儿童小脑髓母细胞瘤几种标记物的免疫组化表达分析

目的 :研究儿童髓母细胞瘤的组织发生和Ki67、p5 3、C erbB 2与其发生及预后的关系。方法 :采用SP免疫组化法检测 7例正常小脑、2 2例髓母细胞瘤Ki67、p5 3、C erbB 2、GFAP和NSE的表达。结果 :髓母细胞瘤中GFAP、NSE表达率分别为 45 5 %、5 9 1%。髓母细胞瘤中Ki67、p5 3和C erbB 2的表达率显著高于正常小脑 ,P <0 0 5。未分化组、经典型、肿瘤直径 >5cm组髓母细胞瘤Ki67、p5 3高表达 ,P <0 0 5 ;C erbB 2则与肿瘤坏死和肿瘤大小有关 ,P <0 0 5。结论 :髓母细胞瘤起源于原始神经外胚叶组织 ,具有双向分化潜能。Ki67、p5 3和C erbB 2与髓母细胞瘤的发生及预后有关     

髓母细胞瘤组织学起源和细胞分化的探讨(附10例髓母细胞瘤的光镜和电镜观察)

关于髓母细胞瘤的组织学起源问题,至今仍有争论。本文收集髓母细胞瘤10例、8个半月胎儿小脑1例和成人小脑1例,分别进行光镜和电镜观察。髓母细胞瘤细胞主要是未分化的原始细胞。有的瘤细胞表现神经元性分化特点,光镜下出现菊形团排列,电镜下出现轴突样结构、突触样结构和致密核心小泡。有的瘤细胞则表现星形细胞特点,分化出磷钨酸苏木素染色阳性突起的幼稚的成胶质细胞和星形细胞,电镜下细胞的胞体和突起内出现成束的胶质微丝。表明了髓母细胞瘤是一种神经上皮性肿瘤,瘤细胞具有双向分化的潜能。髓母细胞瘤细胞和胎儿小脑外颗粒层细胞在形态上有很大相似性,和成人内颗粒层细胞在形态上没有相似性,说明在神经上皮之中,本瘤更可能起源于小脑外颗粒层或其残余,而不是起源于颗粒神经元。     

亲神经性黑色素型肿瘤

中枢神经系统黑色素型肿瘤由黑色素后与各类黑色素型肿瘤共同构成，本院１０年期间诊治ＣＮＳ黑色素瘤、黑色素型髓母细胞瘤、黑色素型神经鞘瘤、黑色素型脑膜瘤和黑色素型神经节细胞瘤共１３例，占同期颅内肿瘤的０．５％。黑色素后出现与黑痣、表皮样囊肿共生现象。黑色素型肿瘤具有双向生长模式和亲神经性的生物学行为，黑色素瘤与黑色素型肿瘤可否被认为是来自一个共同胚细胞异常分化的表现形式，尚待探讨。     

髓母细胞瘤淋巴结转移一例

髓母细胞瘤淋巴结转移一例宋志娥，顾子普，朱宝全，肖素华，刘明远髓母细胞瘤占颅内肿瘤的１．４％，占儿童颅内肿瘤的１５％－２０％。好发于儿童小脑蚓部，恶性度高，不仅复发率高，且有３０％－５０％肿瘤细胞可以随脑脊液播散；有５％病例向颅外转移至骨、肺，但淋巴...     

后颅凹占位性病变CT影像学探讨

收集１１７例经手术和病理证实的后颅凹占位病变病例，其中肿瘤１１４例，囊肿３例。髓母细胞瘤、星形细胞瘤及室管膜瘤多发生于青少年。小脑桥脑角好发听神经瘤、脑膜瘤、胆脂瘤，往往有四脑室侧移和后移。小脑蚓部好发髓母细胞瘤，占８２．４％，可引起四脑室前移。四脑室好发室管膜瘤，占８０％，引起四脑室扩大。小脑半球好发血管母细胞瘤、星形细胞瘤及多胶母细胞瘤、转移瘤，往往引起四脑室侧移及前移。后颅凹各种占位性病变都有ＣＴ影像学特征。可依据症状，与四脑室之间的关系，多可准确定位及定性诊断，本文定位诊断符合率为８９．７％。定位诊断准确率提高，可进一步提高定性诊断准确率。     

节细胞神经母细胞瘤的临床病理学及免疫组化研究

节细胞神经母细胞瘤（ｇａｎｇｌｉｏｎｅｕｒｏｂｌａｓｔｏｍａ，ＧＮＢ）与神经母细胞瘤（ｍｅｕｒｏｂｌａｓｔｏｍａ，ＮＢ）和神经节细胞瘤（ｇａｎ－ｇｌｉｏｎｅｕｒｏｍａ，ＧＮ）是同源性不同分化程度的肿瘤。前者的分化程度界于后两者之间。本文报告我院４０年来１１例ＧＮＢ的研究结果，探讨这种可见肿瘤的临床病理学特征、免疫组化及癌基因产物表达情况。１０例患者为２～６岁，１例为４４岁；８例男性，３例女性；原发部位７例在腹膜后，４例在纵隔。组织学分型，依据肿瘤内成热节细胞与神经母细胞的比例和分布不同，参照ｓｈｉｍａｄａ分类法分为中间混合型（包括Ａ型３例、Ｂ型２例）和结节型６例。免疫组化染色结果为ＮＳＥ９／９、ＣＧＡ８／１１Ｓ－１００９／１１、Ｐ５３蛋白３／１１、Ｃ—ｅｒｂ—Ｂ２９／１１、Ｐ２１蛋白５／６。ＮＳＥ、ＣＧＡ和Ｓ—１００可作为ＧＮＢ的标记物，具体应用时应２～３项合用并结合组织学图像，以提高诊断正确率。ＧＮＢ内肿瘤基因产物的表达提示其发生与这些肿瘤基因有关，但未发现它们之间有协同现象。说明该肿瘤的发生机理十分复杂，可能是多环节调节异常的结果。对该肿瘤的深入研究有待于资料的进一步积累。     

肝细胞癌中NOS和VEGF的表达及其与肿瘤血管形成的关系

目的 研究Ⅱ、Ⅲ型一氧化氮合酶（ｉＮＯＳ、ｃＮＯＳ）和血管内皮生长因子（ＶＥＧＦ）在肝细胞癌中的表达及其与肿瘤血管形成的关系。方法 应用免疫组化方法检测７１例肝细胞癌患者手术切除石蜡包埋标本ｉＮＯＳ、ｅＮＯＳ、ＶＥＧＦ的表达,抗ＣＤ３４单克隆抗体显示血管内皮细胞。根据ＣＤ３４阳性的血管内皮细胞计数来测定肿瘤微血管密度（ＭＶＤ）。结果 ｉＮＩＳ、ｅＮＯＳ分别在８１．３％、８５．９％的肝癌中阳性表达,     

非小细胞肺癌bFGF表达与微血管密度的意义

目的：探讨非小细胞肺癌（ＮＳＣＬＣ）组织中碱性成纤维细胞生长因子（ｂＦＧＦ）表达和微血管密度（ＭＶＤ）的意义。方法：采用免疫组化ＡＢＣ法检测７８例ＮＳＣＬＣ标本中ｂＦＧＦ表达和ＭＶＤ，并根据病理类型、组织学分化程度、有无区域淋巴结转移以及预后进行分析。结果：在ＮＳＣＬＣ中腺癌的ｂＦＧＦ表达阳性率和ＭＶＤ值显著高于鳞癌（Ｐ〈０．０５）；所有ＮＳＣＬＣ病例中，ｂＦＧＦ表达阳性率与肿瘤组织学分化程度有关     

层粘蛋白和纤维连接蛋白的表达与肺癌转移和预后的关系

目的：探讨原发性肺癌ＬＮ和ＦＮ的表达与转移及预后的关系。方法：采用免疫组化ＬＳＡＢ法检测１７９例肺癌标本中ＬＮ和ＦＮ的表达。结果：中、高分化的肺鳞癌的ＬＮ的表达强度明显不同于低分化者（ｔ＊＝３．０７，２．６７，Ｐ均＜０．０１），ＬＮ的表达强度在有无淋巴结转移的两组鳞癌间，差异具有显著性意义（χ２＝１１．１３，Ｐ＜０．０５），ＬＮ和ＦＮ的表达强度在鳞癌５年以上生存组明显不同于半年内死亡组（ｔ△＝２．８５，２．４９，Ｐ△＜０．０１，＜０．０５），ＦＮ表达强度在３组不同生存期的肺腺癌间，差异具有显著性意义（Ｈｃ＝７．５３，Ｐ＜０．０５）。结论：ＬＮ和ＦＮ的表达可作为评估肺癌淋巴结转移及预后的有价值的指标。     

脑胶质瘤中EGFR基因扩增和10号染色体杂合性丢失的研究

目的：探索素皮生长因子受体（ＥＧＦＲ）基因扩增及１０号染色体杂合性丢失（Ｌ０Ｈ１０）与胶质瘤发生、发展的关系。方法：采用Ｓｏｕｔｈｅｒｎ印迹杂交和ＲＦＬＰ方法对５５例各种类型的脑胶质瘤的ＥＧＦＲ基因扩增和１０号染色体杂合性丢失情况进行检测分析。结果：１７例Ⅲ－Ⅳ级恶性星细胞肿瘤中的７例（７／１７），１例髓母细胞瘤（１／１０），１例极性成胶质细胞瘤（１／５）和１例室管膜母细胞瘤，存在ＥＧＦＲ基因的扩     

Expression of glial fibrillary acidic protein in human medulloblastoma cells treated with recombinant glia maturation factor-beta.

Medulloblastoma, a common pediatric brain tumor, is a primitive neuroectodermal tumor which often displays neuronal and/or glial characteristics. We have investigated the consequences of treating cell lines derived from a human medulloblastoma with glia maturation factor-beta (GMF-beta), a protein found in mammalian brain. GMF-beta promotes growth arrest and morphological alteration of cultured glioma and neuroblastoma cells. The proliferation of medulloblastoma cells was arrested 24-48 hr after exposure to human recombinant GMF-beta. During the same period, treated cells acquired a morphology similar to that of mature astrocytes. By 72 hr, all treated cells bound an antibody against glial fibrillary acidic protein (GFAP), a distinguishing biochemical feature of mature astrocytes. Immunoreactivity was accompanied by de novo expression of GFAP mRNA. Our observations are the first demonstration of the induction of morphological and biochemical characteristics of mature astrocytes in cultured medulloblastoma-derived cells by an exogenous factor.     

Diffusion MRI in Evaluation of Pediatric Posterior Fossa Tumors

Background: To evaluate the role of diffusion MRI in differentiating pediatric posterior fossa tumors and determine the cut-off values of ADC ratio to distinguish medulloblastoma from other common tumors. Methods: We retrospectively reviewed MRI of 90 patients (7.5-year median age) with pathologically proven posterior fossa tumors (24 medulloblastoma, 7 ependymoma, 4 anaplastic ependymoma, 13 pilocytic astrocytoma, 30 diffuse intrinsic pontine glioma (DIPG), 4 ATRT, 3 diffuse astrocytoma, 2 high grade astrocytoma, 2 glioblastoma, and 1 low grade glioma). The conventional MRI characteristics were evaluated. Two readers reviewed DWI visual scale and measured ADC values by consensus.  ADC measurement was performed at the solid component of tumors. ADC ratio between the tumors to cerebellar white matter were calculated. Results: The ADC ratio of medulloblastoma was significantly lower than ependymoma, pilocytic astrocytoma and DIPG. The ADC cut-off ratio of ≤ 1.115 allowed discrimination medulloblastoma from other posterior fossa tumors with sensitivity, specificity, PPV and NPV of 95.8%, 81%, 67.6% and 97.9%, respectively. ADC ratio cut-off level to differentiate medulloblastoma from ependymoma was ≤ 0.995 with area under the curve (AUC)= 0.8693. ADC ratio cut-off level for differentiate medulloblastoma from pilocytic astrocytoma at ≤ 1.17 with AUC = 0.9936. ADC cut-off level for differentiate medulloblastoma from DIPG at ≤ 1.195 with AUC = 0.9681. The ADC ratio was correlated with WHO grading by the lower ADC ratio associated with the higher grade. Furthermore, High DWI visual scale was associated with high grade tumor. Conclusion: Diffusion MRI has a significant role in diagnosis of pediatric posterior fossa tumors. ADC ratio can be used to distinguish medulloblastoma from other posterior fossa tumor with good level of diagnostic performance.     

The modulation of astrocytic differentiation in cells derived from a medulloblastoma surgical specimen

Medulloblastomas are cerebellar tumors which are primarily composed of sheets of uniform, small malignant cells and may have astrocytic, neuronal or no features typical of these cell types. The assessment of astrocytic differentiation in medulloblastoma rests largely on the detection in malignant cells of glial fibrillary acidic protein (GFAP), a marker present in the later stages of normal astrocyte differentiation. It is still not known whether cells that do not contain GFAP in medulloblastomas with astrocytic differentiation correspond to highly proliferative astrocyte progenitors in maturation arrest at earlier stages of differentiation. The purpose of the current study was to examine whether cells in short term culture derived from a medulloblastoma tumor specimen with astrocytic differentiation were of the astrocytic lineage and if so, whether they represented proliferative astrocyte progenitors which would morphologically and antigenically mature in response to differentiating agents. A portion of tumor specimen from a 10-month-old child with recurrent posterior fossa medulloblastoma (RB2) that contained GFAP focally in tumor cells was grown in monolayer culture. We examined cellular structure and appearance of western immunoblotting and immunohistochemical studies for GFAP and neuron-specific enolase (NSE) in RB2 cells before and after treatment with retinoic acid (RA) and dibutyryl cyclic AMP (dBcAMP). RB2 in culture consisted of small polygonal cells (93%), large flat cells (3%), and polygonal cells with cytoplasmic processes (4%). In untreated RB2, 30% of cells expressed GFAP and staining for NSE was negative. RA treatment produced flattened cells and decreased GFAP. DBcAMP reversibly induced fine cytoplasmic processes containing GFAP in 85% of cells within 96h. Neither agent induced NSE. The results suggest that cultured cells which are derived from a medulloblastoma with astrocytic differentiation do not spontaneously differentiate but that treatment with dBcAMP suppresses proliferation, enhances cytoplasmic process formation and increases cytoplasmic GFAP. Cells in culture and in medulloblastoma tumor specimens which do not contain GFAP may represent astrocyte progenitors in maturation arrest.     

72例标危型髓母细胞瘤放疗剂量对生存的影响

目的 回顾分析标危型髓母细胞瘤采用全脑全脊髓放疗剂量≤24 Gy和>24 Gy对预后的影响。方法 标危型髓母细胞瘤定义为年龄>3岁、未发生转移、肿瘤全切或近全切(残留≤1.5 cm³)。2003—2013年共入组72例初治儿童、青少年标危型髓母细胞瘤患者。患者术后接受全脑全脊髓+局部瘤床放疗和8个疗程辅助化疗,化疗方案为顺铂、司莫司汀或卡莫司汀联合长春新碱。按放疗剂量≤24 Gy和>24 Gy分为A、B组(20、52例),比较两组患者复发率和生存率。Kaplan-Meier法计算复发率和生存率并Logrank法检验组间差异。结果 A组接受全脑全脊髓放疗19.2~24.0 Gy,B组接受全脑全脊髓放疗24.1~30.6 Gy。放疗后66例(92%)患者完成全部辅助化疗。共11例患者复发。随访满3年患者48例,其中复发11例,死亡7例。全组3年EFS率为83%,3年OS率为86%。A组和B组患者3年EFS率分别为84%和83%(P=0.609), 3年OS率分别为85%和87%(P=0.963)。结论 标危型髓母细胞瘤经规范综合治疗效果较好,其中全脑全脊髓放疗剂量减少至19.2~24.0 Gy未影响疗效。     

HO-1和Nrf-2在髓母细胞瘤中的表达和意义

  目的  髓母细胞瘤是儿童后颅凹常见恶性肿瘤, 本研究目的在于检测Nrf-2和HO-1在髓母细胞瘤中的表达, 并探讨其在髓母细胞瘤发生发展的意义。  方法  应用免疫组化SP法检测41例髓母细胞瘤及27例瘤旁对照脑组织中Nrf-2和HO-1的表达, 并结合研究病例的临床资料(患者性别、年龄、临床症状、肿瘤大小、肿瘤病理分型), 进行相关性分析。  结果  在髓母细胞瘤病例中, Nrf-2和HO-1的阳性表达率(分别为82.9%, 78.0%)与瘤旁对照组织的阳性表达率(分别为37.0%, 29.6%)相比明显升高, 差异具有显著统计学意义(P < 0.001), 并且二者之间呈显著正相关关系(P < 0.05)。但Nrf-2和HO-1的表达与分析的病例的临床特征无显著相关性(P > 0.05)。  结论  Nrf-2和HO-1的高表达可能在髓母细胞瘤的发生发展中发挥重要作用。      

Pediatric brain tumours at a tertiary care hospital in Karachi.

The objectives of this study were to determine the epidemiology of brain tumors during infancy and childhood and to define and segregate childhood brain tumors vis-a-vis their morphological characteristics. The present study includes pediatric brain tumors, ICD-10 category C71 encountered during 10 years (January 1989 through December 1998) at a tertiary care hospital in Karachi. Eighty one cases were included, 58 (71.6%) in males and 23 (28.4%) in females with a male to female ratio of 2.5:1. The cases were divided into 3 age groups each covering five years of life (0-4, 5-9, 10-14 years), with the greatest number in the second age group i.e. 5-9 years followed by the third age group and the 0-4 year age group. The mean age for all cases, both genders was 8.8 years (95% CI 7.9; 9.6) with a marginal variation for cases occurring in the cerebrum and cerebellum. The malignancies occurred at a younger age in the males for each subcategory by site and morphology. The morphological distribution of cases was astrocytoma (28 cases, 34.6%), primitive neuroectodermal tumor or PNET (40 cases; 49.4%), ependymoma (8 cases, 10%), mixed glioma (4 cases; 5%) and a case of oligodendroglioma. The 81 malignancies included in this study were further categorized by site into two groups, supratentorial (27 cases; 33.3%) and infratentorial (54 cases; 66.7%). The morphological categorization of supratentorial tumors was astrocytoma (17 cases; 63%), ependymoma (5 cases; 18.5%), mixed glioma (2 cases; 7.4%). PNET with rhabdoid differentiation, oligodendroglioma and pinealoblastoma comprised 1 case (3.7%) each. The 17 supratentorial astrocytoma were sub-categorized as follows - pilocytic astrocytoma (5 cases; 29.4%), grade II astrocytoma (6 cases; 35.3%); grade III astrocytoma (2 cases; 11.8%), anaplastic astrocytoma (1 case; 5.9%) and glioblastoma multiforme (3 cases; 17.7%). The morphological categorization of infratentorial tumors was astrocytoma (11 cases; 20.4%), medulloblastoma (38 cases; 70.4%), ependymoma (3 cases; 5.6%) and mixed glioma - astroependymoma (2 cases, 3.7%). The morphological sub-categorization of infratentorial astrocytoma was pilocytic astrocytoma (7 cases, 63.6%), with gemistocytic astrocytoma, grade II, grade III and anaplastic astrocytoma comprising 1 (9.1%) case each. The morphological categorization of medulloblastoma was classical medulloblastoma (15 cases; 39.5%), desmoplastic medulloblastoma (8 cases; 21.1%), medulloblastoma with astrocytic differentiation (12 cases; 31.5%), medulloblastoma with neural differentiation (2 cases; 5.3%), and neuroblastic medulloblastoma (1 case; 2.6%). The pediatric brain tumors in Karachi reflect a developing country scenario, with a strong male predisposition and a late presentation with a peak in the 5-9 year age group. There is a predominance of medulloblastoma and a paucity of astrocytomas. The current study is a single institution study and needs cautious interpretation. Population-based studies are required to determine the cancer burden due to pediatric malignancies of the brain in this population and for the morphological categorization of brain tumors in Karachi.     

Risk-adapted craniospinal radiotherapy followed by high-dose chemotherapy and stem-cell rescue in children with newly diagnosed medulloblastoma (St Jude Medulloblastoma-96): long-term results from a prospective, multicentre trial

BACKGROUND: Current treatment for medulloblastoma, which includes postoperative radiotherapy and 1 year of chemotherapy, does not cure many children with high-risk disease. We aimed to investigate the effectiveness of risk-adapted radiotherapy followed by a shortened period of dose-intense chemotherapy in children with medulloblastoma. METHODS: After resection, patients were classified as having average-risk medulloblastoma (< or = 1.5 cm2 residual tumour and no metastatic disease) or high-risk medulloblastoma (> 1.5 cm2 residual disease or metastatic disease localised to neuraxis) medulloblastoma. All patients received risk-adapted craniospinal radiotherapy (23.4 Gy for average-risk disease and 36.0-39.6 Gy for high-risk disease) followed by four cycles of cyclophosphamide-based, dose-intensive chemotherapy. Patients were assessed regularly for disease status and treatment side-effects. The primary endpoint was 5-year event-free survival; we also measured overall survival. This study is registered with ClinicalTrials.gov, number NCT00003211. FINDINGS: Of 134 children with medulloblastoma who underwent treatment (86 average-risk, 48 high-risk), 119 (89%) completed the planned protocol. No treatment-related deaths occurred. 5-year overall survival was 85% (95% CI 75-94) in patients in the average-risk group and 70% (54-84) in those in the high-risk group (p=0.04); 5-year event-free survival was 83% (73-93) and 70% (55-85), respectively (p=0.046). For the 116 patients whose histology was reviewed centrally, histological subtype correlated with 5-year event-free survival (p=0.04): 84% (74-95) for classic histology, 77% (49-100) for desmoplastic tumours, and 57% (33-80) for large-cell anaplastic tumours. INTERPRETATION: Risk-adapted radiotherapy followed by a shortened schedule of dose-intensive chemotherapy can be used to improve the outcome of patients with high-risk medulloblastoma.     

髓母细胞瘤CT诊断(附93例报告)

目的探讨CT对髓母细胞瘤的诊断价值.方法对93例髓母细胞瘤的CT表现与手术病理对照进行回顾性分析,93例患者全部行CT检查,其中65例经MRI检查,全部病例经手术及病理证实.结果髓母细胞瘤好发于10岁以下儿童（88%）,且肿瘤位于小脑蚓部,成人则常发生在一侧小脑半球.肿瘤血运较丰富,可有囊变、坏死（25%）,偶有钙化（7%）.其影像学特点是肿瘤呈高或略高密度肿块影,有中等度较均一增强,有8%增强不显著.结论髓母细胞瘤恶性度高、预后差,其CT表现有一定的特异性.     

Loss of Heterozygosity Analysis of Chromosome 17p13.1–13.3 and its Correlation with Clinical Outcome in Medulloblastomas

Cytogenetic and molecular genetic studies have shown that deletions on the short arm of chromosome 17 distal to p53 locus are the most common genetic events in medulloblastoma. We examined the occurrences and frequencies of allelic deletions on chromosome 17p13.1-13.3 by loss of heterozygosity (LOH) analysis to investigate the possible involvement of 17p13.1-13.3 in medulloblastoma development. We also performed survival analysis to determine whether LOH analysis of 17p13.1-13.3 can be used to predict prognosis in medulloblastoma. Loss of heterozygosity was analyzed by polymerase chain reaction on chromosome 17p13.1-13.3 using three microsatellite markers, TP53 on 17p13.1, D17S796 on 17p13.1-13.2, and D17S1574 on 17p13.3, in 17 medulloblastoma DNAs extracted either from archival tissue or fresh frozen tissue specimens. Allelic deletions were detected in five of 17 informative cases (29%) on TP53, eight of 17 informative cases (47%) on D17S796, and four of 17 informative cases (24%) on D17S1574. Overall, nine of 17 cases (53%) showed LOH on chromosome 17p13.1-13.3. The 5-year progression free survival (PFS) and 5-year overall survival rates were identical (59%). The 5-year PFS for nine medulloblastoma patients with LOH on 17p13.1-13.3 was 56%, and the 5-year PFS for eight medulloblastoma patients without LOH on 17p13.1-13.3 was 63%. In our survival analysis, we did not find a significant association between survival and LOH on 17p13.1-13.3. Our results support the notion that deletions of chromosome 17p13.1-13.3 may be involved in the pathogenesis of medulloblastoma. From survival analysis, we conclude that LOH on chromosome 17p13.1-13.3 may not be a significant predictor of prognosis in medulloblastoma.     

Expression of major histocompatibility complex on human medulloblastoma cells with neuronal differentiation

Medulloblastomas are among the most common malignant brain tumors in children. These tumors consist of immature bipotential cells that may differentiate into neuronal and glial cells. We have established two cell lines for human medulloblastoma. One was derived from a 2-year-old girl with a cerebellar tumor (designated as ONS-76) and another from a 9-year-old girl with a metastatic tumor in the right frontal lobe (ONS-81). The in vitro population-doubling times were 18.6 and 19.2 h, respectively. Immunohistochemical studies showed that both cells possessed neurofilament protein (Mr 145,000 and 200,000) and neuron-specific enolase, without glial fibrillary acidic protein or S-100 protein. Human gamma-interferon enhanced class I major histocompatibility complex antigens on these medulloblastoma cells. Class II major histocompatibility complex antigens were also induced by human interferon-gamma. We here report for the first time the expression of class II major histocompatibility antigens, which play an important role in immune response, on human medulloblastoma cells with neuronal differentiation.