1were validated in44independent OGs tissue samples with different1p LOH status using IHC method.
Results:The result of IHC validated that the expression of HMGB1, MAP2and ATP6V1E1was higher in OGs with1p LOH than in OGs without1p LOH, while the expression of UBA1was higher in OGs without1p LOH than in OGs with1p LOH.
Conclusion:The results of IHC show the difference in the expression of proteins in OGs tissues with different1p LOH.These specific proteins may be useful in diagnosis, prognosis and treatment selection for OG patients.
Part Ⅱ:Correlation analysis between MAP2, ATP6V1E1and prognosis of oligodendroglioma patients
Objective:To discuss the correlation between MAP2, ATP6V1E1and prognosis of patients.
Methods:33OG patients was followed-up with KPS score, compared the change of KPS score with IHC score of MAP2and ATP6V1E1, and discuss the correlation.
Results:The change of KPS score was significantly related to the IHC score of MAP2and ATP6V1E1. The correlation was further improve after we combined the IHC scores of these two proteins.
Conclusion:MAP2and ATP6V1E1may be related to sensitivity of chemotherapy and the prognosis. It can be used in judgment of prognosis, the direction of therapy, and further discussion of pathogenesis.
引文
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19. Fallon KB, Palmer CA, Roth KA, et al:Prognosticvalue of 1p,19q,9p, 10q, and EGFR-FISHanaiyses in recurrent oligodendrogliomas[J]. J NeuropatholExp Neurol 2004:63:314-322.
20. Ino Y, Betensky RA, Zlatescu MC, et al:Molecularsubtypes of anaplastic oligodendroglioma:Implications for patient management at diagnosis[J].Clin Cancer Res 2001:7:839-845.
21. van den Bent MJ, Chinot O, Boogerd W, et al:Second-line chemotherapy with temozolomide inrecurrent oligodendroglioma after PCV (procarbazine,lomustine and vincristine) chemotherapy:EORTC Brain Tumor Group phase Ⅱ study 26972[J].Ann Oncol 2003:14:599-602.
22. van den Bent MJ, Dellatre JY, Brandes AA, etal:First analysis of EORTC trial 26951, a randomizedphase Ⅲ study of adjuvant PCV chemotherapy inpatients with highly anaplastic olidogdneroglioma[R].Presented at the American Society of Clinical Oncology41st Annual Meeting, Orlando, FL, May 2005:13-17.
23. Bauman GS, Ino Y, Ueki K, et al:Allelic loss ofchromosome 1p and radiotherapy plus chemotherapyin patients with oligodendrogliomas[J]. Int J RadiatOncol Biol Phys 2000:48:825-830.
1. Cairncross G, Macdonald D, Ludwin S et al. Chemotherapy for anaplasticoligodendroglioma. National Cancer Institute of Canada Clinical TrialsGroup[J]. J Clin Oncol 1994; 12:2013-2021.
2. van den Bent MJ, Kros JM, Heimans JJ et al. Response rate and prognosticfactors of recurrent oligodendroglioma treated with procarbazine, CCNU,and vincristine chemo therapy [J]. Dutch Neuro-oncology Group. Neurology1998;51:1140-1145.
3. Smith JS, Perry A, Borell TJ, et al:Alterationsof chromosome arms 1p and 19q as predictors ofsurvival in oligodendrogliomas, astrocytomas, andmixed oligoastrocytomas[J]. J Clin Oncol 2000:18:636-645.
4. Reifenberger G, Kros JM, Burger P et al. Oligodendroglioma. In:KleihuesP, Cavenee WK, eds. World Health Organization Classification of Tumours[M].Pathology and Genetics of Tumours of the Nervous System. Lyon,France:IARC Press,2000:55-70.
5. Kamiya M, Nakazato Y:The expression of cellcycle regulatory proteins in oligodendroglial tumors[J].Clin Neuropathol 2002:21:52-65.
6. Reifenberger G, Reifenberger J, Liu L, et al:Molecular Genetics of Oligodendroglial Tumors[A], inNagai M (ed):Brain Research and Therapy. Toyko,Japan, Springer-Verlag,1996:187-209.
7. Reifenberger G, Reifenberger J, Liu L, et al:Molecular genetic analysis of oligodendroglial tumorsshows preferential allelic deletions on 19q andlp[J]. Am J Pathol 1994:145:1175-1190.
8. Reifenberger J, Reifenberger G, Gies U, et al:Analysis of p53 mutation and epidermal growthfactor receptor amplification in recurrent gliomaswith malignant progression[J]. J Neuropathol ExpNeurol 1996:55:822-831.
9. Maintz D, Fiedler K, Koopmann J, et al:Moleculargenetic evidence for subtypes of oligoastrocytomas[J].J Neuropathol Exp Neurol 1997:56:1098-1104.
10. Bigner SH, Rasheed BK, Wiltshire R, et al.Morphologic and molecular genetic aspects of oligodendroglialneoplasms[J]. Neuro-Oncol 1999:1:52-60.
11. Van den Bent MJ, Taphoorn MJ, Brandes AA,et al:Phase Ⅱ study of first-line chemotherapy withtemozolomide in recurrent oligodendroglial tumors:The European Organization for Research and Treatmentof Cancer Brain Tumor Group Study 26971 [J].J Clin Oncol 2003:21:2525-2528.
12. Kreiger PA, Okada Y, Simon S, et al:Losses ofchromosomes 1p and 19q are rare in pediatricoligodendrogliomas[J]. Acta Neuropathol (Berl) 2005:109:387-392.
13. Smith JS, Perry A, Borell TJ, et al:Alterationsof chromosome arms 1p and 19q as predictors ofsurvival in oligodendrogliomas, astrocytomas, andmixed oligoastrocytomas[J]. J Clin Oncol 2000:18:636-645.
14. Buckner, JC, Ballman KV, Scheithauer RM, etal:NCCTG 94-72-53:Diagnostic and prognostic significanceof 1p and 19q deletions in patients (pts)with low-grade oligodendroglioma and astrocytoma[J].J Clin Oncol 2005:23:114s.
15. Felsberg J, Erkwoh A, Sabel MC, et al:Oligodendroglialtumors:Refinement of candidate regionson chromosome arm 1p and correlation oflp/19q status with survival[J]. Brain Pathol 2004:14:121-130
16. Nayak A, Ralte AM, Sharma MC, et al:p53protein alterations in adult astrocytic tumors andoligodendrogliomas[J]. Neurol India 2004:52:228-232.
17. Johnson MD, Vnencak-Jones CL, TomsSA, et al:Allelic losses in oligodendroglial andoligodendroglioma-like neoplasms:Analysis usingmicrosatellite repeats and polymerase chain reaction[J].Arch Pathol Lab Med 2003:127:1573-1579.
18. Fallon KB, Palmer CA, Roth KA, et al:Prognosticvalue of 1p,19q,9p, 10q, and EGFR-FISHanalyses in recurrent oligodendrogliomas[J]. J NeuropatholExp Neurol 2004:63:314-322.
19. Ino Y, Betensky RA, Zlatescu MC, et al:Molecularsubtypes of anaplastic oligodendroglioma:Implications for patient management at diagnosis[J].Clin Cancer Res 2001:7:839-845.
20. van den Bent MJ, Chinot O, Boogerd W, et al:Second-line chemotherapy with temozolomide inrecurrent oligodendroglioma after PCV (procarbazine,lomustine and vincristine) chemotherapy:EORTC Brain Tumor Group phase Ⅱ study 26972[J].Ann Oncol 2003:14:599-602.
21. van den Bent MJ, Dellatre JY, Brandes AA, etal:First analysis of EORTC trial 26951, a randomizedphase Ⅲ study of adjuvant PCV chemotherapy inpatients with highly anaplastic olidogdneroglioma[R].Presented at the American Society of Clinical Oncology41st Annual Meeting, Orlando, FL, May 2005:13-17.
22. Bauman GS, Ino Y, Ueki K, et al:Allelic loss ofchromosome 1p and radiotherapy plus chemotherapyin patients with oligodendrogliomas[J]. Int J RadiatOncol Biol Phys 2000:48:825-830.
23. Shaw E, Arusell R, Scheithauer B, et al:Prospectiverandomized trial of low-versus high-doseradiation therapy in adults with supratentorial lowgradeglioma: Initial report of a North Central CancerTreatment Group/Radiation Therapy OncologyGroup/Eastern Cooperative Oncology Group study[J].J Clin Oncol 2002:20:2267-2276.
24. CBTRUS Statistical Report:Primary Brain Tumorsin the United States, 1997-2001 [R]. Hinsdale, IL,Central Brain Tumor Registry of the United States,2004.
25. Buccoliero AM, Arganini L, Ammannati F, etal:Oligodendrogliomas lacking O6-methylguanine-DNA-methyltransferase expression[J]. J Chemother 2005:17:321-326.
26. Nijjar TS, Simpson WJ, Gadalla T, et al:Oligodendroglioma:The Princess Margaret Hospital experience(1958-1984)[J]. Cancer 1993:71:4002-4006.
27. Lebrun C, Fontaine D, Ramaioli A, et al:Longtermoutcome of oligodendrogliomas:Nice BrainTumor Study Group[J]. Neurology 2004:62:1783-1787
28. Cairncross G, Seiferheld W, Shaw E, et al:Anintergroup randomized controlled clinical trial (RCT)of chemotherapy plus radiation (RT) versus RT alonefor pure and mixed anaplastic oligodendrogliomas:Initial report of RTOG 94-02[J]. J Clin Oncol 2004:22:107s(abstr TA-09).
29. Schiffer D, Dutto A, Cavalla P, et al:Prognosticfactors in oligodendroglioma[J]. Can J Neurol Sci 1997:24:313-319.
30. Daumas-Duport C, Tucker ML, Kolles H, et al:Oligodendrogliomas:Part Ⅱ:A new grading systembased on morphological and imaging criteria[J]. J Neurooncol 1997:34:61-78.
31. Dehghani F, Schachemnayr W, Laun A, et al:Prognostic implication of histopathological, immunohistochemicaland clinical features of oligodendrogliomas:A study of 89 cases[J]. Acta Neuropathol (Berl) 1998:95:493-504.
32. Cairncross JG, Macdonald DR:Successfulchemotherapy for recurrent malignant oligodendroglioma[J].Ann Neurol 1988:23:360-364.
33. Paleologos NA, Macdonald DR, Vick NA, et al:Neoadjuvant procarbazine, CCNU, and vincristine foranaplastic and aggressive oligodendroglioma[J]. Neurology 1999:53:1141-1143.
34. Fortin D, Macdonald DR, Stitt L, et al:PCV foroligodendroglial tumors:In search of prognosticfactors for response and survival[J]. Can J Neurol Sci 2001:28:215-223.
35. Jeremic B, Shibamoto Y, Gruijicic D, et al:Combined treatment modality for anaplastic oligodendroglioma:A phase Ⅱ study[J]. J Neurooncol 1999:43:179-185.
36. Cairncross G, Seiferheld W, Shaw E, et al:AnIntergroup randomized controlled clinical trial (RCT)of chemotherapy plus radiotherapy (RT) versus RTalone for pure and mixed anaplastic oligodendroglioma:Initial report of RTOG 94-02 [R]. Presented at theSociety for Neuro-Oncology 9th Annual ScientificMeeting, Toronto, Canada, November2004:18-21.
37. Chahlavi A, Kanner A, Peereboom D, et al:Impact of chromosome 1p status in response ofoligodendroglioma to temozolomide:Preliminary results[J].J Neurooncol 2003:61:267-273.
38. Vogelbaum M, Berkey B, Peereboom D, et al:Phase Ⅱ trial of pre-irradiation and concurrent temozolomidein patients with newly diagnosed anaplasticoligodendrogliomas and mixed anaplastic oligodendrogliomas[J].J Clin Oncol 2005:23:119s, (abstr 1520).
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8. Mukasa A, Ueki K, Matsumoto S, et al. Distinction in gene expression profiles of oligodendrogliomas with and without allelic loss of 1p [J]. Oncogene, 2002,21:3961-3968.
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1. Tanaka Y, Yokoo H, Komori T, et al. A distinct pattern of olig2-positive celluar distribution in papillary glioneuronal tumors:a manifestation of the oligodendroglial phenotype? [J]. Acta Neuropathol,2005,110:39-47.
2. Smith JS, Perry A, Borell TJ, et al. Alterations of chromosome armslp and 19q as predictors of survival in oligodendrogliomas, astrocytomas, and mixed oligoastrocytomas [J]. J Clin Oncol,2000,18:636-645.
3. Mukasa A, Ueki K, Matsumoto S, et al. Distinction in gene expression profiles of oligodendrogliomas with and without allelic loss of 1p [J]. Oncogene, 2002,21:3961-3968.
4. Martin J.B. Taphoorn, Martin J, et al. Health-Related Quality of Life in Patients Treated forAnaplastic Oligodendroglioma With Adjuvant Chemotherapy:Results of a European Organisation for Research andTreatment of Cancer Randomized Clinical Trial [J]. J Clin Oncol,2007:25:5723-5730.
5. Herbert H. Engelhard, Ana Stelea, and Arno Mundt. Oligodendroglioma andAnaplastic Cligodendroglioma:Clinical Features, Treatment, and Prognosis [J]. Surg Neurol 2003;60:443-56.
6. Kurt A. Jaeckle, Karla V. Ballman, Ravi D. Rao, et al. Current Strategies in Treatment of Oligodendroglioma:Evolution of Molecular Signatures of Response [J]. J Clin Oncol,2006:24:1246-1252.
7. Gregory Cairncross, and Robert Jenkins. Gliomas With lp/19q Codeletion:a.k.a. Oligodendroglioma [J]. Cancer J 2008; 14:352-357.
8. T. Mikkclscn, T. Doyle, J. Anderson, et al. Temozolomide single-agent chemotherapy for newly diagnosedanaplastic oligodendroglioma [J]. J Neurooncol, 2009:92:57-63.
9. van den Bent MJ, Kros JM, Heimans JJ et al. Response rate and prognosticfactors of recurrent oligodendroglioma treated with procarbazine, CCNU,and vincristine chemotherapy[J]. Dutch Neuro-oncology Group. Neurology 1998;51:1140-1145.
10. Smith JS, Perry A, Borell TJ, et al:Alterationsof chromosome arms 1p and 19q as predictors ofsurvival in oligodendrogliomas, astrocytomas, andmixed oligoastrocytomas[J]. J Clin Oncol 2000:18:636-645.
11. Bigner SH, Rasheed BK, Wiltshire R, et al:Morphologic and molecular genetic aspects of oligodendroglialneoplasms[J]. Neuro-Oncol 1999:1:52-60.
12. Van den Bent MJ, Taphoorn MJ, Brandes AA,et al:Phase Ⅱ study of first-line chemotherapy withtemozolomide in recurrent oligodendroglial tumors:The European Organization for Research and Treatmentof Cancer Brain Tumor Group Study 26971 [J].J Clin Oncol 2003:21:2525-2528.
13. Kreiger PA, Okada Y, Simon S, et al:Losses ofchromosomes 1p and 19q are rare in pediatricoligodendrogliomas[J]. Acta Neuropathol (Berl) 2005:109:387-392.
14. Smith JS, Perry A, Borell TJ, et al:Alterationsof chromosome arms 1p and 19q as predictors ofsurvival in oligodendrogliomas, astrocytomas, andmixed oligoastrocytomas[J]. J Clin Oncol 2000:18:636-645.
15. Buckner, JC, Ballman KV, Scheithauer RM, etal:NCCTG 94-72-53:Diagnostic and prognostic significanceof 1p and 19q deletions in patients (pts)with low-grade oligodendroglioma and astrocytoma[J].J Clin Oncol 2005:23:114s.
16. Felsberg J, Erkwoh A, Sabel MC, et al:Oligodendroglialtumors:Refinement of candidate regionson chromosome arm 1p and correlation oflp/19q status with survival[J]. Brain Pathol 2004:14:121-130
17. Nayak A, Ralte AM, Sharma MC, et al:p53protein alterations in adult astrocytic tumors andoligodendrogliomas[J]. Neurol India 2004:52:228-232.
18. Johnson MD, Vnencak-Jones CL, TomsSA, et al:Allelic losses in oligodendroglial andoligodendroglioma-like neoplasms:Analysis usingmicrosatellite repeats and polymerase chain reaction[J].Arch Pathol Lab Med 2003:127:1573-1579.
19. Fallon KB, Palmer CA, Roth KA, et al:Prognosticvalue of 1p,19q,9p, 10q, and EGFR-FISHanaiyses in recurrent oligodendrogliomas[J]. J NeuropatholExp Neurol 2004:63:314-322.
20. Ino Y, Betensky RA, Zlatescu MC, et al:Molecularsubtypes of anaplastic oligodendroglioma:Implications for patient management at diagnosis[J].Clin Cancer Res 2001:7:839-845.
21. van den Bent MJ, Chinot O, Boogerd W, et al:Second-line chemotherapy with temozolomide inrecurrent oligodendroglioma after PCV (procarbazine,lomustine and vincristine) chemotherapy:EORTC Brain Tumor Group phase Ⅱ study 26972[J].Ann Oncol 2003:14:599-602.
22. van den Bent MJ, Dellatre JY, Brandes AA, etal:First analysis of EORTC trial 26951, a randomizedphase Ⅲ study of adjuvant PCV chemotherapy inpatients with highly anaplastic olidogdneroglioma[R].Presented at the American Society of Clinical Oncology41st Annual Meeting, Orlando, FL, May 2005:13-17.
23. Bauman GS, Ino Y, Ueki K, et al:Allelic loss ofchromosome 1p and radiotherapy plus chemotherapyin patients with oligodendrogliomas[J]. Int J RadiatOncol Biol Phys 2000:48:825-830.
1. Cairncross G, Macdonald D, Ludwin S et al. Chemotherapy for anaplasticoligodendroglioma. National Cancer Institute of Canada Clinical TrialsGroup[J]. J Clin Oncol 1994; 12:2013-2021.
2. van den Bent MJ, Kros JM, Heimans JJ et al. Response rate and prognosticfactors of recurrent oligodendroglioma treated with procarbazine, CCNU,and vincristine chemo therapy [J]. Dutch Neuro-oncology Group. Neurology1998;51:1140-1145.
3. Smith JS, Perry A, Borell TJ, et al:Alterationsof chromosome arms 1p and 19q as predictors ofsurvival in oligodendrogliomas, astrocytomas, andmixed oligoastrocytomas[J]. J Clin Oncol 2000:18:636-645.
4. Reifenberger G, Kros JM, Burger P et al. Oligodendroglioma. In:KleihuesP, Cavenee WK, eds. World Health Organization Classification of Tumours[M].Pathology and Genetics of Tumours of the Nervous System. Lyon,France:IARC Press,2000:55-70.
5. Kamiya M, Nakazato Y:The expression of cellcycle regulatory proteins in oligodendroglial tumors[J].Clin Neuropathol 2002:21:52-65.
6. Reifenberger G, Reifenberger J, Liu L, et al:Molecular Genetics of Oligodendroglial Tumors[A], inNagai M (ed):Brain Research and Therapy. Toyko,Japan, Springer-Verlag,1996:187-209.
7. Reifenberger G, Reifenberger J, Liu L, et al:Molecular genetic analysis of oligodendroglial tumorsshows preferential allelic deletions on 19q andlp[J]. Am J Pathol 1994:145:1175-1190.
8. Reifenberger J, Reifenberger G, Gies U, et al:Analysis of p53 mutation and epidermal growthfactor receptor amplification in recurrent gliomaswith malignant progression[J]. J Neuropathol ExpNeurol 1996:55:822-831.
9. Maintz D, Fiedler K, Koopmann J, et al:Moleculargenetic evidence for subtypes of oligoastrocytomas[J].J Neuropathol Exp Neurol 1997:56:1098-1104.
10. Bigner SH, Rasheed BK, Wiltshire R, et al.Morphologic and molecular genetic aspects of oligodendroglialneoplasms[J]. Neuro-Oncol 1999:1:52-60.
11. Van den Bent MJ, Taphoorn MJ, Brandes AA,et al:Phase Ⅱ study of first-line chemotherapy withtemozolomide in recurrent oligodendroglial tumors:The European Organization for Research and Treatmentof Cancer Brain Tumor Group Study 26971 [J].J Clin Oncol 2003:21:2525-2528.
12. Kreiger PA, Okada Y, Simon S, et al:Losses ofchromosomes 1p and 19q are rare in pediatricoligodendrogliomas[J]. Acta Neuropathol (Berl) 2005:109:387-392.
13. Smith JS, Perry A, Borell TJ, et al:Alterationsof chromosome arms 1p and 19q as predictors ofsurvival in oligodendrogliomas, astrocytomas, andmixed oligoastrocytomas[J]. J Clin Oncol 2000:18:636-645.
14. Buckner, JC, Ballman KV, Scheithauer RM, etal:NCCTG 94-72-53:Diagnostic and prognostic significanceof 1p and 19q deletions in patients (pts)with low-grade oligodendroglioma and astrocytoma[J].J Clin Oncol 2005:23:114s.
15. Felsberg J, Erkwoh A, Sabel MC, et al:Oligodendroglialtumors:Refinement of candidate regionson chromosome arm 1p and correlation oflp/19q status with survival[J]. Brain Pathol 2004:14:121-130
16. Nayak A, Ralte AM, Sharma MC, et al:p53protein alterations in adult astrocytic tumors andoligodendrogliomas[J]. Neurol India 2004:52:228-232.
17. Johnson MD, Vnencak-Jones CL, TomsSA, et al:Allelic losses in oligodendroglial andoligodendroglioma-like neoplasms:Analysis usingmicrosatellite repeats and polymerase chain reaction[J].Arch Pathol Lab Med 2003:127:1573-1579.
18. Fallon KB, Palmer CA, Roth KA, et al:Prognosticvalue of 1p,19q,9p, 10q, and EGFR-FISHanalyses in recurrent oligodendrogliomas[J]. J NeuropatholExp Neurol 2004:63:314-322.
19. Ino Y, Betensky RA, Zlatescu MC, et al:Molecularsubtypes of anaplastic oligodendroglioma:Implications for patient management at diagnosis[J].Clin Cancer Res 2001:7:839-845.
20. van den Bent MJ, Chinot O, Boogerd W, et al:Second-line chemotherapy with temozolomide inrecurrent oligodendroglioma after PCV (procarbazine,lomustine and vincristine) chemotherapy:EORTC Brain Tumor Group phase Ⅱ study 26972[J].Ann Oncol 2003:14:599-602.
21. van den Bent MJ, Dellatre JY, Brandes AA, etal:First analysis of EORTC trial 26951, a randomizedphase Ⅲ study of adjuvant PCV chemotherapy inpatients with highly anaplastic olidogdneroglioma[R].Presented at the American Society of Clinical Oncology41st Annual Meeting, Orlando, FL, May 2005:13-17.
22. Bauman GS, Ino Y, Ueki K, et al:Allelic loss ofchromosome 1p and radiotherapy plus chemotherapyin patients with oligodendrogliomas[J]. Int J RadiatOncol Biol Phys 2000:48:825-830.
23. Shaw E, Arusell R, Scheithauer B, et al:Prospectiverandomized trial of low-versus high-doseradiation therapy in adults with supratentorial lowgradeglioma: Initial report of a North Central CancerTreatment Group/Radiation Therapy OncologyGroup/Eastern Cooperative Oncology Group study[J].J Clin Oncol 2002:20:2267-2276.
24. CBTRUS Statistical Report:Primary Brain Tumorsin the United States, 1997-2001 [R]. Hinsdale, IL,Central Brain Tumor Registry of the United States,2004.
25. Buccoliero AM, Arganini L, Ammannati F, etal:Oligodendrogliomas lacking O6-methylguanine-DNA-methyltransferase expression[J]. J Chemother 2005:17:321-326.
26. Nijjar TS, Simpson WJ, Gadalla T, et al:Oligodendroglioma:The Princess Margaret Hospital experience(1958-1984)[J]. Cancer 1993:71:4002-4006.
27. Lebrun C, Fontaine D, Ramaioli A, et al:Longtermoutcome of oligodendrogliomas:Nice BrainTumor Study Group[J]. Neurology 2004:62:1783-1787
28. Cairncross G, Seiferheld W, Shaw E, et al:Anintergroup randomized controlled clinical trial (RCT)of chemotherapy plus radiation (RT) versus RT alonefor pure and mixed anaplastic oligodendrogliomas:Initial report of RTOG 94-02[J]. J Clin Oncol 2004:22:107s(abstr TA-09).
29. Schiffer D, Dutto A, Cavalla P, et al:Prognosticfactors in oligodendroglioma[J]. Can J Neurol Sci 1997:24:313-319.
30. Daumas-Duport C, Tucker ML, Kolles H, et al:Oligodendrogliomas:Part Ⅱ:A new grading systembased on morphological and imaging criteria[J]. J Neurooncol 1997:34:61-78.
31. Dehghani F, Schachemnayr W, Laun A, et al:Prognostic implication of histopathological, immunohistochemicaland clinical features of oligodendrogliomas:A study of 89 cases[J]. Acta Neuropathol (Berl) 1998:95:493-504.
32. Cairncross JG, Macdonald DR:Successfulchemotherapy for recurrent malignant oligodendroglioma[J].Ann Neurol 1988:23:360-364.
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