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Biomedical subjects

M Westphal

Publications and source records attributed to M Westphal.

At least 19 recordsLinked to original sources
PubMed1999

Allelic losses at 1p, 9q, 10q, 14q, and 22q in the progression of aggressive meningiomas and undifferentiated meningeal sarcomas.

Meningiomas are usually benign tumors; however, they can recur after surgical resection and occasionally show histological progression to a higher malignancy grade. Five such rare cases of aggressively recurring meningiomas were present in our departmental cohort of 923 primary meningeal neoplasms operated over a 17-year period. Four other aggressively recurring meningeal tumors with a very similar clinical and histomorphological appearance (three undifferentiated meningeal sarcomas, one hemangiopericytoma) was also included in this study. We investigated whether disease progression can be traced by genetic alterations and whether a pattern of genetic alterations is specific for meningiomas. A total of 40 specimens from primary tumors and multiple recurrences of the nine patients were analyzed with 26 polymorphic allelic markers for deletions on 1p, 1q, 9q, 10q, 14q, and 22q. Loss of heterozygosity (LOH) at 22q was observed in all meningiomas cases at the earliest time point analyzed. Allelic loss at 1p was seen in the original tumor in two cases and upon meningioma recurrence in two others. Deletion on 10q occurred during tumor progression in two cases, and on 9q and 14q in one case. While allelic loss at 22q appears to be an early event in aggressive meningioma disease, there is a clear correlation of further deletions on chromosome arms 1p, 9q, 10q, and 14q with histopathological and clinical progression, as shown in these intraindividual trackings. None of these genetic findings were present in the non-meningiomatous meningeal tumors, indicating that meningothelial cells have their own lineage-specific genetic pathways towards clinical malignancy.

Adult↗
PubMed1999

Levels of vascular endothelial growth factor, hepatocyte growth factor/scatter factor and basic fibroblast growth factor in human gliomas and their relation to angiogenesis.

Angiogenesis is a possible target in the treatment of human gliomas. To evaluate the role of 3 growth factors, vascular endothelial growth factor (VEGF), hepatocyte growth factor/scatter factor (HGF/SF) and basic fibroblast growth factor (bFGF), in the angiogenic cascade, we determined their levels in extracts of 71 gliomas by enzyme-linked immunosorbent assay (ELISA). The levels of bFGF were only marginally different between gliomas of World Health Organization (WHO) grade II (low grade) and grades III and IV (high grade). In contrast, the mean concentrations of VEGF were 11-fold higher in high-grade tumors and those of HGF/SF 7-fold, respectively. Both were highly significantly correlated with microvessel density (p < 0.001) as determined by immunostaining for factor VIII-related antigen. In addition, VEGF and HGF/SF appeared to be independent predictive parameters for glioma microvessel density as determined by multiple regression analysis. We measured the capacity of all 3 factors to induce endothelial tube formation in a collagen gel. In this assay, bFGF was found to be an essential cofactor with which VEGF as well as HGF/SF were able to synergize independently. According to the concentrations of angiogenic factors, extracts from high-grade tumors were significantly more potent in the tube formation assay than the low-grade extracts (p = 0.02). Adding neutralizing antibodies to bFGF, VEGF and HGF/SF together with the extracts, tube formation was inhibited by up to 98%, 62% and 54%, respectively. Our findings suggest that bFGF is an essential cofactor for angiogenesis in gliomas, but in itself is insufficient as it is present already in the sparsely vascularized low-grade tumors. Upon induction of angiogenesis in high-grade tumors, bFGF may synergize with rising levels of not only VEGF but possibly also with HGF/SF, which appears here to be an independent angiogenic factor.

Cells, Cultured↗
PubMed1999

Isolation and culture of human neuromicrovascular endothelial cells for the study of angiogenesis in vitro.

Neovascularization in the adult central nervous system occurs as a response to several pathophysiological conditions such as ischemia, wound repair, or neoplasia. Endothelial cells from different blood vessel types, different organs, and different species are heterogeneous; therefore, the appropriate cell type should be used to study specific aspects of vascular pathology. We have developed a method to isolate human cerebral microvascular endothelial cells (CMECs) from small, freshly obtained specimens of normal brain adherent to human arteriovenous malformations (AVMs). The isolation procedure involves enzymatic digestions and gradient centrifugations, yielding over 95% pure primary cultures. Alternative isolation methods using magnetic beads, panning, or cloning were not superior with regard to cell purity or yield. CMECs were identified by their immunoreactivity for vWF, CD34, EN4, binding of Ulex europeus lectin, and uptake of DiI-Ac-LDL. They displayed ultrastructural features characteristic of blood-brain barrier endothelial cells and expressed GLUT-1. CMECs were subcultured; however, prolonged culture led to reduced culture purity. Vascular endothelial growth factor, basic fibroblast growth factor and hepatocyte growth factor/scatter factor stimulated the directional motility of CMECs, with dose-response profiles similar to human umbilical vein endothelial cells (HUVECs). In contrast, to stimulate proliferation, lower concentrations of growth factors tended to be necessary for CMECs than for the large vessel endothelial cells. CMECs formed capillary tube-like structures in an in vitro angiogenesis assay using matrigel. This study expands the spectrum of available tissue sources for the isolation of human neuromicrovascular endothelial cells, which are essential for the in vitro study of blood-brain barrier function and cerebral angiogenesis.

Arteriovenous Malformations↗
PubMed1999

Two-step presurgical endovascular treatment of five arteriovenous malformations partially fed by single vessels en passage.

PURPOSE: To describe a method for the preoperative embolization of arteriovenous malformations (AVM) containing vessels en passage (VeP). First, before embolization of the primary AVM, the distal portion of the VeP beyond the AVM, which supplies the parenchymal compartment, is blocked through placement of an endovascular ligature (fibered coils). This protects the post lesional parenchymal tissue and isolates malformational compartments before embolization. Thus the proximal AVM-supplying segment of the VeP can be safely embolized. PATIENTS AND METHODS: Five of 204 AVM patients admitted for preoperative embolization between 1989 and 1997 fulfilled the following treatment criteria for the placement of an endovascular ligature in a VeP before embolization: 1. The diameter of the distal portion of the VeP behind the AVM was large whereas the parenchymal blush was poor; 2. The VeP fed a large portion of the AVM; 3. The VeP was judged to be accessible only late in the surgical procedure; 4. The VeP and its off branches were an integral part of the AVM periphery and thus not suitable for microdissection. RESULTS: In all five cases the leptomeningeal collateral perfusion (the arterial supply to parenchymal brain areas) served to supply brain areas distal to the AVM after primary blockage of a VeP by endovascular ligature with fibered coils. Embolization and complete surgical dissection of the AVM was then achieved in all cases. No neurological deficits occurred. CONCLUSION: Experience with our five cases indicates that a preparatory endovascular ligature of a VeP between parenchyma and the malformational compartment followed by embolization of the AVM can serve as an alternative to open surgical dissection of a vessel en passage and that it safely allows effective preoperative embolization.

Adolescent↗
PubMed1999

Management of spinal dural arteriovenous fistulae using an interdisciplinary neuroradiological/neurosurgical approach: experience with 47 cases.

OBJECTIVE: Spinal dural arteriovenous fistulae (SDAVFs) are frequently diagnosed after unacceptable delays and are therefore treated at a disadvantageously advanced stage. There is controversy regarding their treatment and the respective roles of interventional neuroradiologists and neurosurgeons. We present our series of 47 patients to illustrate the necessity for early treatment and the value of an interdisciplinary approach. METHODS: All patients exhibited suspicious magnetic resonance imaging and/or myelographic findings. Subsequent spinal angiography revealed the SDAVFs. Twelve patients were treated primarily by surgical interruption of the arterialized intradural draining vein, and eight patients underwent surgery after unsuccessful embolization. Twelve patients were surgically treated several months after embolization because of the recruitment of collateral vessels. Definitive embolization was achieved for 15 patients. All patients were monitored with magnetic resonance imaging and at least one control angiographic examination. Follow-up periods ranged from 2 months to 8 years. RESULTS: There was an obvious male prevalence, with 35 male and 12 female patients. Only six of the patients were less than 50 years of age. The SDAVFs were found twice as often on the left side, compared with the right. A total of 85% of the SDAVFs were located between T2 and L2. Presenting signs were most often progressive paraparesis, with 66% of the patients exhibiting progression to a condition in which they could not walk without support or were confined to a wheelchair. For 50% of the patients, the time at which the correct diagnosis was established was more than 15 months after the onset of the first symptoms. After treatment, 18 patients showed improvement (38%), the conditions of 26 patients (55%) were unchanged (without further deterioration), and the conditions of three patients (6%) had deteriorated. CONCLUSION: Attempts at embolization should be made at the time of angiography, because no adverse effects were recorded in our series and there was a 30% chance of the patients being cured by that modality alone. Even if recanalization occurs, the internal labeling of a feeding vessel with radio-opaque embolization material allows exact intraoperative fluorographic localization of the origin of the draining vein, facilitating minimally invasive surgical exposure.

Adult↗
PubMed1999

The contractile vacuole network of Dictyostelium as a distinct organelle: its dynamics visualized by a GFP marker protein.

The contractile vacuole system is an osmoregulatory organelle composed of cisternae and interconnecting ducts. Large cisternae act as bladders that periodically fuse with the plasma membrane, forming pores to expel water. To visualize the entire network in vivo and to identify constituents of the vacuolar complex in cell fractions, we introduced a specific marker into Dictyostelium cells, GFP-tagged dajumin. The C-terminal, GFP-tagged region of this transmembrane protein is responsible for sorting to the contractile vacuole complex. Dajumin-GFP negligibly associates with the plasma membrane, indicating its retention during discharge of the bladder. Fluorescent labeled cell-surface constituents are efficiently internalized by endocytosis, while no significant cycling through the contractile vacuole is observed. Endosomes loaded with yeast particles or a fluid-phase marker indicate sharp separation of the endocytic pathway from the contractile vacuole compartment. Even after dispersion of the contractile vacuole system during mitosis, dajumin-GFP distinguishes the vesicles from endosomes, and visualizes post-mitotic re-organization of the network around the nucleus. Highly discriminative sorting and membrane fusion mechanisms are proposed to account for the sharp separation of the contractile vacuole and endosomal compartments. Evidence for a similar compartment in other eukaryotic cells is discussed.

Animals↗
PubMed1999

The rate of homozygous CDKN2A/p16 deletions in glioma cell lines and in primary tumors.

The rate of homozygous deletions of CDKN2A/p16 is variable between different tumor entities, and in addition it is higher in established cell lines in comparison with primary tumors. Such incongruencies may reflect statistical sampling errors, true differences depending on tissue derivatisation and CDKN2A/p16 loss under selective pressure in tissue culture. Clarification of these issues is warranted in the context of defining tumor suppressor genes such as CDKN2A/p16 as targets for gene replacement therapies. We therefore compared established cell lines derived from human glioblastomas and their corresponding primary tumors by multiplex PCR methodology. Archival early passages were included to determine the time point at which the p16 status of a cell line changes if it is different from the original tumor. It was found that in 2 of 11 cases (18%) the primary tumor had no p16 alteration whereas the corresponding cell lines had a homozygous p16 deletion. Tracking the in vitro evolution of these two cell lines we found that CDKN2A/p16 was lost already in the earliest passages. This suggests a clonal outgrowth advantage of a subpopulation of p16 deleted tumor cells rather than instability of the CDKN2A/p16 genotype in vitro. Including 20 additional glioblastoma-derived cell lines we detected that in 19 of the total 31 lines at least one exon was lost bringing the rate of p16 loss in the whole panel to 61%. This compares to a rate of 49% which was found in original glioma tissue from 47 unselected other patients. It is concluded, that in cell culture selective pressure favours the outgrowth of pre-existing CDKN2A/p16 negative clones, which account for the difference of CDKN2A/p16 status between cell lines and tumors. In no case did we see a change of the CDKN2A/p16 status during prolonged tissue culture periods of up to 8 years.

Adult↗
PubMed1999

Preoperative embolization of intracranial meningiomas with a fibrin glue preparation.

BACKGROUND AND PURPOSE: Preoperative embolization expands the spectrum of meningioma that can be operated on safely. Our goal was to achieve the distalmost loading of the vascular bed and confluent tumor necrosis with a fibrin glue preparation in the preoperative embolization of meningiomas. METHODS: Between 1992 and 1997, 80 patients with a meningioma had diagnostic angiography with a standard transfemoral Seldinger technique, performed with a 6F guiding catheter and digital subtraction angiography. Preoperative embolization was carried out in the same session with an additional microcatheter system. Fibrin glue was the only component used. In all cases, CT was performed immediately after embolization; in nine patients, MR imaging was also performed. RESULTS: Angiography verified the elimination of tumor blush in all patients. The high-density areas seen on postembolization CT scans, caused by the fibrin glue dispersed in the embolized supply area, were found to be necrotic at surgery and were easily removed by suction. Two (2.5%) of the 80 patients had complications associated with embolization that resulted in neurologic deficits. CONCLUSION: The most effective preoperative embolization of tumors requires a distalmost loading of the vascular bed. Fibrin glue, which is easy to use and safe to handle, causes confluent tumor necrosis within the injected vascular territory.

Adult↗
PubMed1998

G protein beta subunit-null mutants are impaired in phagocytosis and chemotaxis due to inappropriate regulation of the actin cytoskeleton.

Chemotaxis and phagocytosis are basically similar in cells of the immune system and in Dictyostelium amebae. Deletion of the unique G protein beta subunit in D. discoideum impaired phagocytosis but had little effect on fluid-phase endocytosis, cytokinesis, or random motility. Constitutive expression of wild-type beta subunit restored phagocytosis and normal development. Chemoattractants released by cells or bacteria trigger typical transient actin polymerization responses in wild-type cells. In beta subunit-null cells, and in a series of beta subunit point mutants, these responses were impaired to a degree that correlated with the defect in phagocytosis. Image analysis of green fluorescent protein-actin transfected cells showed that beta subunit- null cells were defective in reshaping the actin network into a phagocytic cup, and eventually a phagosome, in response to particle attachment. Our results indicate that signaling through heterotrimeric G proteins is required for regulating the actin cytoskeleton during phagocytic uptake, as previously shown for chemotaxis. Inhibitors of phospholipase C and intracellular Ca2+ mobilization inhibited phagocytosis, suggesting the possible involvement of these effectors in the process.

Actins↗
PubMed1998

Scatter factor promotes motility of human glioma and neuromicrovascular endothelial cells.

Malignant gliomas are characterized by rapid growth, infiltration of normal brain tissue, and high levels of tumor-associated angiogenesis. The genetic and local environmental tissue factors responsible for the malignant progression from low to high grade gliomas and the highly malignant behavior of glioblastomas are not well understood. In a study of 77 human brain tissue extracts, high grade (III-IV) tumors had significantly greater scatter factor (SF) content than did low grade tumors or non-neoplastic tissue. To investigate the potential significance of SF accumulation in gliomas, we measured the effects of SF on DNA synthesis and motility of cultured human glioma cell lines. SF stimulated DNA synthesis in 7/10 glioma cell lines and in 3/3 neuromicrovascular endothelial cell (NMVEC) lines, consistent with our previous report that SF stimulated cell proliferation of a few human glioma cell lines. SF markedly stimulated the chemotactic migration of 10/10 glioma cell lines as well as 3/3 NMVEC lines. In addition, SF stimulated the 2-dimensional migration of glioma cells on culture surfaces coated with specific extracellular matrix molecules (collagen i.v., laminin, and fibronection). As expected based on these biologic responses to SF, 10/10 glioma lines and 4/4 NMVEC lines expressed mRNA for c-met, the SF receptor. To assess the possible in vivo significance of these migration assays, we compared the chemotactic response of a glioma cell line to human brain cyst fluids and tumor extracts that contained high or low SF concentrations. Fluids and extracts with high SF content tended to induce higher levels of chemotactic migration than did fluids and extracts with low SF content. Addition of anti-SF monoclonal antibody (MAb) inhibited migration induced by fluids and extracts with high SF content by about 30-50%.

Brain Neoplasms↗
PubMed1998

[Congestive myelopathy caused by spinal dural arteriovenous fistulas. Anamnesis, clinical aspects, diagnosis, therapy and prognosis].

Congestive myelopathy, formerly referred to as varicosis spinalis or Foix-Alajouanine syndrome, is caused by a spinal dural arteriovenous fistula (SDAVF). So far, the blood supply from the meningeal arteries draining through the fistula into the medullary venous system can only be verified by spinal angiography. Patients predominantly male and over the age of 60 are afflicted. Initially reversible functional disorders caused by the congestion of the spinal cord veins eventually become irreversible, the most common symptom being an increasingly paretic gait disorder, the signs of which generally begin symmetrically and progress from distal to proximal signs. Simultaneously, predominantly transverse sensory dysfunctions develop, as well as bladder and bowel dysfunctions, most often leading to incontinence. MRI typically shows a central medullary signal enhancement with slight swelling of the afflicted region, initially indicative of a reversible congestive edema and later of an irreversible infarction, and extended perimedullar vessels. Thus, if the clinical course and the characteristic MRI findings suggest the possibility of disease related to congestive myelopathy, spinal angiography becomes indispensable. Since ensuing the success of therapy and prognosis depends on rapid determination of the extent of the illness, a speedy diagnostic reaction is mandatory to institute the treatment necessary to prevent paraplegia.

Adult↗
PubMed1998

Trk A, B, and C are commonly expressed in human astrocytes and astrocytic gliomas but not by human oligodendrocytes and oligodendroglioma.

Neurotrophins regulate the proliferation and differentiation of neurons in the central nervous system via a family of specialized receptors, including TrkA, TrkB, and TrkC. As little is known about their expression or potential role in human glial tissues and glial tumors, we undertook an immunohistochemical analysis of human glia, glioma tissues and cell cultures of glial tumors to characterize the expression of Trk family members (full-length TrkA, TrkB, the truncated form of TrkB, and TrkC). In normal human brain Trk A, B, and C immunoreactivity was found in neurons and some weak staining was also seen astrocytes. No Trk expression was seen on oligodendrocytes. Strong reactivity was seen in reactive astrocytes in a glial scar. In a total of 34 glioma tissue specimens, which included 16 astrocytic tumors (4 low-grade astrocytomas and 12 glioblastomas multiforme) and 15 oligodendrogliomas (8 low-grade and 7 anaplastic) as well as 3 oligoastrocytomas (WHO grade II), TrkA, B, and C immunoreactivity was observed exclusively in specimens from astrocytic gliomas (16/16), but not in any of the oligodendrocytic gliomas (0/15). In the oligoastrocytomas, staining was restricted to the astrocytic component. In the astrocytoma and oligodendroglioma specimens, Trk A, B, and C immunoreactivity was also seen in the surrounding reactive astrocytes. Trk expression was independent of age, sex or histological grade of the investigated tumors. In six primary cell cultures, one derived from human astrocytes and five established from malignant astrocytomas, only TrkA immunoreactivity could be detected, while TrkB (both full-length and truncated isoforms) and TrkC were absent. The TrkA expression in primary cell cultures decreased with continuous cell passaging, and no Trk could be detected in established cell lines derived from glioblastoma. In conclusion, our data suggest that in human glial tissues Trk A, B, and C may be expressed in a lineage-restricted manner, thereby distinguishing between astrocytes and oligodendrocytes in a marker-like fashion. Trk expression, like GFAP expression appears to be increased in activated (reactive)/neoplastic astrocytes.

Adult↗
PubMed1998

Preoperative functional magnetic resonance imaging (fMRI) of the motor system in patients with tumours in the parietal lobe.

Intracranial lesions may compromise structures critical for motor performance, and mapping of the cortex, especially of the motor hand area, is important to reduce postoperative morbidity. We investigated nine patients with parietal lobe tumours and used functional MRI sensitized to changes in blood oxygenation to define the different motor areas, especially the primary sensorimotor cortex, in relation to the localization of the tumour. Activation was determined by pixel-by-pixel correlation of the signal intensity time course with a reference waveform equivalent to the stimulus protocol. All subjects showed significant activation of the primary sensorimotor cortex while performing a finger opposition task with the affected and unaffected side. In five patients the finger opposition task additionally activated the ipsilateral sensorimotor cortex and the supplementary motor area (SMA). Extension and flexion of the foot, additionally performed in two patients, also activated the sensorimotor cortex, in one case within the perifocal oedema of the tumour. Tumour localization near the central sulcus induced displacement of the sensorimotor cortex as compared to the unaffected side in all patients with a relevant mass effect. The results of our study demonstrate that functional MRI at 1.5 T with a clinically used tomograph can reproducibly localize critical brain regions in patients with intracranial lesions.

Adult↗
PubMed1998

Tissue culture of human neurocytomas induces the expression of glial fibrilary acidic protein.

Cell cultures were established from three human neurocytoma specimens (primary and recurrent). The phenotypic evolution was analyzed by immunocytology in different culture conditions in the presence and absence of serum including the addition of epidermal growth factor, rat caudate extract, retinoic acid, and N-acetyl cystein. The cells were grown on glass cover slides or an extracellular matrix (ECM) from bovine corneal endothelial cells. Immunostainings were performed after overnight incubation and were repeated after 5 and 10 days of culture. The cultures were compared to an oligoastrocytoma also arising at the foramen of Monro and an ependymoma of the frontal lateral ventricle, two tumors supposedly originating from the same tissue matrix as the neurocytoma. After overnight incubation, 90% of the neurocytoma cells were positive for A2B5 and synaptophysin. GFAP reactivity appeared in the periphery of cell processes in less than 1% of the cells. The staining patterns and morphology were nearly identical under the different culture conditions. After 5 days, almost all cells were strongly positive for GFAP, while the number of cells remaining positive for synaptophysin and A2B5 was unchanged from the earlier time point. Again, there were no fundamental differences between the incubation conditions. At this point, cultures maintained on ECM were compared to their counterparts on untreated glass cover slides with identical staining results, although many fewer cells had attached. An identical immuno-reactive pattern was found on day 10. In contrast to the neurocytoma cultures, there was an immediate strong GFAP signal in both the mixed glioma and the ependymoma. A2B5 was also positive, but synaptophysin was absent. Because the neurocytoma specimens were synaptophysin positive but GFAP negative by immunohistochemistry, it is concluded that neurocytomas may represent a human neuronoglial precursor tumor that switches its phenotype in culture to astroglial differentiation despite very diverse culture conditions.

Adult↗
PubMed1998

Microtubule-mediated centrosome motility and the positioning of cleavage furrows in multinucleate myosin II-null cells.

To study centrosome motility and the interaction of microtubules with the cell cortex in mitotic, post-mitotic and interphase cells, (alpha)-tubulin was tagged in Dictyostelium discoideum with green fluorescent protein. Multinucleate cells formed by myosin II-null mutants proved to be especially suited for the analysis of the control of cleavage furrow formation by the microtubule system. After docking of the mitotic apparatus onto the cell cortex during anaphase, the cell surface is activated to form ruffles on top of the asters of microtubules that emanate from the centrosomes. Cleavage furrows are initiated at spaces between the asters independently of the positions of spindles. Once initiated, the furrows expand as deep folds without a continued connection to the microtubule system. Occurrence of unilateral furrows indicates that a closed contractile ring is dispensable for cytokinesis in Dictyostelium. The progression of cytokinesis in the multinucleate cells underlines the importance of proteins other than myosin II in specifying a cleavage furrow. The analysis of centrosome motility suggests a major role for a minus-end directed motor protein, probably cytoplasmic dynein, in applying traction forces on guiding microtubules that connect the centrosome with the cell cortex.

Anaphase↗
PubMed1998

Expression and synthesis of insulin-like growth factor-binding proteins in human glioma cell lines.

We previously demonstrated the presence of insulin-like growth factors (IGFs) and IGF-receptors in human glioma cell lines derived from primary glioblastomas. The biological action of IGFs is modulated by specific IGF-binding proteins (IGFBP)-1 to -7. By means of polymerase chain reaction (PCR), we detected mRNA transcripts for IGFBP-1 in 42%, IGFBP-2 in 65%, IGFBP-3 in 97%, IGFBP-4 in 3%, IGFBP-5 in 74%, IGFBP-6 in 94% and IGFBP-7 in 87% of the glioma cell lines. The specificity of the PCR reaction was verified by direct sequencing of the PCR product. In addition, the content of the most prevalent IGFBP-3 was measured in conditioned medium from glioma cells by specific radioimmunoassay with levels ranging from < 1 to 620 ng/ml. Moreover, the presence of membrane-bound IGFBPs (44, 50 and 60 kDa) as well as IGF-II receptors was demonstrated by using 125I-labelled IGF-II as a ligand. In conclusion, IGFBPs may modulate the IGF-mediated effects in these cell lines.

Aged↗
PubMed1998

Absence of polyomavirus JC in glial brain tumors and glioma-derived cell lines.

The human neurotropic papovavirus JC, a close relative of simian virus 40, has been associated with the formation of brain tumors in humans because of its ability to induce such tumors in other primates under experimental conditions. Here we have analyzed 30 brain tumors classified as either oligodendroglioma or astrocytoma and 22 cell lines derived from human gliomas for the presence of JC viral sequences using polymerase chain reaction with two different sets of primers. None of the tumors or cell lines contained JC viral sequences. Similarly, we failed to detect expression of JC T antigen in any of 26 human glioma lines analyzed in this study. We conclude that JC virus is not a major cause of human brain tumors.

Brain Neoplasms↗