胶质瘤患者尿液,血液和瘤组织中表皮生长因子的含量及其意义

对５０例胶质瘤患者的血、尿和瘤组织ＥＧＦ含量进行了检测。结果发现，恶性胶质瘤患者尿液ＥＧＦ含量显著高于低恶度胶质瘤患者尿液ＥＧＦ含量。直线相关研究显示，尿ＥＧＦ含量与瘤组织ＥＧＦ含量及肿瘤分级呈正相关。胶质瘤患者血浆ＥＧＦ含量虽与肿瘤分级呈正相关，但不如尿液ＥＧＦ含量与肿瘤分级的相关性明显，若两者结合，可能对胶质瘤的恶性程度的预估更为可靠。肿瘤肉眼全切除术后胶质瘤患者血尿ＥＧＦ含量低于术前，近期疗效较好；手术活检或部分切除者１０例，术后血、尿ＥＧＦ含量不降低或有所增高，近期疗较差。说明检测尿ＥＧＦ有助于胶质瘤的临床诊断及恶性程度的评估，也可作为胶质瘤的标记之一     

细胞内p53蛋白积聚：人脑星形细胞瘤恶性进展的因素之一

用单克隆抗体Pabl 801行免疫组化研究48例不同恶性程度的人脑星形细胞瘤,发现17例(35.4%)p53蛋白染色阳性,其中核阳性者12例,胞浆阳性者5例。30例高恶度的星形细胞瘤中有14例(47%)阳性,其余18例低恶度的肿瘤有3例(17%)阳性,二者具有显著性差异。高恶度的肿瘤中p53染色阳性细胞百分比亦高于低恶度的肿瘤。该结果提示细胞内p53蛋白积聚是人脑星形细胞瘤由低恶度进展到高恶度的一个重要因素。     

非小细胞肺癌患者血清及肿瘤组织一氧化氮合酶活性变化及临床意义

目的　研究非小细胞肺癌患者血清和肿瘤组织中一氧化氮合酶 (NOS)的活性变化及其临床意义。方法　采用分光光度法检测 30例非小细胞肺癌患者血清及肿瘤组织中 NOS的活性 ,并分析其临床意义。结果　 (1)肺癌患者血清 NOS活性较正常人显著增高 (P<0 .0 1) ;(2 )术后血清 NOS活性较术前显著降低 (P<0 .0 1) ;(3)血清及肿瘤组织中 NOS活性随肺癌的恶性程度加重而增高 (P<0 .0 1)。结论　非小细胞肺癌患者血清及肿瘤组织中NOS活性的增高与肿瘤的生长及恶性行为有关     

大肠癌患者癌组织胃泌素表达与血清胃泌素水平的临床研究

目的：观察大肠癌患者血清胃泌素及肿瘤组织的ＧＡＳ表达情况。方法：采用放射免疫及免疫组化技术测定７０例大肠癌患者血清胃泌素水平。结果：胃泌素阳性表达率，中、低分化癌比高分化癌为高；粘液腺癌、印戒细胞癌、未分化腺癌较乳头状腺癌和管状腺癌为高，差异均非常显著（Ｐ＜０．０１）。结论：胃泌素阳性细胞过度表达可能是大肠癌分化不良的一个标志，且可能是肿瘤恶性程度增高的原因之一。血清胃泌素测定对诊断大肠癌灵敏度和特异性不高，但由于其升高为癌组织胃泌素阳性表达所致，与肿瘤的分化程度、恶性度、大小及分期密切相关。大肠癌病人术前血清胃泌素水平增高，则提示其肿瘤恶性程度较高，分期较晚，预后不良。     

隔蛋白7在神经上皮肿瘤中的表达

目的研究隔蛋白7（SEPT7）在神经上皮肿瘤中的表达。方法采用逆转录-聚合酶链反应（RT—PCR）方法检测47例胶质瘤标本以及4个胶质瘤细胞系中SEPT7的mRNA表达水平,以及免疫组化法研究了肿瘤标本以及组织芯片中SEPT7的表达状况。结果胶质瘤中SEPT7的表达水平随肿瘤恶性程度增加而明显降低,低恶度胶质瘤与高恶度胶质瘤的mRNA、蛋白表达水平差异有统计学意义;胶质瘤细胞系TJ905、TJ899未检测到SEPT7的表达,U251、TJ862细胞系中SEPT7表达水平较正常组织显著降低。结论RT—PCR和免疫组化检测表明SEPT7在神经上皮肿瘤中表达下调,可能与肿瘤的发生、发展有关联,值得进一步研究。     

血管内皮生长因子在食管癌组织中的表达及其临床意义研究

 目的 探讨食管癌组织中VEGF的表达水平与食管癌生物学特性的关系. 方法 应用免疫组化法分析人食管癌组织中VEGF的表达和微血管密度;应用RT-PCR法检测食管癌组织及人食管癌细胞株VEGFmRNA的表达. 结果 食管癌组织的VEGF阳性表达率为70.9%,VEGF在肿瘤组织的表达水平明显高于癌旁组织,其表达水平与肿瘤的病理学分级、肿瘤的浸润深度及淋巴结转移等行为有关.食管癌组织中微血管分布不均,血管密集区主要集中在癌灶边缘;MVD与肿瘤的分化程度和淋巴结转移相关;MVD与VEGF的表达之间存在正相关关系.食管癌组织的VEGFmRNA表达比癌旁组织增高,以VEGF189、VEGF165和VEGF121三种亚型为主. 结论 VEGF在食管癌组织中呈高表达状态,该现象与肿瘤的恶性程度、转移情况及微血管形成能力相关.     

脑肿瘤伽玛刀治疗后再开颅切除原因分析

目的探讨伽玛刀治疗脑瘤后需要再开颅切除的原因。材料与方法结合临床表现特点，３７例伽玛刀治疗后均有不同程度的颅内压增高，局部颅神经损害加重，ＣＴ或ＭＲ复查脑瘤增大或水肿扩大，并通过手术切除肿瘤，解除颅高压或神经压迫症状。结果伽玛刀治疗前脑瘤直径大于３．０ｃｍ，肿瘤影响脑脊液循环，压迫脑干或重要颅神经损伤严重，脑肿瘤水肿严重，肿瘤恶性程度或复发是伽玛刀治疗后需开颅切除的重要因素。结论病理证实伽玛射线对脑肿瘤细胞具有致死性杀伤作用，但对周边瘤细胞，尤其是胶质瘤摧毁不彻底，提高伽玛刀治疗脑肿瘤疗效和减少并发症的关键在于掌握适应证和治疗技术。     

端粒酶逆转录酶及VEGF在卵巢肿瘤中的表达

目的探讨卵巢肿瘤组织中端粒酶逆转录酶(TRT)和血管内皮生长因子(VEGF)的表达及相关性.方法对89例卵巢肿瘤(良性肿瘤44例、交界性肿瘤9例、恶性肿瘤33例)采用免疫组织化学S-P法测定其TRT和VEGF的表达,并进行相关分析.结果 TRT和VEGF在不同卵巢肿瘤组中的表达明显各异,两者在良性组、交界性组、恶性组中的阳性率分别是9.1%、55.6%、83.3%和11.4%、66.4%、86.1%.它们的阳性表达强度亦随着肿瘤的恶性度增高而逐渐增强;各组比较均有显著性差异(P＜0.01).相关分析显示TRT和VEGF的表达密切正相关(P＜0.01).结论 TRT和VEGF在卵巢肿瘤组织中的高表达与恶性度关系密切,二者的同时检测可作为判断卵巢肿瘤恶性度的重要指标.     

脑膜瘤DNA流式细胞术分析的临床病理学意义

目的探讨脑膜瘤细胞DNA倍体和增殖活性与脑膜瘤组织病理分型及生物学特性的关系.方法采用流式细胞仪检测42例脑膜瘤细胞DNA倍体和S期比例(SPF)、增殖指数(PI),结合肿瘤病理学类型进行相关性分析.结果在不典型、恶性脑膜瘤细胞中,非整倍体比例、SPF、PI显著性增高(P＜0.01);在组织亚型之间,各参数无显著性差异(P＞0.05):SPF、PI在非整倍体细胞系和复发脑膜瘤细胞中显著性增高(P＜0.01).结论流式细胞术分析是研究脑膜瘤细胞动力学和生物学特性的重要方法.DNA非整倍体可作为判定肿瘤恶性程度的指标.SPF、PI作为细胞增殖的指标,对脑膜瘤恶性程度和预后的评估具有重要意义.     

Heparanase及bFGF在胃癌组织中的表达及其与胃癌侵袭转移的关系

目的:探讨乙酰肝素酶(Heparanase HPA)及碱性成纤维细胞生长因子(bFGF)在胃癌组织中的表达及其与胃癌生物学行为的关系.方法:RT-PCR法检测HPA mRNA在胃癌组织中的表达,同时应用免疫组织化学法检测bFGF蛋白在胃癌组织中的表达.结果:HPA mRNA的高表达与胃癌的大体类型、浸润深度、细胞分化程度及组织学生长方式、淋巴结转移、腹膜转移、TNM分期呈正相关:而与肿瘤大小无明显关系.bFGF与浸润深度及TNM分期呈正相关.HPA与bFGF共同表达的病例腹膜转移率、淋巴结转移率、腹腔脱落癌细胞检出率均明显增高.结论:HPA在胃癌组织中的表达增高.HPA及bFGF的表达与胃癌的恶性程度密切相关,在胃癌的侵袭转移中发挥重要作用.两者共同表达时恶性程度明显增高.     

脑肿瘤细胞PCNA和Ki—67表达的对比观察

观察45例（4组）原发性脑肿瘤的免疫组化研究发现：增殖细胞核抗原（PCNA）和Ki67抗原（Ki－67）阳性率均为100％，两种阳性细胞密度均随肿瘤恶性程度增加而升高，并与肿瘤体积呈正相关，两种阳性细胞密度间也呈正相关，各肿瘤组PCNA阳性细胞密度均高于同组Ki－67阳性细胞密度。提示PCNA和Ki－67表达水平均能较客观地反应脑肿瘤的增殖速度和恶性程度。PCNA能用于石蜡切片是检测增殖期细胞更实用的标记物。     

Brain tumor and role of beta-carotene, a-tocopherol, superoxide dismutase and glutathione peroxidase

The erythrocyte levels of the antioxidant enzymes SOD and GPx, and serum levels of antioxidants vitamins beta-carotene and beta-tocopherol were estimated in various types of brain tumors, and were compared with the levels in controls. Statistically significant (P<.001) diminished levels of beta-carotene, beta-tocopherol, SOD and GPx, were observed in all the brain tumor patients as compared to controls. Malignant tumor also showed a relative decrease in antioxidant levels as compared to benign tumors. Comparison of histopathological sections of brain tumors also suggested a inverse relationship between antioxidant level and grades of malignancy. Marked decrease in antioxidant levels may have a role in genesis of considerable oxidative stress in brain tumors. Furthermore, the degree of decline in antioxidant levels may indicate severity of malignancy in brain tumors.     

Brain tumors

Brain tumors generally arise as the culmination of a multistep process that involves a variety of genetic abnormalities. Theoretically, replacement of abnormal genes with normal genes is essential to brain tumor treatment. However, it is very difficult to replace all damaged genes. Currently, most clinical protocols for gene therapy in brain tumors include transfer of a gene which can induce tumor cells to die or which can enhance the environment to generate a systemic immune response against the tumor. The former strategy includes suicide gene therapies, tumor suppressor gene therapy and oncolytic virus therapy. The latter adopts immunogene therapy. In this report, we also focus on other gene therapies, such as therapies to control the cell cycle or apoptosis, and promote antiangiogenesis. Gene therapy is generally accepted to be rather safe in recent years. In fact, the current single-gene therapies for brain tumor are limited and probably restricted to a few tumors. Several agents with different mechanisms of action would be necessary to kill heterogenously mixed tumor cells. Further molecular techniques and basic studies may overcome the malignancy of cancers.     

Expression of hypoxia-inducible carbonic anhydrases in brain tumors

Malignant brain tumors exhibit distinct metabolic characteristics. Despite high levels of lactate, the intracellular pH of brain tumors is more alkaline than normal brain. Additionally, with increasing malignancy, brain tumors display intratumoral hypoxia. Carbonic anhydrase (CA) IX and XII are transmembrane isoenzymes that are induced by tissue hypoxia. They participate in regulation of pH homeostasis by catalyzing the reversible hydration of carbon dioxide. The aim of our study was to investigate whether brain tumors of different histology and grade of malignancy express elevated levels of CA IX and XII as compared to normal brain. We analyzed 120 tissue specimens from brain tumors (primary and metastatic) and normal brain for CA IX and XII expression by immunohistochemistry, Western blot, and in situ hybridization. Whereas normal brain tissue showed minimal levels of CA IX and XII expression, expression in tumors was found to be upregulated with increased level of malignancy. Hemangioblastomas, from patients with von Hippel-Lindau disease, also displayed high levels of CA IX and XII expression. Comparison of CA IX and XII staining with HIF-1alpha staining revealed a similar microanatomical distribution, indicating hypoxia as a major, but not the only, induction factor. The extent of CA IX and XII staining correlated with cell proliferation, as indicated by Ki67 labeling. The results demonstrate that CA IX and XII are upregulated in intrinsic and metastatic brain tumors as compared to normal brain tissue. This may contribute to the management of tumor-specific acid load and provide a therapeutic target.     

Brain Metastases from Solid Tumors: an Institutional Study from South India

Background: Brain metastases are the most common intra-cranial neoplasms. The incidence is on a rise dueto advanced imaging techniques. Aims: The objective of the study was to analyse the clinical and demographicprofile of patients with brain metastases from primary solid tumors. Materials and Methods: This is a retrospectivesingle institutional study covering 130 consecutive patients with brain metastases from January 2007 to August2014. Results: Some 64.6% of the patients were females. The majority were in the sixth decade of life. The siteof the primary tumor was the lungs in 50.8% of the cases. The overall median time from the diagnosis of theprimary malignancy to detection of brain metastases was 21.4 months. Survival was found to be significantlyimproved in patients with solitary brain lesions when compared to patients with multiple brain metastases,and in patients undergoing surgical excision with or without cranial irradiation when compared to wholebrain irradiation alone. The majority of the cases belonged to the recursive partitioning analysis class II group.Whole brain radiation therapy was delivered to 79% of the patients. Conclusions: Most of the patients withbrain metastases in the study belonged to recursive partitioning analysis classes II or III, and hence had poorprognosis. Most of the patients in the Indian context either do not satisfy the indications for surgical excision orare incapable of bearing the high cost associated with stereotactic radiosurgery. Treatment should be tailoredon an individual basis to all these patients.     

Patterns of enrollment of infants with central nervous system tumours on cooperative group studies: a report from the Canadian Pediatric Brain Tumour Consortium

In children under the age of 3, the most common solid tumours are brain tumors. Treatment for many of these patients includes surgery, chemotherapy and rarely radiation therapy. Many clinical trials have been performed in an attempt to establish the best treatment for these patients. Patients enrolled on clinical trials contribute to the establishment of the best therapy. We performed a national survey of all children less than the age of three with brain tumours and examined the contribution these patients made to clinical trials. A data bank was established using data collected from Canadian pediatric oncology centers on children less than age 3 diagnosed with brain tumours between 1990 and 2005. Data were collected on the use of adjunctive treatment after surgery, treatment on a protocol, reasons patients were not registered on a protocol, and reasons for discontinuation of therapy. From the 579 cases in the data bank, 302 (52%) patients were treated with further therapy after surgery. The use of further therapy after surgery was significantly higher in patients with cerebellar and brain stem tumors, patients who were over 1 year of age, patients with ependymal and embryonal tumors, and patients with high grade malignant tumors. Only 62 (21%) patients were enrolled on a protocol for therapy. No factor was significant for being enrolled on a protocol. Reasons for not being registered on a protocol were mainly that there was no open COG/POG/CCG study or the study was not open at the institution. The therapy was stopped because of completion of the protocol in 50% and because of disease progression in 34%. In Canada, about half of children under the age of 36 months with brain tumors are undergoing therapy following surgery for their malignancy but only a small fraction of them are enrolled on a clinical trial. There needs to be improved availability of clinical trials for these patients so that novel therapies can be evaluated and survival improved.     

Matrix Metalloproteinase 2 (MMP-2) Immunoreactive Protein is Associated with Poor Grade and Survival in Brain Neoplasms

Matrix metalloproteinases play an important role in the invasion of tumor cells and the progression of cancer. The 72kDa type IV collagenase, a matrix metalloproteinase 2 (MMP-2) has been shown to contribute to the invasion and metastasis in diverse malignant neoplasms. Object. To elaborate the potential role of MMP-2 in brain tumor invasion we studied the expression and localization of this enzyme protein in 101 brain tumors representing different types of brain neoplasms. For the first time, we also correlated the expression of MMP-2 protein to patient survival. Methods. Using immunohistochemistry and a monoclonal antibody specific for MMP-2 we found that MMP-2 protein was primarily localized in tumor cells and vasculature cells as well as inflammatory cells. The expression of MMP-2 was absent or negligible in benign tumors (pilocytic astrocytoma and meningioma). Thirty-three percent (6/18) of astrocytomas, 38% (3/8) of anaplastic astrocytomas, 14% (1/7) of anaplastic oligodendrogliomas, 54% (19/35) of glioblastomas and 100% (6/6) of metastatic brain tumors were positive for MMP-2. A correlation between MMP-2 expression and survival was found in malignant brain tumors. The mean survival of patients with an MMP-2 negative tumor was 36 months, when it was only 7–14 months in patients with an MMP-2 positive tumor. Conclusions. Our data suggest that MMP-2 is associated with histological malignancy and poor survival in brain tumors.     

单发脑转移瘤的外科治疗

本文报告了５１例单发脑转移瘤，全部为手术和病理检查所证实。５１例中，男性３２例，女性１９例，平均年龄为４６．８岁。这些患者的主要表现为颅内压增高。本研究结果表明年龄较小、身体条件好的单发脑转移瘤患者，如果他们的原发灶经过适当处理，或转移性脑瘤是可切除的，都应尽早地行手术治疗，并同时行减压术。术后患者应行全脑放疗和化疗，以便延长其生命，改善生活质量。     

Brief Descriptive Epidemiology of Primary Malignant Brain Tumors from North-East India

Brain tumors are a mixed group of neoplasms that originate from the intracranial tissues and the meningeswith degrees of malignancy varying greatly from benign to aggressive. Not much is known about the epidemiologyof primary malignant brain tumors (PMBTs) in our population in North-East India. In this analysis, an attemptwas made to identify the age groups, gender distribution, topography and different histological types of PMBTwith data from a hospital cancer registry. A total of 231 cases of PMBT were identified and included for thepresent analysis. Our analysis has shown that most of PMBT occur at 20-60 years of age, with a male to femaleratio of 2.3:1. Some 70.5% of cases occurred in cerebral lobes except for the occipital lobe, and astrocytictumors were the most common broad histological type. In our population the prevalence of PMBT is 1% of allcancers, mostly affecting young and middle aged patients. As brain tumors are rare, so case-control analyticepidemiological studies will be required to establish the risk factors prevalent in our population.     

PET: Brain tumor biochemistry

Most mechanisms of drugs which are used in brain tumor chemotherapy are well characterized: alkylation of DNA components (nitrosoureas), binding with tubulin protein resulting in metaphase arrest (vincristine), chromatid breaks and chromosome translocations (procarbazine), or inhibition of ribonucleotide reductase (hydroxyurea) [1]. These drugs exert their effects mainly during certain cell cycle phases of proliferating cells, particularly when DNA is synthesized. From this it can be assumed that the efficacy of these drugs depends on the fraction of proliferating cells. Thus it would be of great importance to estimate the proliferation rate of brain tumors which could guide chemotherapy in individual patients. Positron emission tomography (PET) measures quantitatively thein vivo tissue uptake of tracer substances. In tumors, the uptake appears to be altered in a characteristic way determined by biochemical properties of tumor tissue. Some aspects of brain tumor metabolism which are theoretically related to proliferation have been investigated with PET. In the following, the literature is reviewed with regard to: 1) tracer substances whose uptake has been thought to reflect tumor malignancy (¹¹C-methionine,¹⁸F-fluoro-deoxyglucose), and 2) tracers which theoretically could reflect mechanisms specifically related to DNA synthesis (¹¹C-putrescine, ligands for peripheral benzodiazepine receptors).