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At least 19 recordsLinked to original sources
PubMed2000

Gamma knife radiosurgery as a primary treatment for prolactinomas.

OBJECT: The purpose of this study was to estimate the efficacy of gamma knife radiosurgery (GKS) in controlling tumor growth and endocrinopathy associated with prolactinomas. METHODS: Between 1993 and 1997, 164 of 469 patients with pituitary adenomas treated by GKS harbored prolactinomas. The dose to the tumor margin ranged from 9 to 35 Gy (mean 31.2 Gy), and the visual pathways were exposed to a dose of less than 10 Gy. The mean tumor diameter was 13.4 mm. The mean follow-up time for 128 cases was 33.2 months (range 6-72 months). Tumor control was observed in all but two patients who underwent surgery 18 and 36 months, respectively, after GKS. Clinical cure was achieved in 67 cases. Clinical improvement was noted with a decrease in the hyperprolactinemia after GKS. Nonetheless, in 31 (29%) of 108 patients who were followed for more than 2 years no improvement in serum prolactin levels was demonstrated, although this could be normalized by bromocriptine administration after treatment. Nine infertile women became pregnant 2 to 13 months after GKS and all gave birth to normal children. There was no visual deterioration related to GKS. Five women experienced premature menopause. In these patients there was subtotal disappearance of the tumor and an empty sella developed. CONCLUSIONS: Gamma knife radiosurgery as a primary treatment for prolactinomas can be safe and effective both for controlling tumor growth and for normalization of prolactin hypersecretion. A higher margin dose (> or = 30 Gy) seemed to be associated with a better clinical outcome. Gamma knife radiosurgery may make prolactinomas more sensitive to the bromocriptine.

Humans↗
PubMed1997

Hydroxyurea for treatment of unresectable and recurrent meningiomas. I. Inhibition of primary human meningioma cells in culture and in meningioma transplants by induction of the apoptotic pathway.

Meningiomas, which invade intracranial bone structures and the adjacent connective tissue, are frequently unresectable because of their aggressive and recalcitrant growth behavior. They have a high recurrence rate, and in approximately 10% of these tumors there is an increased risk of malignancy. Significant morbidity and mortality rates associated with recurrent meningiomas demand nonsurgical approaches. To date, adjuvant hormonal treatment has not proven beneficial. The anticancer drug hydroxyurea was therefore tested for its potential use in the treatment of meningiomas. Early-passaged cell cultures were established from 20 different meningiomas. The addition of 5 x 10(-4) and 10(-3) M hydroxyurea over a period of 5 to 9 days resulted in a remarkable decrease in cell proliferation and even blocked tumor cell growth when compared with untreated cells. A significant arrest of meningioma cell growth in the S phase of the cell cycle was revealed on DNA flow cytometry. Electron micrographs of hydroxyurea-treated tumor cells showed ultrastructural features consistent with apoptosis, and light microscopy demonstrated DNA fragmentation by in situ DNA strand break labeling. Short-term treatment of meningioma cell cultures with hydroxyurea for 24 to 48 hours resulted in discrete oligonucleosomal fragments (DNA ladder), another characteristic sign of apoptosis. In addition to the in vitro studies, tissue from five different meningiomas was transplanted into nude mice followed by treatment with 0.5 mg/g body weight hydroxyurea over 15 days. In situ DNA strand break labeling demonstrated DNA fragmentation in distinct regions with different tumor cell densities in all hydroxyurea-treated meningioma transplants. These data provide evidence that hydroxyurea is a powerful inhibitor of meningioma cell growth, most likely by causing apoptosis in the tumor cells. Thus, hydroxyurea may be a suitable chemotherapeutic agent for the long-term treatment of unresectable or semi- to malignant meningiomas, or for preventing recurrent growth of meningiomas after resection.

Animals↗
PubMed2003

Multiple meningiomas consisting of fibrous meningioma and anaplastic meningioma.

A 61-year-old woman presented with progressive dementia over a period of 4 months. Computed tomographic (CT) scans and magnetic resonance (MR) imaging showed 2 meningiomas located at the left parasagittal region and the left sphenoid ridge. These tumors had distinct MRI findings; the left parasagittal tumour showed a clear peritumoral CSF space without brain oedema, but the sphenoid ridge tumour was large with marked peritumoral oedema. Total excision of these 2 tumours was attempted with favourable clinical improvement and histological studies revealed meningiomas of different histological types. The left parasagittal tumour was a fibrous meningioma and the left sphenoid ridge tumour was an anaplastic meningioma with typical brain invasion. These tumours showed a MIB-1 staining index of 1% and 30%, respectively. There was also a difference in the immunohistochemical findings for neurofibromin (NF1 product) expression; the left parasagittal tumour expressed neurofibromin but the left sphenoid ridge tumour lacked neurofibromin expression, suggesting an NF1-gene mutation. This case may be a rare example of the simultaneous occurrence of meningiomas with distinct genotypes.

Female↗
PubMed2001

Expression of PDGF and its receptor as well as their relationship to proliferating activity and apoptosis of meningiomas in human meningiomas.

In this study, we detected the expression of platelet-derived growth factor (PDGF) and its receptor in 61 human meningiomas by immunohistochemistry and in situ hybridisation. The results showed that almost all the 61 meningiomas expressed PDGFBB and PDGF beta receptor and the positive rate of PDGFAA was 49%. Only two meningiomas expressed PDGF alpha receptor. The positive rate and the immunostaining intensity of PDGFBB and PDGF beta receptor were higher in atypical meningiomas than in benign types. There was no significant difference between the different types of benign meningiomas. The expression of PDGFB chain mRNA was coincident with that of PDGFB chain protein. There was no correlation between the expression of PDGFAA and the types or grades of meningiomas. The correlation between overexpression of PDGFBB/R beta and tumour grade provides a useful parameter in evaluating the prognosis of patients with meningiomas. The proliferative activity of meningiomas was evaluated by the proliferating cell nuclear antigen labelling index (PCNA LI). In the 61 meningiomas, the average PCNA LI (%) was 1.8+/-1.3, 1.9+/-1.3, 1.7+/-0.8 and 11.6+/-5.3 (in fibrous, meningothelial, transitional and atypical meningiomas, respectively). Statistic analysis shows that the PCNA LI is higher in atypical meningiomas than that in benign types, and there was no significant difference between the different types of benign meningiomas. The expression of PDGFBB and PDGF beta receptor was significant enhanced in ascending order from low PCNA LI meningiomas to high ones. This result suggested that PDGFBB/R beta autocrine loop may stimulate the growth of meningiomas. In this study, we also detected the cell apoptosis of meningiomas by terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) method. The average apoptosis labelling index (%) was 0.11+/-0.05, 0.08+/-0.04, 0.09+/-0.03 and 0.35+/-0.15 in fibrous, meningothelial, transitional and atypical meningiomas respectively. The apoptosis labelling index was higher in atypical meningiomas than that in benign types. There was a positive correlation between the apoptosis labelling index and PC NA LI of meningioma. When the positive rate of PDGFBB and/or PDGF beta receptor was higher in meningioma, the apoptotic cells was also increased. In conclusion, the overexpression of PDGFBB and its relevant receptor PDGFR beta in meningiomas was correlated with grade of meningiomas and the proliferative activity of meningiomas; PDGFBB/R beta autocrine loop may play an critical role in the pathogenesis of meningiomas.

Adult↗
PubMed1989

Meningioma, meningeal hemangiopericytoma (angioblastic meningioma), peripheral hemangiopericytoma, and acoustic schwannoma. A comparative immunohistochemical study.

The relationship between meningeal hemangiopericytoma (angioblastic meningioma), meningiomas of meningothelial derivation, and peripheral hemangiopericytoma is controversial; and immunohistochemical studies have yielded conflicting results. Likewise, immunohistochemistry has been touted as a reliable means of differentiating fibrous meningioma from acoustic schwannoma. By the immunoperoxidase method, we studied 40 meningiomas (11 meningotheliomatous, four transitional, 11 fibrous, three secretory, four metaplastic, one xanthomatous, one papillary, four atypical, one malignant), five arachnoid granulations, 13 angioblastic meningiomas, nine peripheral hemangiopericytomas, and seven acoustic schwannomas. Antisera to vimentin, epithelial membrane antigen (EMA), keratin, S-100 protein, carcinoembryonic antigen (CEA), desmin, factor VIII, Ulex europeaus, and glial fibrillary acidic protein (GFAP) were utilized. All meningiomas and arachnoid granulations stained for vimentin and EMA; 15% and 12% of meningiomas were S-100 and keratin positive, respectively. The latter was noted primarily in areas of secretory (pseudopsammomatous) differentiation. In contrast, all angioblastic meningiomas stained for only vimentin. This profile of immunoreactivity was also seen in the peripheral hemangiopericytomas, with the exception of single cases that stained focally for EMA and S-100 protein, respectively. Acoustic schwannomas all stained positively for S-100 protein, vimentin, and were variably reactive for EMA, a pattern not distinct from meningioma. We conclude that (a) meningiomas express both epithelial and mesenchymal markers as do arachnoid granulations, (b) that angioblastic meningiomas demonstrate only mesenchymal markers, (c) that angioblastic meningiomas express identical markers to peripheral hemangiopericytoma and should thus be considered a variant thereof, (d) among meningiomas, CEA and keratin appear to be relatively specific markers for the "secretory" variant, and (e) because of overlap in S-100 and EMA reactivity, these markers are unreliable in differentiating meningioma from acoustic schwannoma.

Antibodies, Neoplasm↗
PubMed2002

A role for chromosome 9p21 deletions in the malignant progression of meningiomas and the prognosis of anaplastic meningiomas.

Meningiomas display significant variability in terms of recurrence and survival rates, even within tumor grade. Although several recent modifications of the grading system have improved our ability to predict biologic behavior, additional prognostic markers are needed. Inactivation of the cell cycle regulator, p16 (CDKN2A), has recently been observed in a small subset of atypical and the majority of anaplastic meningiomas. To assess the potential clinical utility of this marker, we performed dual-color FISH on 117 well-characterized archival meningiomas using paired commercial probes to the chromosome 9 centromeric (CEP9) and p16 (9p21) regions. Benign meningiomas (N = 42) were divided into non-recurring versus recurring groups. Atypical meningiomas (N = 52) consisted of proliferative and brain invasive subsets. The 23 anaplastic meningiomas were not further stratified. Deletion of p16 or monosomy 9 was seen in 17% of benign, 52% of atypical, and 74% of anaplastic meningiomas (p < 0.001). No statistically significant differences were found among subsets of benign or subsets of atypical meningioma, though there were more recurrences in those with deletion. Despite potential effects on cell cycle regulation, p16 deletions were not restricted to meningiomas with a high proliferative index. Most importantly, p16 deletion was strongly associated with survival in the anaplastic meningioma cohort, with a risk ratio for death of 6.79 (p = 0.016). Conversely, absence of deletion identified a subset of anaplastic meningioma patients (26%) with prolonged survival. We conclude that chromosome 9p21 deletions are associated with malignant progression of meningiomas and poor prognosis in anaplastic meningiomas.

Adult↗
PubMed1997

Hydroxyurea for treatment of unresectable and recurrent meningiomas. II. Decrease in the size of meningiomas in patients treated with hydroxyurea.

In this paper the authors present the first evidence that meningiomas respond to treatment with hydroxyurea. Hydroxyurea was administered as an adjunct chemotherapeutic treatment in patients with recurrent and unresectable meningiomas. Hydroxyurea was used because experimental data demonstrated that it inhibits growth of cultured human meningioma cells and meningioma transplants in nude mice by inducing apoptosis. The authors therefore treated four selected patients with hydroxyurea. All patients had undergone multiple gross resections and all except one received radiotherapy. Three patients with recurrent Grade I meningiomas assessed according to World Health Organization (WHO) guidelines received hydroxyurea because of an increased tumor growth rate, documented by magnetic resonance (MR) imaging, within a 6- or 12-month interval. A fourth patient with a malignant meningioma (WHO Grade III) began a course of treatment with hydroxyurea immediately after his sixth palliative operation without waiting for another relapse to be demonstrated on MR imaging. Because of their location and invasive growth behavior none of the meningiomas could have been removed completely by surgical intervention. All patients received hydroxyurea at a dosage level of 1000 to 1500 mg/day (approximately 20 mg/kg/day). In a man with a large sphenoid wing meningioma invading the right cavernous sinus and the temporal base, the intracranial tumor mass was reduced by 60% during 6 months of treatment. A woman with a large ball-shaped meningioma of the right sphenoid wing invading the cavernous sinus exhibited a 74% decrease of the initial tumor volume in 10 months of treatment with oral hydroxyurea. Serial MR images obtained monthly revealed that the process of size reduction was continuous and proportionate. The shrinkage of the tumor was accompanied by a complete remission of symptomatic trigeminal neuralgia after 2 months and by improved abducent paresis after 5 months. The third patient had a slowly growing meningioma that exhibited a 15% reduction in mass when reassessed after 5 months of hydroxyurea treatment. The fourth patient with the malignant meningioma in the left cerebellopontine angle has had no recurrence for 24 months. Long-term treatment with hydroxyurea may result in full remission of tumors in meningioma patients. The preliminary data indicate that hydroxyurea provides true medical treatment in patients with unresectable and recurrent meningiomas, replacing palliative surgery and radiotherapy in the management of this disease.

Adult↗
PubMed1997

Correlation of histopathologic classification with proliferative activity and DNA ploidy in 120 intracranial meningiomas, with special reference to atypical meningioma.

Histologic classification of 120 meningiomas was correlated with their proliferative fraction and DNA ploidy using immunohistochemistry and flow cytometry to differentiate histologically atypical meningiomas from benign ones. Histologically, the 120 meningiomas included 101 benign (43 meningotheliomatous, 40 transitional, 11 fibroblastic, 2 secretory, 2 microcystic, 2 angiomatous, and 1 psammomatous), 15 atypical, and 4 malignant meningiomas. As a histologic spectrum between the benign and malignant meningiomas, atypical meningiomas were defined by the presence of two of the following criteria; high cellularity, focal necrosis, uninterrupted growth pattern, and certain cytologic findings i.e., high nuclear/cytoplasmic ratio, coarse chromatin, and prominent nucleoli. In 56 cases, immunostaining for proliferating cell nuclear antigen showed higher proliferating cell fraction in atypical and malignant meningiomas than that in benign meningiomas (p < 0.05). In the flow cytometric analysis, aneuploidy was more often seen in atypical meningiomas compared to benign meningiomas (p < 0.05). We found that benign, atypical, and malignant meningiomas could be histologically classified and correlated with proliferative activity and DNA ploidy pattern. Therefore, atypical meningiomas should be distinguished from benign meningiomas by histopathologic examination and confirmed by studies on their proliferation fractions and DNA ploidies.

Aneuploidy↗
PubMed1985

[Clinico-pathological study of meningiomas in childhood--with special reference to malignant meningiomas].

Six cases of meningiomas which accounted for 3.6% out of 167 intracranial tumors in children were studied with clinico-pathological method. Four meningiomas located in the convexity, two meningiomas developed within the lateral ventricle. CT scan with contrast material showed homogeneous enhanced tumors in four cases. Heterogeneous enhanced tumors were observed in two malignant meningiomas. There was evidence of recurrence in three cases. Two of in these cases were malignant meningiomas. Three patients received postoperative radiotherapy. One case of malignant meningiomas died seven years after the first operation. Five cases are still alive. Macroscopically three cases had cyst formation. Four convexity meningiomas were attached to the dura matter. Three malignant meningiomas were ill-defined and invaded the normal brain tissue. One case of malignant meningiomas invaded the skull. Six meningiomas were classified histologically into two fibrous, one transitional and three malignant meningiomas according to the World Health Organization (WHO) classification of brain tumors. All cases were examined for glial fibrillary acidic protein (GFAP) using the immunohistochemical method. Two cases of malignant meningiomas demonstrated the positive reaction to GFAP. Four cases were negative. These findings suggest that malignant meningiomas grow invasively into the surrounding normal brain tissue.

Adolescent↗
PubMed1996

[A case of thoracic meningioma presenting paraplegia at 4.5 years after removal of a falx meningioma].

A case of a thoracic meningioma presenting paraplegia 4.5 years after removal of a falx meningioma is reported. A 73-year-old woman, complaining of diplopia, was admitted to our department. Neurological examination revealed right abducens palsy. CT demonstrated a well-enhanced right frontal mass beneath the falx. The mass was totally removed under right frontal craniotomy. Its histology was transitional meningioma with rich fibroblasts. 4.5 years after craniotomy, she complained of progressing gait disturbance and nocturnal leg pain. Neurological examination revealed paraplegia, complete loss of leg sensation, loss of patellar and ankle reflex, bilateral positive Babinski reflex and urinary disturbance. Rectal function and anal reflex were preserved. Thoracic MRI demonstrated an intradural extramedullary mass which was well enhanced with Gd-DTPA at Th6-7. Under laminectomy, the mass was totally removed. Its histology was transitional meningioma with rich psammoma bodies and whirl formations. 4 months after removal, her palsy and sensory loss were almost completely recovered. We were able to find 15 cases of combined intracranial and spinal meningiomas in the literature. A young woman of neurofibromatosis suffered from tentorial, intraventricular and C1-2 meningiomas. Of 15 cases without neurofibromatosis including our case, 4 cases were of young boys and 11 cases were of women. Their initial symptoms originated from intracranial meningiomas in 8 cases. Multiple intracranial meningiomas were revealed in only 4 cases. In 9 cases, one case presented a combination of one intracranial meningioma and one spinal meningioma. Histology of intracranial meningioma was almost the same that of spinal meningioma in almost half of the 10 cases. These findings suggest the multi sentricity theory of multiple meningiomas originating in other neuroaxial compartments. Severe spinal dysfunction was recovered after removal in our case. Rectal function and anal reflex were preserved. These anorectal findings suggest that spinal dysfunction is either complete or incomplete. Motor evoked potentials are hopeful tools which can select reversible spinal motor dysfunctions.

Aged↗
PubMed2004

Expression of cytokeratin by malignant meningiomas: diagnostic pitfall of cytokeratin to separate malignant meningiomas from metastatic carcinoma.

Based on clinical and histologic features, differentiating metastatic carcinomas from benign or malignant meningiomas usually is not difficult. Occasionally, however, in some patients without a clinical history of carcinoma, malignant meningiomas can morphologically simulate metastatic carcinoma, necessitating an immunohistochemical study for cytokeratin to make a correct diagnosis. However, the utility of immunohistochemical markers to separate malignant meningioma from metastatic carcinoma has not been investigated. The immunoperoxidase method with antigen retrieval was used to characterize the expression of three cytokeratins (AE1/AE3, CAM 5.2, and Pan cytokeratin), EMA, CEA, Ber-EP4, CD 15, and B72.3 in 12 previously diagnosed malignant meningiomas, 20 benign meningiomas, and 20 metastatic carcinomas. Cytokeratin expression was detected in 75% of malignant meningiomas, 0% of benign meningiomas, and 100% of metastatic carcinomas. While epithelial markers of Ber-EP4, CEA, B72.3 and CD-15 were positive in 90, 80, 70 and 65% of the metastatic carcinoma, respectively, they were negative in all 12 malignant meningioma examined. Vimentin immunoreactivity was seen in all benign and malignant meningiomas, and in 20% of metastatic carcinomas. Our results indicated that cytokeratin is not a reliable immunohistochemical marker to separate a malignant meningioma from metastatic carcinoma. A panel of epithelial markers including Ber-EP4, CEA, B72.3 and CD-15, and vimentin may be needed to separate malignant meningioma from metastatic carcinoma. Cytokeratin expression can be a potential pitfall for confusing a malignant meningioma with a metastatic carcinoma.

Antibodies, Neoplasm↗
PubMed2005

Clinical and histological features of multiple meningiomas compared with solitary meningiomas.

Between 1991 and 2002, 456 patients with an intracranial meningioma were treated. Thirty-nine of these had more than one meningioma (8.6%). The mean age was 58 years (27-85 years). Sex distribution was 8.8:1 (35 female, four male). There was no associated spinal meningioma. No patient had neurofibromatosis. In 19 patients all meningiomas were removed. Twelve showed the same histology, seven had different histological features. In the remaining 20 patients only the symptomatic meningioma was removed. Recurrences occurred in 11 patients (28.2%). Six patients died during follow-up. Multiple meningiomas have their own clinical features. Besides a high female preponderance, PR expression was stronger in multiple meningiomas than in solitary meningiomas while p53 status and MIB-1 LI were similar between the two groups. Progesterone receptor, p53 status and MIB-1 LI were valuable markers for predicting a patient's outcome in multiple meningiomas. The number of meningiomas is growing in patients with recurrent meningiomas.

Adult↗
PubMed2002

Histopathology and MIB-1 labeling index predicted recurrence of meningiomas: a proposal of diagnostic criteria for patients with atypical meningioma.

BACKGROUND: Although various histopathologic features have been associated with aggressive behavior or recurrence of meningiomas, there is little agreement about which features are the most important and in what combination. The objective of this study was to formulate diagnostic criteria for atypical meningioma. METHODS: Eighty-three patients with meningiomas who underwent macroscopic total resection and had been followed until they developed recurrent disease or for at least 10 years were studied. Thirteen histopathologic parameters that related to recurrence of the tumor were evaluated in each patient. All possible combinations of histologic parameters that were related significantly to recurrence were used to formulate scoring models. The model that included the fewest parameters and that could distinguish tumor recurrence best within 10 years was chosen as the final model. RESULTS: The final model included three parameters: loss of architecture, mitoses > or= 1.5/mm2, and necrosis. Of the 52 tumors with a score < 2 (0 or 1 of the 3 parameters), all except 1 tumor did not recur within 10 years, and they were all considered benign meningiomas. Of the 31 tumors with a score > or = 2 (2 or 3 of the 3 parameters), 94% recurred within 10 years (76% recurred within 5 years), and they were considered atypical meningiomas. The estimated 5-year and 10-year recurrence rates for the benign meningiomas were 0.0% and 1.9%, respectively, for benign meningiomas and 71.0% and 93.5%, respectively, for atypical meningiomas (P < 0.001). The estimated 5-year and 10-year mortality rates also were significantly different (0.0% and 0.0% vs. 22.1% and 26.7%, respectively; P < 0.001). The MIB-1 labeling index (LI) for the entire group studied ranged from 0.4 to 33.5 (mean LI, 8.4). Fifty-two tumors with an LI of < 10 did not recur within 10 years. Of the 31 tumors with an LI > or = 10, 97% recurred (71% within 5 years). CONCLUSIONS: Histopathology and MIB-1 LI were able to predict clinical outcomes of patients with meningioma. The authors propose that atypical meningioma may be diagnosed when two of the following three criteria are present: loss of architecture, mitoses > or = 1.5/mm2, and necrosis.

Adolescent↗
PubMed1990

Hormonal dependency of cerebral meningiomas. Part 2: In vitro effect of steroids, bromocriptine, and epidermal growth factor on growth of meningiomas.

Cell culture and biochemical techniques have been employed to examine the effects of steroids, bromocriptine, and epidermal growth factor (EGF) on the growth and proliferative potential of meningiomas. In cell culture, the growth of meningiomas was not altered by progestogens, antiprogestogens, or 17beta-estradiol. The progestogen, norethisterone, had no effect on the uptake by meningiomas cell cultures of 3H-thymidine. Furthermore, cytosolic deoxyribonucleic acid (DNA) polymerase activity of meningiomas did not correlate with the progesterone receptor status of the same tumors. In contrast, the androgen antagonists, cyproterone acetate and 11-alpha-hydroxyprogesterone, and the dopamine agonist, bromocriptine, all inhibited the in vitro growth of meningioma cells. The growth of meningioma cell cultures was stimulated by EGF, and there was a positive correlation between the EGF content and DNA polymerase activity in meningioma cytosols. These results demonstrate that female sex steroids do not influence growth of meningiomas in vitro, whereas antiandrogens and bromocriptine have an antiproliferative effect. Consequently, bromocriptine and antiandrogens may have a role in the medical treatment of meningiomas. In addition, these results suggest that EGF may be involved in the genesis and/or progression of meningiomas.

Bromocriptine↗
PubMed2005

Microarray-based gene expression profiling of benign, atypical and anaplastic meningiomas identifies novel genes associated with meningioma progression.

To identify gene expression profiles associated with human meningiomas of different World Health Organization (WHO) malignancy grades, we analyzed 30 tumors (13 benign meningiomas, WHO grade I; 12 atypical meningiomas, WHO grade II; 5 anaplastic meningiomas, WHO grade III) for the expression of 2,600 genes using cDNA-microarray technology. Receiver operator curve (ROC) analysis with a cutoff value of 45% selection probability identified 37 genes with decreased and 27 genes with increased expression in atypical and anaplastic meningiomas, compared to benign meningiomas. Supervised classification of the tumors did not reveal specific expression patterns representative of each WHO grade. However, anaplastic meningiomas could be distinguished from benign meningiomas by differential expression of a distinct set of genes, including several ones associated with cell cycle regulation and proliferation. Investigation of potential correlations between microarray expression data and genomic aberrations, detected by comparative genomic hybridization (CGH), demonstrated that losses on chromosomes 10 and 14 were associated with distinct expression profiles, including increased expression of several genes related to the insulin-like growth factor (IGF) (IGF2, IGFBP3 and AKT3) or wingless (WNT) (CTNNB1, CDK5R1, ENC1 and CCND1) pathways. Taken together, our microarray-based expression profiling revealed interesting novel candidate genes and pathways that may contribute to meningioma progression.

Chromosome Mapping↗
PubMedDate not supplied

Immunohistochemical characteristics of haemangiopericytic meningiomas: comparison with typical meningiomas, haemangioblastomas and haemangiopericytomas from extracranial sites.

The relationship between malignant vascular meningeal tumours and typical meningiomas remains controversial, despite the need for accurate diagnostic distinction between the two, and some forms of vascular meningioma may be more closely allied to haemangioblastomas or extracranial haemangiopericytomas than to true meningiomas. In order to try to clarify the diagnostic characteristics and origins of the entity known as haemangiopericytic meningioma, 10 histologically typical cases were stained by the immunoperoxidase technique with a panel of seven antibodies. The results were compared with those obtained from typical and angiomatous meningiomas, haemangioblastomas and haemangiopericytomas from extracranial sites. Both the haemangiopericytic meningiomas and the extracranial haemangiopericytomas showed a similar staining pattern, which differed from that of the typical and angiomatous meningiomas in the strikingly focal nature of the vimentin staining and the lack of reactivity with antibodies to epithelial elements. The haemangioblastomas were less consistent in their individual staining characteristics, but had a quite different overall pattern from all the other tumour types. It is, therefore, suggested that so-called haemangiopericytic meningiomas are in fact primary haemangiopericytomas of the meninges, antigenically distinct from true meningiomas and displaying a malignant potential appropriate to haemangiopericytomas arising in any other sites.

Antibodies, Monoclonal↗
PubMed1995

Evidence of meningioma infiltration into cranial nerves: clinical implications for cavernous sinus meningiomas.

Anatomical and biological studies of cavernous sinus meningiomas help us understand the biological heterogeneity of these tumors. The question of whether cavernous sinus meningiomas infiltrate cranial nerves is clinically important because of the effect on treatment planning. In the authors' experience of treating 36 patients with cavernous sinus meningiomas, tumor invasion into a cranial nerve was documented in two patients in whom a cranial nerve was resected during the cavernous sinus dissection. In both patients, histological examination using hematoxylin and eosin and bodian stains showed infiltration of the cranial nerves by a benign meningioma which, to the best of the authors' knowledge, is a condition previously unreported. This histological finding of meningioma invasion into a cranial nerve demonstrates the biological heterogeneity of cavernous sinus meningiomas and raises concern about the invasive character of meningioma. Because not all tumor cells can be identified radiologically or by direct visualization at surgery, occult tumor infiltration predisposes a patient to recurrence despite the best neurosurgical efforts. Evidence of cranial nerve infiltration by meningioma suggests that, in some circumstances, cavernous sinus dissection in the hope of total removal of a meningioma may be futile and, in the long term, may provide no advantage over treatment options with lower morbidity.

Adult↗
PubMed2000

Intracranial injection of human meningioma cells in athymic mice: an orthotopic model for meningioma growth.

OBJECT: Although human meningioma cells have been heterotopically implanted in nude mice, introducing these cells into intracranial locations seems more likely to reproduce normal patterns of tumor growth. To provide an orthotopic xenograft model of meningioma, the authors implanted a controlled quantity of meningioma cells at subdural and intracerebral sites in athymic mice. METHODS: Malignant (one tumor), atypical (two tumors), or benign (three tumors) meningiomas were placed into primary cell cultures. Cells (10(6)/10 microl) from these cultures and from an immortalized malignant meningioma cell line, IOMM-Lee, were injected with stereotactic guidance into the frontal white matter or subdural space of athymic mice. Survival curves were plotted for mice receiving tumor cells of each histological type and according to injection site. Other mice were killed at intervals and their heads were sectioned whole. Hematoxylin and eosin staining of these sections revealed the extent of tumor growth. CONCLUSIONS: The median length of survival for mice with malignant, atypical, or benign tumors was 19, 42, or longer than 84 days, respectively. Atypical and malignant tumors were invasive, but did not metastasize extracranially. Malignant tumors uniformly showed leptomeningeal dissemination and those implanted intracerebrally grew locally and spread noncontiguously to the ventricles, choroid plexus, convexities, and skull base. Tumors formed in only 50% of mice injected with benign meningioma cells, whereas injection of more aggressive cells was uniformly successful at tumor production. The three types of human meningiomas grown intracranially in athymic mice maintained their relative positions in the spectrum of malignancy. However, atypical meningiomas became more aggressive after xenografting and acquired malignant features, implying that there had been immune constraint in the original host. Tumor cells injected into brain parenchyma migrated to more optimal environments and grew best there. This model provides insights into the biology of meningiomas and may be useful for testing new therapies.

Aged↗