scholarly journals Familial multiple meningioma

2020 ◽  
Author(s):  
Keyword(s):  
Multiple Meningioma

Whole exome sequencing in a case of sporadic multiple meningioma reveals shared NF2, FAM109B, and TPRXL mutations, together with unique SMARCB1 alterations in a subset of tumor nodules

2015 ◽  
Vol 208 (6) ◽  
pp. 327-332 ◽  
Author(s):  
Miguel Torres-Martín ◽  
M. Elena Kusak ◽  
Alberto Isla ◽  
Rommel R. Burbano ◽  
Giovanny R. Pinto ◽  
...  
Keyword(s):  
Exome Sequencing ◽  
Whole Exome Sequencing ◽  
Whole Exome ◽  
Multiple Meningioma

scholarly journals Unresectable Recurrent Multiple Meningioma: A Case Report with Radiological Response to Somatostatin Analogues

2016 ◽  
Vol 9 (2) ◽  
pp. 520-525 ◽  
Author(s):  
Ana Ortolá Buigues ◽  
Irene Crespo Hernández ◽  
Manuela Jorquera Moya ◽  
Jose Ángel Díaz Pérez
Keyword(s):  
Somatostatin Receptors ◽  
Somatostatin Analogues ◽  
Somatostatin Analogue ◽  
Continuous Administration ◽  
Antiangiogenic Effect ◽  
Neurological Improvement ◽  
Radiological Response ◽  
Multiple Meningioma ◽  
Multiple Recurrences

Medical treatment of meningiomas is reserved for cases in which surgery and radiotherapy have failed. Given that a high percentage of meningiomas express somatostatin receptors, treatment with somatostatin analogues has been proposed. In addition, these medications have been shown to have an antiproliferative and antiangiogenic effect in vitro. To date, very few cases with clinical response and none with radiological response have been described. The case described here is the first to report a radiological response. A 76-year-old Caucasian male was first diagnosed with unresectable meningioma at age 47. The patient experienced multiple recurrences and underwent three surgeries and radiotherapy over the years from the initial diagnosis. Despite treatment, the disease continued its progression. Based on an Octreoscan positive for tumour uptake, therapy with extended-release somatostatin analogues was started. Although no clinical neurological improvement was observed, magnetic resonance imaging scans revealed a discreet but continuous radiological response over time. After >2 years of continuous administration of lanreotide, the patient remains progression free. In highly selected cases, somatostatin analogue treatment for meningioma may be beneficial. Based on our findings, treatment with somatostatin analogues should be maintained longer than previously described before evaluating treatment response.

Rare case of multiple meningiomas in nonneurofibromatosis patient at unusual locations

2017 ◽  
Vol 31 (2) ◽  
pp. 240-243 ◽  
Author(s):  
Vikrant Setia ◽  
Deepashu Sachdeva ◽  
Shrinivas Odugoudar ◽  
Pravin Borde ◽  
Daljit Singh
Keyword(s):  
Posterior Fossa ◽  
Rare Case ◽  
Intracranial Lesion ◽  
Multiple Meningiomas ◽  
Intraventricular Meningioma ◽  
Intracranial Lesions ◽  
Multiple Meningioma

Abstract Multiple meningioma is a condition in which more than one intracranial lesion is seen in different location and these lesions may occur with or without signs of neurofibromatosis. Incidence of multiple meningioma range from 1 to 10% in different series. We report a case of multiple meningioma in a 33 years old female who had 14 intracranial lesions both supratentorially and infratentorially, and underwent surgery for large right lateral intraventricular meningioma. She had two meningiomas located in posterior fossa associated with supratentorial meningioma, which has been rarely reported.

scholarly journals MULTIPLE MENINGIOMA

2000 ◽  
Vol 56 (3) ◽  
pp. 275
Author(s):  
PRAKASH SINGH
Keyword(s):  
Multiple Meningioma

Evidence for clonal spread in the development of multiple meningiomas

1995 ◽  
Vol 83 (4) ◽  
pp. 705-709 ◽  
Author(s):  
Jeffrey J. Larson ◽  
John M. Tew ◽  
Matthias Simon ◽  
Anil G. Menon
Keyword(s):  
X Chromosome ◽  
Progenitor Cell ◽  
Underlying Mechanism ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Content Type ◽  
Multiple Meningiomas ◽  
Multiple Meningioma ◽  
Polymerase Chain ◽  
Clonal Spread

✓ Meningiomas are common intracranial tumors that arise from the arachnoid cells of the meninges. Occasionally patients develop multiple meningiomas. Because the underlying mechanism of multiple meningioma formation is unknown, the authors examined the pattern of X chromosome inactivation in multiple meningiomas. Fifteen intracranial meningiomas were resected in four patients with multiple meningiomas to determine whether the tumors in patients with multiple meningiomas originate from a common progenitor cell or arise independently. Specimens were examined using polymerase chain reaction assays to detect the pattern of X chromosome inactivation. In each patient, all tumors showed inactivation of the same X chromosome, suggesting that tumors arose from the same clone of cells (p <0.0005). The authors conclude that multiple meningiomas arise from the uncontrolled spread of a single progenitor cell.

scholarly journals Nomegestrol Acetate or Chlormadinone Acetate Progestative Treatment in Women: Meningioma Behavior at Treatment Discontinuation

2021 ◽  
Author(s):  
Simona Mihaela Florea ◽  
Sebastien Boissonneau ◽  
Thibault Passeri ◽  
Anne Laure Bernat ◽  
Emmanuel Mandonnet ◽  
...  
Keyword(s):  
Treatment Discontinuation ◽  
Intracranial Meningioma ◽  
Close Monitoring ◽  
Chlormadinone Acetate ◽  
Multiple Meningiomas ◽  
Urgent Surgery ◽  
Nomegestrol Acetate ◽  
Multiple Meningioma ◽  
Stopping Treatment

Abstract Background: Associations between progestins and meningiomas is now well established. While the link between cyproterone acetate (CA) and meningioma was thoroughly studied, there is far less available data regarding the link between chlormadinone acetate (CHA) or nomegestrol acetate (NA) and risk of intracranial meningiomaMethods: We are presenting a series of 28 patients diagnosed with single or multiple meningiomas while treated with CHA-NA, in which the clinical and radiological course were analyzed after treatment discontinuation.Results: 28 women, with a mean age of 56 years old, were diagnosed with one or multiple meningioma while being treated with either CHA or NA. After stopping treatment, 89.3% showed either tumor shrinkage or tumor stabilization on follow-up MRIs. Multiple meningiomas were more likely observed in patients with long periods of treatment (>10 years, p 0.03) and seem to have a better clinical course (p 0.01). Most of the lesions were located on the skull base (55.4%). Four patients with multiple meningiomas showed discordant tumors evolution, with some tumors growing while others were decreasing. Most of the growing meningiomas were either convexity or midline lesions and more posteriorly located. Conclusion: Our study demonstrated a significant percentage of tumor diminution or stabilization after NA and CHA discontinuation. Therefore, treatment discontinuation with close monitoring should be the first measure taken if urgent surgery is not indicated. However, our results seem to be less encouraging than previously described in patients treated by CA, with more patients showing tumor growth despite treatment discontinuation. Further studies are needed to differentiate the effect of the different progestins treatment on meningiomas.

Rosai-Dorfman Disease Mimicking Multiple Meningioma

Neurosurgery ◽  
1995 ◽  
Vol 36 (6) ◽  
pp. 1185???1187 ◽  
Author(s):  
Miriam Kim ◽  
John Provias ◽  
Mark Bernstein
Keyword(s):  
Rosai Dorfman Disease ◽  
Multiple Meningioma

scholarly journals Primary Pulmonary Multiple Meningioma

Haigan ◽  
2007 ◽  
Vol 47 (6) ◽  
pp. 791-792 ◽  
Author(s):  
Takashi Ibe ◽  
Mitsuhiro Kamiyoshihara ◽  
Atsushi Takise ◽  
Yasuki Iwasaki ◽  
Masakiyo Yatomi ◽  
...  
Keyword(s):  
Multiple Meningioma

EPCO-29. GENOMIC PROFILING OF SPORADIC MULTIPLE MENINGIOMAS

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi8-vi8
Author(s):  
Zeynep Erson-Omay ◽  
Tanyeri Barak ◽  
Shaurey Vetsa ◽  
Arushii Nadar ◽  
Danielle Miyagishima ◽  
...  
Keyword(s):  
Underlying Mechanism ◽  
Copy Number Variations ◽  
Genomic Profiling ◽  
Multiple Meningiomas ◽  
Whole Exome ◽  
Radiation History ◽  
History Of ◽  
Multiple Meningioma ◽  
Genomic Characterization

Abstract INTRODUCTION In rare cases, sporadic meningiomas can occur as multiple tumors in the same patient without a known germline mutation. While the underlying mechanism that leads to the formation of these multiple lesions has been hypothesized to be monoclonal or independent, the genomic profiles to support these theories remain understudied. METHODS Patients with an absence of family history of meningioma and prior radiation history with multiple metachronous meningiomas were included. All tissue underwent whole exome sequencing and analysis of somatic single nucleotide variations (SNV), small insertion/deletion (INDEL) events together with copy number variations (CNV) was performed. The genomic findings were correlated with clinical data. RESULTS A cohort of 13 meningiomas and one dural specimen, from five individuals was studied. The majority (9/13 tumors) of tumors had NF2 mutation/Chr22 loss. Four out of 5 cases had a monoclonal origination, whereas one case displayed an independent clonal formation. The somatic profile of dura was unrevealing. In contrast to the current understanding, we found monoclonal formation of multiple meningiomas is not exclusive to NF2 driven cases, as non-NF2 mutated meningiomas can too display a monoclonal etiology. Moreover, multiple monoclonal-originating lesions did not always display a homogenous profile, but rather exhibited heterogeneity through branching evolution, where some lesions acquired genomic alterations associated with aggressive behavior. The histological characterization of multiple meningioma cases does not necessarily overlap with the genomic clustering. CONCLUSION To our knowledge, this is the first study to use unbiased comprehensive genomic methods to reveal the heterogeneity of multiple meningioma genomic profiles. Our extensive genomic characterization of this cohort revealed that monoclonal formation can be observed both in NF2 and non-NF2 mutant meningiomas and can introduce heterogeneity. Therefore, in order to understand the full scope of each individual’s disease, detailed genomic profiling of all lesions, when possible, should be performed.

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