Meningioma múltiplo familiar é um tumor benigno raro do sistema nervoso central, que se caracteriza pelo surgimento de múltiplos meningiomas ou, raramente, de um único, em dois ou mais parentes de sangue, sem outros sinais aparentes de síndromes. Dependendo da localização, da velocidade de crescimento e do tamanho dos tumores, os pacientes podem apresentar um comprometimento neurológico sutil, que piora gradualmente, ou um comprometimento súbito e grave, ou podem ser completamente assintomáticos.
Introdução
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Meningioma múltiplo familiar é um tumor benigno raro do sistema nervoso central, que se caracteriza pelo surgimento de múltiplos meningiomas ou, raramente, de um único, em dois ou mais parentes de sangue, sem outros sinais aparentes de síndromes. Dependendo da localização, da velocidade de crescimento e do tamanho dos tumores, os pacientes podem apresentar um comprometimento neurológico sutil, que piora gradualmente, ou um comprometimento súbito e grave, ou podem ser completamente assintomáticos.
Escala de raridade
<1/50kMuito rara
1/20kRara
1/10kPouco freq.
1/5kIncomum
1/2k
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Sinais e sintomas
O que aparece no corpo e com que frequência cada sintoma acontece
Linha do tempo da pesquisa
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Genética e causas
O que está alterado no DNA e como passa nas famílias
Genes associados
5 genes identificados com associação a esta condição. Padrão de herança: Autosomal dominant.
Transcriptional activator which specifically regulates expression of TBX22 in the posterior region of the developing palate. Required during later stages of palate development for growth and medial fusion of the palatal shelves. Promotes maturation and normal function of calvarial osteoblasts, including expression of the osteoclastogenic cytokine TNFSF11/RANKL. Necessary for normal development of the membranous bones of the skull (By similarity). May play a role in tumor suppression (Probable)
Nucleus
CEBALID syndrome
An autosomal dominant developmental disorder characterized by global developmental delay, intellectual disability with severe expressive language delay, craniofacial dysmorphism, and structural brain abnormalities. Most patients have an atypical form of rhombencephalosynapsis, a distinctive brain malformation characterized by partial or complete loss of the cerebellar vermis with fusion of the cerebellar hemispheres. Other frequent features include perisylvian polymicrogyria, abnormal posterior clinoid processes, cerebellar hypoplasia or dysplasia, and persistent trigeminal artery.
Involved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology). Component of SWI/SNF chromatin remodeling complexes that carry out key enzymatic activities, changing chromatin structure by altering DNA-histone contacts within a nucleosome in an ATP-dependent manner. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). Durin
Nucleus
Meningioma
A common neoplasm of the central nervous system derived from arachnoidal cells. The majority of meningiomas are well differentiated vascular tumors which grow slowly and have a low potential to be invasive, although malignant subtypes occur. Most cases are sporadic. Familial occurrence of meningioma is rare.
Negative regulator in the hedgehog/smoothened signaling pathway (PubMed:10559945, PubMed:10564661, PubMed:10806483, PubMed:12068298, PubMed:12975309, PubMed:15367681, PubMed:22365972, PubMed:24217340, PubMed:24311597, PubMed:27234298, PubMed:28965847). Down-regulates GLI1-mediated transactivation of target genes (PubMed:15367681, PubMed:24217340, PubMed:24311597). Down-regulates GLI2-mediated transactivation of target genes (PubMed:24217340, PubMed:24311597). Part of a corepressor complex that a
CytoplasmNucleus
Medulloblastoma
Malignant, invasive embryonal tumor of the cerebellum with a preferential manifestation in children.
Core component of the BAF (hSWI/SNF) complex. This ATP-dependent chromatin-remodeling complex plays important roles in cell proliferation and differentiation, in cellular antiviral activities and inhibition of tumor formation. The BAF complex is able to create a stable, altered form of chromatin that constrains fewer negative supercoils than normal. This change in supercoiling would be due to the conversion of up to one-half of the nucleosomes on polynucleosomal arrays into asymmetric structures
Nucleus
Rhabdoid tumor predisposition syndrome 1
A familial cancer syndrome predisposing to renal or extrarenal malignant rhabdoid tumors and to a variety of tumors of the central nervous system, including choroid plexus carcinoma, medulloblastoma, and central primitive neuroectodermal tumors. Rhabdoid tumors are the most aggressive and lethal malignancies occurring in early childhood.
Growth factor that plays an essential role in the regulation of embryonic development, cell proliferation, cell migration, survival and chemotaxis. Potent mitogen for cells of mesenchymal origin (PubMed:26599395). Required for normal proliferation and recruitment of pericytes and vascular smooth muscle cells in the central nervous system, skin, lung, heart and placenta. Required for normal blood vessel development, and for normal development of kidney glomeruli. Plays an important role in wound
Secreted
Basal ganglia calcification, idiopathic, 5
A form of basal ganglia calcification, an autosomal dominant condition characterized by symmetric calcification in the basal ganglia and other brain regions. Affected individuals can either be asymptomatic or show a wide spectrum of neuropsychiatric symptoms, including parkinsonism, dystonia, tremor, ataxia, dementia, psychosis, seizures, and chronic headache. Serum levels of calcium, phosphate, alkaline phosphatase and parathyroid hormone are normal. The neuropathological hallmark of the disease is vascular and pericapillary calcification, mainly of calcium phosphate, in the affected brain areas.
Variantes genéticas (ClinVar)
1,738 variantes patogênicas registradas no ClinVar.
Classificação de variantes (ClinVar)
Distribuição de 1 variantes classificadas pelo ClinVar.
Vias biológicas (Reactome)
21 vias biológicas associadas aos genes desta condição.
Diagnóstico
Os sinais que médicos procuram e os exames que confirmam
Tratamento e manejo
Remédios, cuidados de apoio e o que precisa acompanhar
Onde tratar no SUS
Hospitais de referência no Brasil e o protocolo oficial do SUS (PCDT)
🇧🇷 Atendimento SUS — Meningioma familiar múltiplo
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Dados de DATASUS/CNES, SBGM, ABNeuro e Ministério da Saúde. Sempre confirme a disponibilidade diretamente com o estabelecimento.
Pesquisa ativa
Ensaios clínicos abertos e novidades científicas recentes
Pesquisa e ensaios clínicos
Nenhum ensaio clínico registrado para esta condição.
Publicações mais relevantes
STING activation induces cytotoxic and immune responses in meningiomas via inflammatory cell death pathways.
Meningiomas are common tumors of the central nervous system that are typically treated with surgery or radiation, but lack established systemic therapies. Activation of the stimulator of interferon genes pathway with an agonist such as 8803 can trigger anti-tumor immune responses. Using integrated molecular approaches, here we show that this pathway is targetable in both neoplastic and immune populations within the meningioma microenvironment. Meningioma tumor cells exhibit promoter hypomethylation and increased chromatin accessibility of the STING genomic locus, associated with robust expression of this gene. Treatment of diverse patient meningiomas ex vivo with 8803 induces direct tumor cytotoxicity through inflammatory cell death pathways, including induction of gasdermin D membrane pore formation. Release of necrotic tumor debris triggered by 8803 activates macrophages and upregulates matrix metalloproteinase production, facilitating degradation of extra-cellular collagen. Injection of preclinical meningiomas with 8803 induces survival benefits, including in an immunocompetent orthotopic setting, through remodeling of the tumor microenvironment, immune infiltration, and downregulation of tumor-mediated immune suppression, thereby nominating 8803 for treatment consideration in meningiomas.
Association Between miRNAs and the Diagnosis, Prognosis, and Recurrence of Patients with Meningioma: A Systematic Review.
To evaluate the diagnostic, prognostic, and recurrence-related roles of microRNAs (miRNAs) in meningioma based on expression profiles across different biological samples. This systematic review was conducted in accordance with Cochrane Collaboration and PRISMA guidelines. A search was performed in PubMed, Scopus, Web of Science, and Google Scholar without language restrictions. Cohort and case–control studies assessing miRNA expression in tumor tissue, serum, or cerebrospinal fluid from patients with histologically confirmed meningioma were included. Risk of bias was evaluated using the Newcastle–Ottawa Scale. Bioinformatic pathway enrichment analyses were conducted for recurrently miRNAs. Twenty-three studies involving 1615 participants were included, of whom 1461 had meningiomas (WHO grades 1–3). Overall, 153 miRNAs were evaluated, including 90 upregulated, 45 downregulated, and 18 without significant differential expression. miR-21, miR-34a, and members of the miR-181 family were consistently associated with tumor grade and progression. Tumor recurrence was most frequently linked to miR-224-5p, miR-331-5p, miR-29c-3p, and miR-219-5p. Circulating miRNAs, particularly miR-497 and miR-219, demonstrated diagnostic potential in serum and cerebrospinal fluid. Pathway analyses highlighted enrichment in metabolic and signaling pathways, including sphingolipid, sulfur, and fatty acid metabolism. This review identifies miR-21, miR-224-5p, miR-331-5p, miR-29c-3p, and circulating miR-497 and miR-219 as the most promising miRNA biomarkers for meningioma diagnosis, grading, and recurrence monitoring. Despite methodological heterogeneity, the consistency of these findings across independent studies supports their translational potential. Nonetheless, large, standardized studies with independent validation cohorts are required prior to clinical implementation. The online version contains supplementary material available at 10.1007/s10571-026-01665-2.
KMT2C Loss Promotes NF2-Wildtype Meningioma Progression and Ferroptosis Sensitivity via Epigenetic Repression of Hippo Signaling.
High-grade meningiomas remain clinically challenging due to their aggressive behavior and limited therapeutic options. Although mutations and dysregulation of KMT2 family members have been implicated in various cancers, their functional significance in meningioma remains unclear. While NF2 alterations are the most common drivers of meningioma pathogenesis, the mechanisms regulating NF2 transcription in NF2-intact tumors are poorly understood. Here, we demonstrate that KMT2C expression is markedly reduced in high-grade meningiomas and that loss of KMT2C promotes proliferation and invasion in NF2-wild-type meningioma cells. Mechanistically, KMT2C deficiency suppresses NF2 transcription and inactivates Hippo signaling, leading to enhanced oncogenic activity and increased sensitivity to ferroptosis. Loss of KMT2C impairs the acetyltransferase activity of CBP/EP300, resulting in a global reduction of H3K27ac and transcriptional silencing of NF2. Pharmacological restoration of histone acetylation with the HDAC inhibitor Trichostatin A (TSA) effectively suppressed tumor growth. Collectively, our findings identify KMT2C as a key epigenetic regulator linking promoter histone acetylation, NF2-Hippo pathway activity, and ferroptosis susceptibility. These results provide mechanistic insights into high-grade meningioma progression and highlight ferroptosis induction and epigenetic modulation as promising therapeutic strategies for NF2-wild-type, KMT2C-deficient meningiomas.
Risk for Cancer With Glucagon-Like Peptide-1 Receptor Agonists and Dual Agonists : A Systematic Review and Meta-analysis.
Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are used for type 2 diabetes mellitus (T2DM) and overweight or obesity, but their association with cancer is unclear. To investigate the risk for obesity-related cancer associated with GLP-1RAs. PubMed, Embase, Web of Science, Scopus, and the Cochrane Central Register of Controlled Trials from inception to August 2025. Randomized placebo-controlled trials reporting any of the following cancer outcomes: thyroid, pancreatic, colorectal, gastric, esophageal, liver, gallbladder, breast, ovarian, endometrial, or kidney cancer; multiple myeloma; or meningioma. Risk of bias was evaluated using the Cochrane Risk of Bias 2 tool, and certainty of evidence was assessed using the GRADE (Grading of Recommendations Assessment, Development and Evaluation) approach. Odds ratios (ORs) were pooled using random-effects meta-analysis. The review included 48 trials involving 94 245 participants. GLP-1RAs probably have little or no effect on risk for thyroid cancer (OR, 1.37 [95% CI, 0.82 to 2.31]; 1 fewer to 9 more cases per 10 000 patients treated), pancreatic cancer (OR, 0.84 [CI, 0.53 to 1.35]; 9 fewer to 6 more per 10 000), breast cancer (OR, 0.95 [CI, 0.60 to 1.49]; 10 fewer to 12 more per 10 000), or kidney cancer (OR, 1.12 [CI, 0.78 to 1.60]; 5 fewer to 13 more per 10 000) (moderate certainty). GLP-1RAs may have little or no effect on colorectal, esophageal, liver, gallbladder, ovarian, or endometrial cancer; multiple myeloma; or meningioma (low certainty). The effect on gastric cancer is very uncertain. Results were consistent in sensitivity analyses of trials with low risk of bias and studies of semaglutide or tirzepatide and across subgroups stratified by follow-up duration, population, GLP-1RA class, weight loss profile, dose, and duration of action. The included trials were not designed to evaluate cancer outcomes and had short follow-up. GLP-1RAs may have little or no effect on risk for obesity-related cancers. Longer-term studies are needed to clarify potential risks or benefits. None. (PROSPERO: CRD42024608365). LZTR1- and SMARCB1-related schwannomatosis are characterized by a predisposition to develop multiple non-intradermal schwannomas. Individuals most commonly present between the second and fourth decade of life. The most common presenting feature is localized or diffuse pain or asymptomatic mass. Schwannomas most often affect peripheral nerves and spinal nerves. Meningiomas have only been reported in individuals with SMARCB1-related schwannomatosis. Malignancy remains a risk especially in individuals with SMARCB1-related schwannomatosis. The diagnosis of LZTR1- or SMARCB1-related schwannomatosis is established in a proband with characteristic clinical findings and a heterozygous germline pathogenic variant in LZTR1 or SMARCB1 identified by molecular genetic testing. Treatment of manifestations: Comprehensive, multimodal approach to pain management, guided by a pain management specialist or neurologist; referral to mental health professionals as needed for anxiety and/or depression; surgery for schwannomas associated with uncontrolled localized pain or a neurologic deficit; meningioma treatment as for sporadic meningioma. Surveillance: Annual neurologic examination and pain assessment; brain and spine MRI or whole-body MRI every two to three years beginning at age 12 years, with fine cuts through internal auditory canal in those w/LZTR1-related schwannomatosis; assessment for anxiety and depression annually or as needed. Agents/circumstances to avoid: Radiation can increase the risk for malignant transformation and should be avoided when possible. Evaluation of relatives at risk: It is appropriate to evaluate apparently asymptomatic older and younger at-risk relatives of an affected individual in order to identify as early as possible those who would benefit from surveillance and clinical management. LZTR1- and SMARCB1-related schwannomatosis are inherited in an autosomal dominant manner with reduced penetrance. Fewer than 20% of individuals diagnosed with LZTR1- or SMARCB1-related schwannomatosis have an affected parent. In families in which the proband represents a simplex case, the proportion of probands with a de novo pathogenic variant is approximately 30% for LZTR1-related schwannomatosis and 10% for SMARCB1-related schwannomatosis. Each child of an individual with LZTR1- or SMARCB1-related schwannomatosis has up to a 50% chance of inheriting a pathogenic variant. Once a germline LZTR1 or SMARCB1 pathogenic variant has been identified in an affected family member, predictive testing for at-risk asymptomatic family members and prenatal and preimplantation genetic testing are possible.
French translation and preliminary psychometric evaluation of the Meningioma Quality of Life questionnaire (MQOL-FR).
Disease-specific instruments to assess quality of life in meningioma patients are scarce, and no validated French meningioma-specific questionnaire is available. We translated the Meningioma Quality of Life questionnaire (MQOL) into French (MQOL-FR) and performed a preliminary psychometric evaluation focused on the total score. In this prospective study of adults with meningioma, MQOL was translated using the EORTC forward-backward procedure with expert-panel reconciliation. Patients completed MQOL-FR, Karnofsky Performance Status (KPS), Functional Assessment of Cancer Therapy-Brain (FACT-Br), and EQ-5D. Internal consistency (Cronbach's alpha), test-retest reliability (intraclass correlation coefficient (ICC), and convergent validity (Pearson correlations) were assessed using available complete data for each score. Of 56 invited patients, 37 completed at least part of MQOL-FR. Across subscales, 32-36 patients contributed to internal consistency analyses, and 26 provided complete data for the MQOL total score (all scorable items completed; item 69 "non applicable/non-scored"). Cronbach's alpha for the total score was 0.88 (95%CI 0.75-0.95). Several subscales (symptoms, emotional, anxiety, functional well-being) showed acceptable reliability, whereas others (vitality, family, social, physical) were less robust. Thirteen patients completed the questionnaire twice; nine had complete paired total-score data. Test-retest reliability for the total score was excellent (ICC 0.93, 95%CI 0.71-0.98). Measurement error indices were SEM 3.8 points and MDC95 10.6 points (0-100 scale). The MQOL total score correlated strongly with the FACT-Br total score (r = 0.84). MQOL-FR showed good internal consistency and excellent test-retest reliability for the total score, with encouraging convergent validity in this cohort. Subscale-level findings should be considered exploratory. Larger multicenter studies are needed to refine subscale performance, evaluate responsiveness to clinical change, and support broader validation in more representative samples.
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International journal of surgical pathologyQuality of life after resection of a meningioma-A cross-cultural comparison of Indian and Australian patients.
PloS oneBAP1 Tumour Predisposition Syndrome Due to Whole BAP1 Gene Deletion.
Case reports in geneticsOculomotor nerve palsy in neurofibromatosis type 2.
Radiology case reportsCoexisting lipomatous meningioma and glioblastoma in Cowden syndrome: A unique tumor association.
Neuropathology : official journal of the Japanese Society of NeuropathologySupratentorial extra-axial RELA fusion-positive ependymoma misdiagnosed as meningioma by intraoperative histological and cytological examinations: a case report.
Journal of medical case reportsExtra-Axial supratentorial anaplastic ependymoma: Unusual location of an aggressive tumor, A case report.
Indian journal of pathology & microbiologyCaspase 8 Expression Patterns in Meningiomas: A Tissue Microarray Digital Image Analysis.
CureusTRAF7 somatic mosaicism in a patient with bilateral optic nerve sheath meningiomas: illustrative case.
Journal of neurosurgery. Case lessonsClinical implications of the 2021 edition of the WHO classification of central nervous system tumours.
Nature reviews. Neurology[Molecular Biological Background of Neurofibromatosis Type 2].
No shinkei geka. Neurological surgeryGenomic profiling of sporadic multiple meningiomas.
BMC medical genomicsInteresting presentation of postnatal depression and infant failure to thrive.
BMJ case reportsGemcitabine Cooperates with Everolimus to Inhibit the Growth of and Sensitize Malignant Meningioma Cells to Apoptosis Induced by Navitoclax, an Inhibitor of Anti-Apoptotic BCL-2 Family Proteins.
CancersExamination of Genetic Susceptibility in Radiation-Associated Meningioma.
Radiation researchPhase 2 study of pembrolizumab in patients with recurrent and residual high-grade meningiomas.
Nature communicationsIntracranial Osteoma: Unusual Etiology of Chronic Daily Headaches.
CureusUtilization of Cerebrospinal Fluid Proteome Analysis in the Diagnosis of Meningioma: A Systematic Review.
CureusDefining the Spectrum, Treatment and Outcome of Patients With Genetically Confirmed Gorlin Syndrome From the HIT-MED Cohort.
Frontiers in oncologyReceptor-Tyrosine Kinase Inhibitor Ponatinib Inhibits Meningioma Growth In Vitro and In Vivo.
CancersThe integrated multiomic diagnosis of sporadic meningiomas: a review of its clinical implications.
Journal of neuro-oncologyReceptor Tyrosine Kinases as Candidate Prognostic Biomarkers and Therapeutic Targets in Meningioma.
International journal of molecular sciencesRelapse of Psychosis Status Post Meningioma Resection.
Health psychology researchNegative Impact of COVID-19 Upon Primary Brain Tumor Care.
CureusGenomic Biomarkers of Meningioma: A Focused Review.
International journal of molecular sciencesMeningiomas in Patients With Malignant Pleural Mesothelioma Harboring Germline BAP1 Mutations.
Journal of thoracic oncology : official publication of the International Association for the Study of Lung CancerIntegrated Molecular-Morphologic Meningioma Classification: A Multicenter Retrospective Analysis, Retrospectively and Prospectively Validated.
Journal of clinical oncology : official journal of the American Society of Clinical OncologyDescription of Two Families with New Mutations in Familial Cerebral Cavernous Malformations Genes.
Journal of stroke and cerebrovascular diseases : the official journal of National Stroke AssociationCoexistent vestibular schwannoma and meningioma in a patient without neurofibromatosis: A case report and review of literature.
World journal of clinical casesGermline BAP1 Mutation in a Family With Multi-Generational Meningioma With Rhabdoid Features: A Case Series and Literature Review.
Frontiers in oncologyManagement experience of pediatric meningioma in a Mexican reference center.
Annals of diagnostic pathologySomatic PIK3CA Mutations in Sporadic Cerebral Cavernous Malformations.
The New England journal of medicineBilateral Diffuse Uveal Melanocytic Proliferation in a Patient with Recurrent Frontal Lobe Meningioma.
Ocular immunology and inflammationIntracranial meningioma in two coeval adult cats from the same litter.
JFMS open reportsIt's All Due to the Thyroid: Lessons Learnt From a Patient's Perspective.
CureusMeningioma genomics: a therapeutic challenge for clinicians.
Journal of integrative neuroscienceBiological Treatments of Neurofibromatosis Type 2 and Other Skull Base Disorders.
Otolaryngologic clinics of North AmericaPatient-specific virtual reality technology for complex neurosurgical cases: illustrative cases.
Journal of neurosurgery. Case lessonsEpidemiological distribution of primary central nervous system tumors in the Western Province of Saudi Arabia: a local registry from neuroscience-affiliated centers.
Epidemiology and healthVenous Anatomy Influence on the Approach Selection of a Petroclival Clear Cell Meningioma With Associated Multiple Spinal Meningiomas: 2-Dimensional Operative Video.
Operative neurosurgery (Hagerstown, Md.)Multiple meningiomas arising within the same hemisphere associated with Li-Fraumeni syndrome.
Surgical neurology internationalA Novel Pathogenic Variant in the MN1 Gene in a Patient Presenting with Rhombencephalosynapsis and Craniofacial Anomalies, Expanding MN1 C-terminal Truncation Syndrome.
Journal of pediatric geneticsSurveillance for subsequent neoplasms of the CNS for childhood, adolescent, and young adult cancer survivors: a systematic review and recommendations from the International Late Effects of Childhood Cancer Guideline Harmonization Group.
The Lancet. OncologyInnumerable Meningiomas Arising in a Patient With Tuberous Sclerosis Complex Decades After Radiation Therapy.
Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology SocietySWI/SNF deficient central nervous system neoplasms.
Seminars in diagnostic pathologyCase report 68Ga-DOTATATE of optic nerve sheath meningioma.
American journal of ophthalmology case reportsKIF11 inhibitors filanesib and ispinesib inhibit meningioma growth in vitro and in vivo.
Cancer lettersCase Series of Skull Base Meningioma Resection in the Octogenarian Population.
Journal of neurological surgery. Part B, Skull baseMeningioma: A Pathology Perspective.
NeurosurgeryA Preliminary Report on Quality of Life and Sexual Function in Brain Tumor Patients.
The journal of sexual medicineEpidemiology and survival of patients with spinal meningiomas: A SEER analysis.
European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical OncologyInterdisciplinary Approaches to Survivorship with a Focus on the Low-grade and Benign Brain Tumor Populations.
Current oncology reportsIntracranial angiomatoid fibrous histiocytoma with rhabdoid features: a mimic of rhabdoid meningioma.
Brain tumor pathologyA Case of Multiple Adenomatous Colon Polyps and Meningiomas.
GastroenterologyEffect of lifestyle and dietary factors in the development of brain tumors.
Journal of family medicine and primary careCo-expression of CD34 and h-caldesmon in a benign meningioma-like dermal neoplasm, a case report.
Dermatology reportsAcute Necrotizing Encephalitis as a Probable Association of COVID-19.
Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care MedicineFamilial Nervous System Tumor Syndromes.
Continuum (Minneapolis, Minn.)mTOR kinase inhibition disrupts neuregulin 1-ERBB3 autocrine signaling and sensitizes NF2-deficient meningioma cellular models to IGF1R inhibition.
The Journal of biological chemistryDemographic study of brain tumour in a neurosurgical department in Terengganu, Malaysia.
The Medical journal of MalaysiaThe importance of genetic counseling and screening for people with pathogenic SMARCE1 variants: A family study.
American journal of medical genetics. Part APredictive Model and Online Calculator for Discharge Disposition in Brain Tumor Patients.
World neurosurgeryIncidence, Mortality, and Survival Trends of Primary CNS Tumors in Cali, Colombia, From 1962 to 2019.
JCO global oncologyNasopharyngeal B-cell lymphoma with pan-hypopituitarism and oculomotor nerve palsy: a case report and review of the literature.
BMC endocrine disordersForkhead Box M1 promotes the growth and tube formation of human malignant meningioma cells via the aryl hydrocarbon receptor signaling pathway.
Folia neuropathologicaFamilial Pediatric Clear Cell Meningioma With Germline SMARCE1 Mutation in the United States.
Journal of neuropathology and experimental neurologyARMC5 Primary Bilateral Macronodular Adrenal Hyperplasia Associated with a Meningioma: A Family Report.
Case reports in endocrinologySubsequent Neoplasm Risk Associated With Rare Variants in DNA Damage Response and Clinical Radiation Sensitivity Syndrome Genes in the Childhood Cancer Survivor Study.
JCO precision oncologyMolecular mechanisms of ARMC5 mutations in adrenal pathophysiology.
Current opinion in endocrine and metabolic researchFamilial Tuberculum Sellae Meningiomas.
The Journal of craniofacial surgeryOccupational and ambient radiation exposures from Lu-177 DOTATATE during targeted therapy.
Applied radiation and isotopes : including data, instrumentation and methods for use in agriculture, industry and medicineGATA-4, a potential novel therapeutic target for high-grade meningioma, regulates miR-497, a potential novel circulating biomarker for high-grade meningioma.
EBioMedicineBenign and malignant tumors of the central nervous system and pregnancy.
Handbook of clinical neurologyThe Potential of MLN3651 in Combination with Selumetinib as a Treatment for Merlin-Deficient Meningioma.
CancersDetermining the unmet needs of patients with intracranial meningioma-a qualitative assessment.
Neuro-oncology practiceEnd of life care for patients with meningioma.
Handbook of clinical neurologyMultiple primary tumors: a case report and review of the literature.
BMC musculoskeletal disordersInherited genetic syndromes and meningiomas.
Handbook of clinical neurologyA Retrospective Interventional Cohort Study to Assess the Safety and Efficacy of Sandostatin LAR for Treatment of Recurrent and/or Refractory Meningiomas.
Frontiers in neurologyIntracranial emergencies during pregnancy requiring urgent neurosurgical treatment.
Clinical neurology and neurosurgeryPiTMaP: A New Analytical Platform for High-Throughput Direct Metabolome Analysis by Probe Electrospray Ionization/Tandem Mass Spectrometry Using an R Software-Based Data Pipeline.
Analytical chemistryThe utility of 3-dimensional-printed models for skull base meningioma surgery.
Annals of translational medicineDemographics and outcomes of meningioma patients treated at a tertiary care center in the Middle East.
Clinical neurology and neurosurgeryAssociações
Organizações que acompanham esta doença — pra ter apoio e orientação
Ainda não temos associações cadastradas para Meningioma familiar múltiplo.
É de uma associação que acompanha esta doença? Fale com a gente →
Comunidades
Grupos ativos de quem convive com esta doença aqui no Raras
Ainda não existe comunidade no Raras para Meningioma familiar múltiplo
Pacientes, familiares e cuidadores se organizam em comunidades pra compartilhar experiências, fazer perguntas e se apoiar. Você pode ser o primeiro.
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Doenças com sintomas parecidos — ajudam quem ainda está buscando diagnóstico
Ainda não achamos doenças com sintomas parecidos o suficiente.
Referências e fontes
Bases de dados externas citadas neste artigo
Publicações científicas
Artigos indexados no PubMed ligados a esta doença no grafo RarasNet — título, periódico e PMID direto da fonte, sem intermediação de IA.
- STING activation induces cytotoxic and immune responses in meningiomas via inflammatory cell death pathways.
- Association Between miRNAs and the Diagnosis, Prognosis, and Recurrence of Patients with Meningioma: A Systematic Review.
- KMT2C Loss Promotes NF2-Wildtype Meningioma Progression and Ferroptosis Sensitivity via Epigenetic Repression of Hippo Signaling.
- Risk for Cancer With Glucagon-Like Peptide-1 Receptor Agonists and Dual Agonists : A Systematic Review and Meta-analysis.
- French translation and preliminary psychometric evaluation of the Meningioma Quality of Life questionnaire (MQOL-FR).
- Familial multiple fetal cerebral arteriovenous malformations: a case report of maternal genetic susceptibility and fetal manifestation.
- Familial multiple discoid fibromas: clinical features and a brief overview of the literature.
- Exome Sequencing and Molecular Modeling Reveal Novel Loci in Familial Multiple Sclerosis: The Importance of BTNL3 and BTNL8 in Disease Pathogenesis.
- Exome Sequencing Uncovers Genetic Drivers of Multiple Sclerosis in a Multiplex Family.
- Familial multiple sclerosis is associated with accelerated progression to secondary progressive phase: a retrospective single-center cohort study.
Bases de dados e fontes oficiais
Identificadores e referências canônicas usadas para montar este verbete.
- ORPHA:263662(Orphanet)
- MONDO:0016995(MONDO)
- GARD:17260(GARD (NIH))
- Variantes catalogadas(ClinVar)
- Busca completa no PubMed(PubMed)
- Q56013917(Wikidata)
Dados compilados pelo RarasNet a partir de fontes abertas (Orphanet, OMIM, MONDO, PubMed/EuropePMC, ClinicalTrials.gov, DATASUS, PCDT/MS). Este conteúdo é informativo e não substitui avaliação médica.
Conteúdo mantido por Agente Raras · Médicos e pesquisadores podem colaborar
