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Meningioma

MedGen UID:
7532
Concept ID:
C0025286
Neoplastic Process
Synonym: Meningioma, somatic
Modes of inheritance:
Not genetically inherited
MedGen UID:
988794
Concept ID:
CN307044
Finding
Source: Orphanet
clinical entity without genetic inheritance.
 
HPO: HP:0002858
Monarch Initiative: MONDO:0016642
OMIM®: 190040; 601728
Orphanet: ORPHA2495

Definition

The presence of a meningioma, i.e., a benign tumor originating from the dura mater or arachnoid mater. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVMeningioma
Follow this link to review classifications for Meningioma in Orphanet.

Conditions with this feature

Neurofibromatosis, type 1
MedGen UID:
18013
Concept ID:
C0027831
Neoplastic Process
Neurofibromatosis 1 (NF1) is a multisystem disorder characterized by multiple café au lait macules, intertriginous freckling, multiple cutaneous neurofibromas, and learning disability or behavior problems. About half of people with NF1 have plexiform neurofibromas, but most are internal and not suspected clinically. Plexiform neurofibromas can cause pain, neurologic deficits, and abnormalities of involved or adjacent structures. Less common but potentially more serious manifestations include optic nerve and other central nervous system gliomas, malignant peripheral nerve sheath tumors, scoliosis, tibial dysplasia, vasculopathy, and gastrointestinal, endocrine, or pulmonary disease.
Neurofibromatosis, type 2
MedGen UID:
18014
Concept ID:
C0027832
Neoplastic Process
Neurofibromatosis 2 (NF2) is characterized by bilateral vestibular schwannomas with associated symptoms of tinnitus, hearing loss, and balance dysfunction. The average age of onset is 18 to 24 years. Almost all affected individuals develop bilateral vestibular schwannomas by age 30 years. Affected individuals may also develop schwannomas of other cranial and peripheral nerves, meningiomas, ependymomas, and, very rarely, astrocytomas. Because NF2 is considered an adult-onset disease, it may be underrecognized in children, in whom skin tumors and ocular findings (retinal hamartoma, thickened optic nerves, cortical wedge cataracts, third cranial nerve palsy) may be the first manifestations. Mononeuropathy that occurs in childhood is an increasingly recognized finding; it frequently presents as a persistent facial palsy or hand/foot drop.
Werner syndrome
MedGen UID:
12147
Concept ID:
C0043119
Disease or Syndrome
Werner syndrome is characterized by the premature appearance of features associated with normal aging and cancer predisposition. Individuals with Werner syndrome develop normally until the end of the first decade. The first sign is the lack of a growth spurt during the early teen years. Early findings (usually observed in the 20s) include loss and graying of hair, hoarseness, and scleroderma-like skin changes, followed by bilateral ocular cataracts, type 2 diabetes mellitus, hypogonadism, skin ulcers, and osteoporosis in the 30s. Myocardial infarction and cancer are the most common causes of death; the mean age of death in individuals with Werner syndrome is 54 years.
Neurocutaneous melanocytosis
MedGen UID:
154259
Concept ID:
C0544862
Congenital Abnormality
Neurocutaneous melanosis, or neuromelanosis, is characterized by the presence of melanin-producing cells within the brain parenchyma or leptomeninges, which may lead to clinically apparent neurologic signs and symptoms, such as seizures. Other neurologic abnormalities, including hydrocephalus, arachnoid cysts, tumors, and syringomyelia, may also occur. The disorder is a rare but severe manifestation of congenital melanocytic nevus syndrome (CMNS; 137550). Some patients with neurocutaneous melanosis or CMNS may develop malignant melanoma. The incidence of neurologic involvement, development of malignant melanoma, and death is significantly associated with the projected adult size of the largest congenital melanocytic nevus, particularly those greater than 40 cm (summary by Kinsler et al., 2008; Kinsler et al., 2013).
Megalencephaly-capillary malformation-polymicrogyria syndrome
MedGen UID:
355421
Concept ID:
C1865285
Disease or Syndrome
PIK3CA-related overgrowth spectrum (PROS) encompasses a range of clinical findings in which the core features are congenital or early-childhood onset of segmental/focal overgrowth with or without cellular dysplasia. Prior to the identification of PIK3CA as the causative gene, PROS was separated into distinct clinical syndromes based on the tissues and/or organs involved (e.g., MCAP [megalencephaly-capillary malformation] syndrome and CLOVES [congenital lipomatous asymmetric overgrowth of the trunk, lymphatic, capillary, venous, and combined-type vascular malformations, epidermal nevi, skeletal and spinal anomalies] syndrome). The predominant areas of overgrowth include the brain, limbs (including fingers and toes), trunk (including abdomen and chest), and face, all usually in an asymmetric distribution. Generalized brain overgrowth may be accompanied by secondary overgrowth of specific brain structures resulting in ventriculomegaly, a markedly thick corpus callosum, and cerebellar tonsillar ectopia with crowding of the posterior fossa. Vascular malformations may include capillary, venous, and less frequently, arterial or mixed (capillary-lymphatic-venous or arteriovenous) malformations. Lymphatic malformations may be in various locations (internal and/or external) and can cause various clinical issues, including swelling, pain, and occasionally localized bleeding secondary to trauma. Lipomatous overgrowth may occur ipsilateral or contralateral to a vascular malformation, if present. The degree of intellectual disability appears to be mostly related to the presence and severity of seizures, cortical dysplasia (e.g., polymicrogyria), and hydrocephalus. Many children have feeding difficulties that are often multifactorial in nature. Endocrine issues affect a small number of individuals and most commonly include hypoglycemia (largely hypoinsulinemic hypoketotic hypoglycemia), hypothyroidism, and growth hormone deficiency.
PTEN hamartoma tumor syndrome with granular cell tumor
MedGen UID:
400984
Concept ID:
C1866376
Neoplastic Process
Hunter-Macdonald syndrome
MedGen UID:
383181
Concept ID:
C2677745
Disease or Syndrome
Glioma susceptibility 2
MedGen UID:
414431
Concept ID:
C2751642
Finding
Any malignant glioma in which the cause of the disease is a mutation in the PTEN gene.
Neurofibromatosis, type III, mixed central and peripheral
MedGen UID:
419422
Concept ID:
C2931480
Disease or Syndrome
BAP1-related tumor predisposition syndrome
MedGen UID:
482122
Concept ID:
C3280492
Disease or Syndrome
BAP1 tumor predisposition syndrome (BAP1-TPDS) is associated with an increased risk for a specific skin lesion, BAP1-inactivated melanocytic tumors (BIMT; formerly called atypical Spitz tumors), and the following cancers, in descending order of frequency: uveal (eye) melanoma (UM), malignant mesothelioma (MMe), cutaneous melanoma (CM), renal cell carcinoma (RCC), and basal cell carcinoma (BCC). Hepatocellular carcinoma, cholangiocarcinoma, and meningioma may also be associated with BAP1-TPDS. Affected individuals can have more than one type of primary cancer. In general, the median age of onset of these tumors is younger than in the general population. UM tends to be a more aggressive class 2 tumor with higher risk for metastasis and reduced survival compared to UM occurring in the general population. Due to the limited number of families reported to date, the penetrance, natural history, and frequencies of BAP1-associated tumors are yet to be determined. Other suspected but unconfirmed tumors in BAP1-TPDS include (in alphabetic order): breast cancer, neuroendocrine carcinoma, non-small-cell lung adenocarcinoma, thyroid cancer, and urinary bladder cancer.
Familial meningioma
MedGen UID:
764829
Concept ID:
C3551915
Finding
Individuals with MN1 C-terminal truncation (MCTT) syndrome have mild-to-moderate intellectual disability, severe expressive language delay, dysmorphic facial features (midface hypoplasia, downslanting palpebral fissures, hypertelorism, exophthalmia, short upturned nose, and small low-set ears), and distinctive findings on brain imaging (including perisylvian polymicrogyria and atypical rhombencephalosynapsis). Mild-to-moderate prelingual hearing loss (usually bilateral, conductive, and/or sensorineural) is common. Generalized seizures (observed in the minority of individuals) are responsive to anti-seizure medication. There is an increased risk for craniosynostosis and, thus, increased intracranial pressure. To date, 25 individuals with MCTT syndrome have been identified.
Cowden syndrome 5
MedGen UID:
767432
Concept ID:
C3554518
Disease or Syndrome
PIK3CA-related overgrowth spectrum (PROS) encompasses a range of clinical findings in which the core features are congenital or early-childhood onset of segmental/focal overgrowth with or without cellular dysplasia. Prior to the identification of PIK3CA as the causative gene, PROS was separated into distinct clinical syndromes based on the tissues and/or organs involved (e.g., MCAP [megalencephaly-capillary malformation] syndrome and CLOVES [congenital lipomatous asymmetric overgrowth of the trunk, lymphatic, capillary, venous, and combined-type vascular malformations, epidermal nevi, skeletal and spinal anomalies] syndrome). The predominant areas of overgrowth include the brain, limbs (including fingers and toes), trunk (including abdomen and chest), and face, all usually in an asymmetric distribution. Generalized brain overgrowth may be accompanied by secondary overgrowth of specific brain structures resulting in ventriculomegaly, a markedly thick corpus callosum, and cerebellar tonsillar ectopia with crowding of the posterior fossa. Vascular malformations may include capillary, venous, and less frequently, arterial or mixed (capillary-lymphatic-venous or arteriovenous) malformations. Lymphatic malformations may be in various locations (internal and/or external) and can cause various clinical issues, including swelling, pain, and occasionally localized bleeding secondary to trauma. Lipomatous overgrowth may occur ipsilateral or contralateral to a vascular malformation, if present. The degree of intellectual disability appears to be mostly related to the presence and severity of seizures, cortical dysplasia (e.g., polymicrogyria), and hydrocephalus. Many children have feeding difficulties that are often multifactorial in nature. Endocrine issues affect a small number of individuals and most commonly include hypoglycemia (largely hypoinsulinemic hypoketotic hypoglycemia), hypothyroidism, and growth hormone deficiency.
Cowden syndrome 6
MedGen UID:
767433
Concept ID:
C3554519
Disease or Syndrome
\n\nSome people do not meet the strict criteria for a clinical diagnosis of Cowden syndrome, but they have some of the characteristic features of the condition, particularly the cancers. These individuals are often described as having Cowden-like syndrome. Both Cowden syndrome and Cowden-like syndrome are caused by mutations in the same genes.\n\nCowden syndrome is associated with an increased risk of developing several types of cancer, particularly cancers of the breast, a gland in the lower neck called the thyroid, and the lining of the uterus (the endometrium). Other cancers that have been identified in people with Cowden syndrome include kidney cancer, colorectal cancer, and an agressive form of skin cancer called melanoma. Compared with the general population, people with Cowden syndrome develop these cancers at younger ages, often beginning in their thirties or forties. People with Cowden syndrome are also more likely to develop more than one cancer during their lifetimes compared to the general population. Other diseases of the breast, thyroid, and endometrium are also common in Cowden syndrome. Additional signs and symptoms can include an enlarged head (macrocephaly) and a rare, noncancerous brain tumor called Lhermitte-Duclos disease. A small percentage of affected individuals have delayed development, intellectual disability, or autism spectrum disorder, which can affect communication and social interaction.\n\nThe features of Cowden syndrome overlap with those of another disorder called Bannayan-Riley-Ruvalcaba syndrome. People with Bannayan-Riley-Ruvalcaba syndrome also develop hamartomas and other noncancerous tumors.  Some people with Cowden syndrome have relatives diagnosed with Bannayan-Riley-Ruvalcaba syndrome, and other affected individuals have the characteristic features of both conditions. Based on these similarities, researchers have proposed that Cowden syndrome and Bannayan-Riley-Ruvalcaba syndrome represent a spectrum of overlapping features known as PTEN hamartoma tumor syndrome (named for the genetic cause of the conditions) instead of two distinct conditions.\n\nAlmost everyone with Cowden syndrome develops hamartomas. These growths are most commonly found on the skin and mucous membranes (such as the lining of the mouth and nose), but they can also occur in the intestine and other parts of the body. The growth of hamartomas on the skin and mucous membranes typically becomes apparent by a person's late twenties.\n\nCowden syndrome is a genetic disorder characterized by multiple noncancerous, tumor-like growths called hamartomas and an increased risk of developing certain cancers.
Schwannomatosis 1
MedGen UID:
887689
Concept ID:
C4048809
Neoplastic Process
Schwannomatosis is characterized by a predisposition to develop multiple schwannomas and, less frequently, meningiomas. Individuals with schwannomatosis 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 occur in about 5% of individuals with schwannomatosis and have only been reported in individuals with SMARCB1-related schwannomatosis. Malignancy remains a theoretic risk especially in individuals with a SMARCB1 pathogenic variant.
Familial adenomatous polyposis 3
MedGen UID:
902388
Concept ID:
C4225157
Disease or Syndrome
NTHL1 tumor syndrome is characterized by an increased lifetime risk for colorectal cancer (CRC), breast cancer, and colorectal polyposis. Colorectal polyps can be adenomatous, hyperplastic, and/or sessile serrated. Duodenal polyposis has also been reported. Additional cancers reported in individuals with NTHL1 tumor syndrome include endometrial cancer, cervical cancer, urothelial carcinoma of the bladder, meningiomas, unspecified brain tumors, basal cell carcinomas, head and neck squamous cell carcinomas, and hematologic malignancies. The cumulative lifetime risk of developing extracolonic cancer by age 60 years has been estimated at 35% to 78%.
Intellectual developmental disorder, autosomal recessive 67
MedGen UID:
1648350
Concept ID:
C4749019
Disease or Syndrome
Tumor predisposition syndrome 2
MedGen UID:
1823959
Concept ID:
C5774186
Disease or Syndrome
Tumor predisposition syndrome-2 (TPDS2) is an autosomal recessive cancer predisposition syndrome characterized by the onset of various types of tumors or malignancies in young adulthood. The most common clinical manifestations include acute myeloid leukemia (AML), myelodysplastic syndrome, colorectal adenomatous polyposis and carcinoma, and uveal melanoma, although other tumors and malignancies have been reported (summary by Palles et al., 2022). For a discussion of genetic heterogeneity of TPDS, see TPDS1 (614327).
Basal cell nevus syndrome 2
MedGen UID:
1841087
Concept ID:
C5830451
Neoplastic Process
The basal cell nevus syndrome (BCNS), also known as Gorlin syndrome, is characterized by numerous basal cell cancers and epidermal cysts of the skin, calcified dural folds, keratocysts of the jaws, palmar and plantar pits, ovarian fibromas, medulloblastomas, lymphomesenteric cysts, fetal rhabdomyomas, and various stigmata of maldevelopment (e.g., rib and vertebral abnormalities, cleft lip or cleft palate, and cortical defects of bones) (summary by Koch et al., 2002). For a discussion of genetic heterogeneity of BCNS, see BCNS1 (109400).
Li-Fraumeni syndrome 2
MedGen UID:
1849727
Concept ID:
C5882668
Disease or Syndrome
Li-Fraumeni syndrome is a rare disorder that greatly increases the risk of developing several types of cancer, particularly in children and young adults.\n\nA very similar condition called Li-Fraumeni-like syndrome shares many of the features of classic Li-Fraumeni syndrome. Both conditions significantly increase the chances of developing multiple cancers beginning in childhood; however, the pattern of specific cancers seen in affected family members is different.\n\nThe cancers most often associated with Li-Fraumeni syndrome include breast cancer, a form of bone cancer called osteosarcoma, and cancers of soft tissues (such as muscle) called soft tissue sarcomas. Other cancers commonly seen in this syndrome include brain tumors, cancers of blood-forming tissues (leukemias), and a cancer called adrenocortical carcinoma that affects the outer layer of the adrenal glands (small hormone-producing glands on top of each kidney). Several other types of cancer also occur more frequently in people with Li-Fraumeni syndrome.

Professional guidelines

PubMed

Krischek B, Goldbrunner R
Adv Exp Med Biol 2023;1416:1-4. doi: 10.1007/978-3-031-29750-2_1. PMID: 37432615
Mair MJ, Berghoff AS, Brastianos PK, Preusser M
J Neurooncol 2023 Jan;161(2):245-258. Epub 2022 Oct 1 doi: 10.1007/s11060-022-04148-8. PMID: 36181606Free PMC Article
Goldbrunner R, Stavrinou P, Jenkinson MD, Sahm F, Mawrin C, Weber DC, Preusser M, Minniti G, Lund-Johansen M, Lefranc F, Houdart E, Sallabanda K, Le Rhun E, Nieuwenhuizen D, Tabatabai G, Soffietti R, Weller M
Neuro Oncol 2021 Nov 2;23(11):1821-1834. doi: 10.1093/neuonc/noab150. PMID: 34181733Free PMC Article

Curated

UK NICE Guideline NG99, Brain tumours (primary) and brain metastases in over 16s, 2021

Recent clinical studies

Etiology

Mair MJ, Berghoff AS, Brastianos PK, Preusser M
J Neurooncol 2023 Jan;161(2):245-258. Epub 2022 Oct 1 doi: 10.1007/s11060-022-04148-8. PMID: 36181606Free PMC Article
Pamir MN, Özduman K
Handb Clin Neurol 2020;170:25-35. doi: 10.1016/B978-0-12-822198-3.00025-2. PMID: 32586497
Fountain DM, Young AMH, Santarius T
Handb Clin Neurol 2020;170:245-250. doi: 10.1016/B978-0-12-822198-3.00044-6. PMID: 32586496
Solomon DA, Pekmezci M
Handb Clin Neurol 2020;169:87-99. doi: 10.1016/B978-0-12-804280-9.00005-6. PMID: 32553300
Marosi C, Hassler M, Roessler K, Reni M, Sant M, Mazza E, Vecht C
Crit Rev Oncol Hematol 2008 Aug;67(2):153-71. Epub 2008 Mar 14 doi: 10.1016/j.critrevonc.2008.01.010. PMID: 18342535

Diagnosis

Loomis E, Wakasa M
Handb Clin Neurol 2020;170:323-331. doi: 10.1016/B978-0-12-822198-3.00051-3. PMID: 32586505
Chen R, Aghi MK
Handb Clin Neurol 2020;170:233-244. doi: 10.1016/B978-0-12-822198-3.00043-4. PMID: 32586495
Nowosielski M, Galldiks N, Iglseder S, Kickingereder P, von Deimling A, Bendszus M, Wick W, Sahm F
Neuro Oncol 2017 Nov 29;19(12):1588-1598. doi: 10.1093/neuonc/nox101. PMID: 28531331Free PMC Article
Chen TC
Neurosurg Clin N Am 2016 Apr;27(2):189-93. Epub 2016 Feb 18 doi: 10.1016/j.nec.2015.11.011. PMID: 27012383
Miedema JR, Zedek D
Arch Pathol Lab Med 2012 Feb;136(2):208-11. doi: 10.5858/arpa.2010-0505-RS. PMID: 22288971

Therapy

Brown R
Curr Oncol Rep 2023 Dec;25(12):1409-1417. Epub 2023 Oct 31 doi: 10.1007/s11912-023-01451-z. PMID: 37906356
Mair MJ, Berghoff AS, Brastianos PK, Preusser M
J Neurooncol 2023 Jan;161(2):245-258. Epub 2022 Oct 1 doi: 10.1007/s11060-022-04148-8. PMID: 36181606Free PMC Article
Smith HL, Wadhwani N, Horbinski C
Neurotherapeutics 2022 Oct;19(6):1691-1704. Epub 2022 May 16 doi: 10.1007/s13311-022-01249-0. PMID: 35578106Free PMC Article
Goldbrunner R, Stavrinou P, Jenkinson MD, Sahm F, Mawrin C, Weber DC, Preusser M, Minniti G, Lund-Johansen M, Lefranc F, Houdart E, Sallabanda K, Le Rhun E, Nieuwenhuizen D, Tabatabai G, Soffietti R, Weller M
Neuro Oncol 2021 Nov 2;23(11):1821-1834. doi: 10.1093/neuonc/noab150. PMID: 34181733Free PMC Article
Marosi C, Hassler M, Roessler K, Reni M, Sant M, Mazza E, Vecht C
Crit Rev Oncol Hematol 2008 Aug;67(2):153-71. Epub 2008 Mar 14 doi: 10.1016/j.critrevonc.2008.01.010. PMID: 18342535

Prognosis

Rosenberg PS, Miranda-Filho A, Whiteman DC
BMC Med Res Methodol 2023 Oct 18;23(1):238. doi: 10.1186/s12874-023-02039-8. PMID: 37853346Free PMC Article
Ostrom QT, Price M, Neff C, Cioffi G, Waite KA, Kruchko C, Barnholtz-Sloan JS
Neuro Oncol 2023 Oct 4;25(12 Suppl 2):iv1-iv99. doi: 10.1093/neuonc/noad149. PMID: 37793125Free PMC Article
Friedenreich CM, Ryder-Burbidge C, McNeil J
Mol Oncol 2021 Mar;15(3):790-800. Epub 2020 Aug 18 doi: 10.1002/1878-0261.12772. PMID: 32741068Free PMC Article
Ostrom QT, Cioffi G, Gittleman H, Patil N, Waite K, Kruchko C, Barnholtz-Sloan JS
Neuro Oncol 2019 Nov 1;21(Suppl 5):v1-v100. doi: 10.1093/neuonc/noz150. PMID: 31675094Free PMC Article
Baldi I, Engelhardt J, Bonnet C, Bauchet L, Berteaud E, Grüber A, Loiseau H
Neurochirurgie 2018 Mar;64(1):5-14. Epub 2014 Sep 22 doi: 10.1016/j.neuchi.2014.05.006. PMID: 25249493

Clinical prediction guides

Chen J, Xue Y, Ren L, Lv K, Du P, Cheng H, Sun S, Hua L, Xie Q, Wu R, Gong Y
Eur Radiol 2024 May;34(5):2997-3008. Epub 2023 Oct 19 doi: 10.1007/s00330-023-10258-2. PMID: 37853176
Maas SLN, Stichel D, Hielscher T, Sievers P, Berghoff AS, Schrimpf D, Sill M, Euskirchen P, Blume C, Patel A, Dogan H, Reuss D, Dohmen H, Stein M, Reinhardt A, Suwala AK, Wefers AK, Baumgarten P, Ricklefs F, Rushing EJ, Bewerunge-Hudler M, Ketter R, Schittenhelm J, Jaunmuktane Z, Leu S, Greenway FEA, Bridges LR, Jones T, Grady C, Serrano J, Golfinos J, Sen C, Mawrin C, Jungk C, Hänggi D, Westphal M, Lamszus K, Etminan N, Jungwirth G, Herold-Mende C, Unterberg A, Harter PN, Wirsching HG, Neidert MC, Ratliff M, Platten M, Snuderl M, Aldape KD, Brandner S, Hench J, Frank S, Pfister SM, Jones DTW, Reifenberger G, Acker T, Wick W, Weller M, Preusser M, von Deimling A, Sahm F; German Consortium on Aggressive Meningiomas (KAM)
J Clin Oncol 2021 Dec 1;39(34):3839-3852. Epub 2021 Oct 7 doi: 10.1200/JCO.21.00784. PMID: 34618539Free PMC Article
Ugga L, Perillo T, Cuocolo R, Stanzione A, Romeo V, Green R, Cantoni V, Brunetti A
Neuroradiology 2021 Aug;63(8):1293-1304. Epub 2021 Mar 2 doi: 10.1007/s00234-021-02668-0. PMID: 33649882Free PMC Article
Paun L, Gondar R, Borrelli P, Meling TR
Neurosurg Rev 2021 Oct;44(5):2583-2596. Epub 2021 Jan 28 doi: 10.1007/s10143-021-01478-5. PMID: 33507444Free PMC Article
Sahm F, Schrimpf D, Stichel D, Jones DTW, Hielscher T, Schefzyk S, Okonechnikov K, Koelsche C, Reuss DE, Capper D, Sturm D, Wirsching HG, Berghoff AS, Baumgarten P, Kratz A, Huang K, Wefers AK, Hovestadt V, Sill M, Ellis HP, Kurian KM, Okuducu AF, Jungk C, Drueschler K, Schick M, Bewerunge-Hudler M, Mawrin C, Seiz-Rosenhagen M, Ketter R, Simon M, Westphal M, Lamszus K, Becker A, Koch A, Schittenhelm J, Rushing EJ, Collins VP, Brehmer S, Chavez L, Platten M, Hänggi D, Unterberg A, Paulus W, Wick W, Pfister SM, Mittelbronn M, Preusser M, Herold-Mende C, Weller M, von Deimling A
Lancet Oncol 2017 May;18(5):682-694. Epub 2017 Mar 15 doi: 10.1016/S1470-2045(17)30155-9. PMID: 28314689

Recent systematic reviews

Upreti T, Dube S, Pareek V, Sinha N, Shankar J
Neuroradiology 2024 Aug;66(8):1301-1310. Epub 2024 Jun 21 doi: 10.1007/s00234-024-03404-0. PMID: 38902484Free PMC Article
Andersen MS, Kofoed MS, Paludan-Müller AS, Pedersen CB, Mathiesen T, Mawrin C, Wirenfeldt M, Kristensen BW, Olsen BB, Halle B, Poulsen FR
J Transl Med 2023 Oct 28;21(1):764. doi: 10.1186/s12967-023-04620-7. PMID: 37898750Free PMC Article
Himič V, Burman RJ, Fountain DM, Hofer M, Livermore LJ, Jeyaretna DS
Acta Neurochir (Wien) 2023 Oct;165(10):2873-2883. Epub 2023 Jul 26 doi: 10.1007/s00701-023-05687-3. PMID: 37491650Free PMC Article
Umana GE, Visocchi M, Roca E, Passanisi M, Fricia M, Tranchina MG, Tomasi SO, Nicoletti GF, Cicero S, Scalia G
J Neurol Surg A Cent Eur Neurosurg 2022 Mar;83(2):161-172. Epub 2021 Dec 20 doi: 10.1055/s-0041-1739217. PMID: 34929751
Paun L, Gondar R, Borrelli P, Meling TR
Neurosurg Rev 2021 Oct;44(5):2583-2596. Epub 2021 Jan 28 doi: 10.1007/s10143-021-01478-5. PMID: 33507444Free PMC Article

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      See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Curated

    • NICE, 2021
      UK NICE Guideline NG99, Brain tumours (primary) and brain metastases in over 16s, 2021

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