- Author: Jeffrey N Bruce, MD; Chief Editor: Jules E Harris, MD, FACP, FRCPC more...
Ependymomas are glial tumors that arise from ependymal cells within the CNS (see the image below).
The World Health Organization (WHO) divides them into 4 types on the basis of histologic appearance:
WHO grade I: Myxopapillary ependymoma, subependymoma
WHO grade II: Ependymoma (with cellular, papillary, and clear cell variants)
WHO grade III: Anaplastic ependymoma
Signs and symptoms
The clinical history associated with ependymomas varies according to the age of the patient and the location of the lesion. Reported symptoms may include the following:
Masses in the fourth ventricle: Progressive lethargy, headache, nausea, and vomiting; multiple cranial-nerve palsies (primarily VI-X), as well as cerebellar dysfunction
In children who present before closure of cranial sutures, enlarging head circumference secondary to obstructive hydrocephalus
Supratentorial ependymomas: Increased intracranial pressure manifested as headache, nausea, vomiting, and cognitive impairment
Changes in personality, mood, and concentration; seizures; focal neurologic deficits
Spinal ependymomas: Progressive neurologic deficit
Physical findings with intracranial ependymomas may include the following:
General or focal neurologic signs reflecting the location of the tumor
Infratentorial ependymomas: Papilledema ataxia; nystagmus
Supratentorial ependymomas: Hemiparesis, sensory loss, visual loss, aphasia, and cognitive impairment
Physical findings with cervical or thoracic ependymomas may include the following:
Spinal tumors in the upper cervical cord: Occipital or cervical pain or paresthesia, neck stiffness, and weakness and wasting of neck muscles
Spastic tetraplegia or hemiplegia and weakness ventrolaterally below the lesion
Altered cutaneous sensation below the lesion
Characteristic findings associated with specific cervical and upper thoracic levels (eg, C4, C5, C6, C7, C8, T1)
Physical findings with thoracic ependymomas may include the following:
These tumors are localized more by the sensory (as opposed to motor) examination
Localizing upper thoracic lesions by testing intercostal muscle strength is difficult
Beevor sign localizes lesions below T10
Abdominal skin reflexes usually are absent below the lesion
Physical findings with lumbar ependymomas may include the following:
These lesions are localized from the root level of sensory loss and motor weakness
Nerve root compression: Radicular pain and weakness
Lesions compressing only the first and second lumbar segments: Lost cremasteric reflexes, preserved abdominal reflexes, and increased knee and ankle jerks
Lesions affecting the third and fourth lumbar segments: If the roots of the cauda equina are not affected, weakness of the quadriceps, loss of the patellar reflexes, and hyperactive Achilles reflexes may be present; if they are affected, flaccid paralysis of the legs and loss of knee and ankle reflexes may occur
Lesions affecting spinal cord and cauda equina concurrently: Spastic paralysis of one leg with increased ankle reflexes ipsilaterally may occur, as well as flaccid paralysis with loss of reflexes contralaterally
Physical findings with myxopapillary ependymomas of the conus and cauda equina may include the following:
Presenting symptom is pain in the back, rectal area, or both lower legs
Spontaneous pain is rare with conus lesions but prominent with cauda equina lesions
Motor dysfunction is symmetric for conus lesions and asymmetric for cauda equina lesions
Autonomic dysfunction is typically an early sign with conus lesions but a late finding with cauda equina lesions
See Clinical Presentation for more detail.
No laboratory studies are helpful in making the diagnosis of ependymoma. On CT and MRI, e pendymomas have some characteristic features that help narrow the differential diagnosis, including the following:
Intracranial ependymoma: Typically isodense on unenhanced CT, with minimal to moderate enhancement on contrast administration; on precontrast and postcontrast MRI, usually hypointense to isointense on T1-weighted images and hyperintense (compared with gray matter) on T2-weighted images
Spinal ependymoma: Most intramedullary tumors are isointense or slightly hypointense to the surrounding spinal cord on T1-weighted images; most tumors are hyperintense to the spinal cord on T2-weighted images
Other diagnostic modalities that may be helpful include the following:
Lumbar puncture and cerebrospinal fluid analysis
See Workup for more detail.
Medical management of ependymomas includes the following[1, 2] :
Adjuvant therapy (ie, conventional radiation therapy, radiosurgery, chemotherapy)
Steroids for treatment of peritumoral edema
Anticonvulsants in patients with supratentorial ependymoma
The National Comprehensive Cancer Network (NCCN) suggests the following for adults:
After gross total resection (GTR) of an intracranial WHO grade II ependymoma, limited field fractionated external beam radiotherapy (LFFEBRT) can be considered
Postoperative LFFEBRT is recommended for WHO grade II ependymoma when subtotal resection is noted on postoperative MRI and for grade III anaplastic ependymoma regardless of extent of resection  ; if postoperative spinal MRI or LP findings are positive, craniospinal radiation therapy is indicated regardless of grade or extent of resection
For recurrent ependymoma, if a patient has not received radiation therapy, such therapy should be administered; if a patient has received radiation therapy, then chemotherapy, radiation therapy, or supportive care should be considered 
In terms of surgical care, a GTR is optimal. Approaches include the following:
Children with posterior fossa lesions: Midline suboccipital approach; hydrocephalus can be managed with a perioperative external ventricular drain, ventriculoperitoneal shunt, or, more rarely, third ventriculostomy
Intramedullary tumors: Standard laminectomy with the patient prone; laminoplasty is performed in children but does not guarantee long-term stability
Filum terminale ependymoma: Gross total en bloc resection whenever possible
Ependymomas are glial tumors that arise from ependymal cells within the central nervous system (CNS). They were first described by Bailey in 1924. The World Health Organization (WHO) classification scheme for these tumors includes 4 divisions based on histologic appearance: WHO grade I, myxopapillary ependymoma and subependymoma; WHO grade II, ependymoma (with cellular, papillary, and clear cell variants); WHO grade III, anaplastic ependymoma. Myxopapillary ependymomas are considered a biologically and morphologically distinct variant of ependymoma, occurring almost exclusively in the region of the cauda equina and behaving in a more benign fashion than grade II ependymoma. Subependymomas are uncommon lesions that share the benign features of myxopapillary ependymomas. Ependymoblastomas are now considered a primitive neuroectodermal tumor (PNET) and are distinct from ependymoma.
See the image below.
Intracranial ependymomas present as intraventricular masses with frequent extension into the subarachnoid space, while spinal ependymomas present as intramedullary masses arising from the central canal or exophytic masses at the conus and cauda equina.
The anatomic distinction between intracranial and spinal locations has an epidemiologic and clinical correlate. In children, approximately 90% of ependymomas are intracranial, with the majority of these usually arising from the roof of the fourth ventricle (infratentorial). In adults and adolescents, 75% of ependymomas arise within the spinal canal, with a significant minority occurring intracranially in the supratentorial compartment.
Treatment of patients with ependymomas depends upon neurosurgical intervention to facilitate definitive diagnosis and to decrease tumor burden. Postoperative adjuvant therapy can include brain or spine radiation, chemotherapy, and radiosurgery.[7, 8, 9, 10]
Ependymomas are traditionally thought to arise from oncogenetic events that transform normal ependymal cells into tumor phenotypes. The precise nature and order of these genetic events are unknown; however, significant progress has been made toward delineating mutations that segregate with various tumor phenotypes. Some evidence now suggests that radial glia may be the cells of origin.[11, 12]
In 1988, Dal Chin and colleagues described cytogenetic studies on a supratentorial ependymoma from a 3-year-old girl that showed a t(10;11;15)(p12.2;q13.1;p12) and loss of one X chromosome. This relatively simple karyotypic change was not observed in the analysis of 4 ependymomas published 1 year later. In 1 of the 4 ependymomas studied, translocations involving chromosomes 9, 17, and 22 were observed together with loss of the normal chromosome 17. A second ependymoma had many chromosomal alterations that included a translocation between chromosomes 1 and 2 and rearrangements involving chromosome 17. Consistent genetic alterations were not detected in the remaining 2 cases.
These initial studies underscore the molecular heterogeneity that can exist among histologically identical tumors. Subsequent studies have identified more consistent genetic defects as follows: a loss of loci on chromosome 22, a mutation of p53 in malignant ependymoma, a recurring breakpoint at band 11q13, abnormal karyotypes with frequent involvement of chromosome 6 and/or 16, and NF2 mutations. Clustering of ependymomas has been reported in some families, with segregation analysis in one family suggesting the presence of an ependymoma tumor suppressor gene in the region of the chromosome 22 locus loss (22pter-22q11.2).[17, 18, 19, 20, 21, 22]
The ultimate goal of genetic studies is to demonstrate a causal relationship between specific mutations and tumor progression. Current efforts in the field are directed toward identifying another tumor suppressor gene on chromosome 22.
Frequency of ependymomas is similar to that in other parts of the world.
Intracranial ependymomas represent 6-9% of primary CNS neoplasms and account for 30% of primary CNS neoplasms in children younger than 3 years.
Depending on the patient population, the reported 10-year overall survival rate for ependymoma can vary from 45-55%. The current 5-year survival rate for patients with intracranial ependymomas is approximately 50%, when rates from children and adults are combined. Stratification based on age reveals 5-year survival rates of 76% in adults and 14% in children.
Grade II and III ependymoma are more common in black Americans than white Americans.
The incidence of ependymoma is approximately equal in males and females.
Ependymomas generally present in young children with a mean age of diagnosis of 4 years, yet 25-40% of patients are younger than 2 years. Spinal ependymomas are most common in patients aged 15-40 years, most of which are of a myxopapillary subtype. Intracranial tumors are seen more often in children, particularly in the infratentorial compartment.
Chamberlain MC, Kormanik PA. Practical guidelines for the treatment of malignant gliomas. West J Med. 1998 Feb. 168(2):114-20. [Medline].
Merchant TE. Current management of childhood ependymoma. Oncology (Williston Park). 2002/05. 16(5):629-42, 644; discussion 645-6, 648.
Timmermann B, Kortmann RD, Kühl J, Meisner C, Slavc I, Pietsch T. Combined postoperative irradiation and chemotherapy for anaplastic ependymomas in childhood: results of the German prospective trials HIT 88/89 and HIT 91. Int J Radiat Oncol Biol Phys. 2000 Jan 15. 46(2):287-95. [Medline].
National Comprehensive Cancer Network. NCCN Practice Guidelines in Oncology: Adult Intracranial Ependymomas. Available at http://www.nccn.org/professionals/physician_gls/PDF/cns.pdf. Accessed: Jan 2009.
Applegate GL, Marymont MH. Intracranial ependymomas: a review. Cancer Invest. 1998. 16(8):588-93. [Medline].
Schwartz TH, Kim S, Glick RS, et al. Supratentorial ependymomas in adult patients. Neurosurgery. 1999 Apr. 44(4):721-31. [Medline].
Verma A, Zhou H, Chin S, Bruggers C, Kestle J, Khatua S. EGFR as a predictor of relapse in myxopapillary ependymoma. Pediatr Blood Cancer. 2011 Dec 20. [Medline].
Tripathy P, Mohapatra D, Mohapatra S. Primary intradural extramedullary ependymoma: report of two cases and review of the literature. Neurol Neurochir Pol. 2011 Jul-Aug. 45(4):397-401. [Medline].
Son DW, Song GS, Han IH, Choi BK. Primary extramedullary ependymoma of the cervical spine : case report and review of the literature. J Korean Neurosurg Soc. 2011 Jul. 50(1):57-9. [Medline]. [Full Text].
Poppleton H, Gilbertson RJ. Stem cells of ependymoma. Br J Cancer. 2007 Jan 15. 96(1):6-10. [Medline].
Taylor MD, Poppleton H, Fuller C, Su X, Liu Y, Jensen P, et al. Radial glia cells are candidate stem cells of ependymoma. Cancer Cell. 2005 Oct. 8(4):323-35. [Medline].
Dal Cin P, Sandberg AA. Cytogenetic findings in a supratentorial ependymoma. Cancer Genet Cytogenet. 1988 Feb. 30(2):289-93. [Medline].
Metzger AK, Sheffield VC, Duyk G, et al. Identification of a germ-line mutation in the p53 gene in a patient with an intracranial ependymoma. Proc Natl Acad Sci U S A. 1991 Sep 1. 88(17):7825-9. [Medline].
Sainati L, Montaldi A, Putti MC, et al. Cytogenetic t(11;17)(q13;q21) in a pediatric ependymoma. Is 11q13 a recurring breakpoint in ependymomas?. Cancer Genet Cytogenet. 1992 Apr. 59(2):213-6. [Medline].
Mazewski C, Soukup S, Ballard E, et al. Karyotype studies in 18 ependymomas with literature review of 107 cases. Cancer Genet Cytogenet. 1999 Aug. 113(1):1-8. [Medline].
Nijssen PC, Deprez RH, Tijssen CC, et al. Familial anaplastic ependymoma: evidence of loss of chromosome 22 in tumour cells. J Neurol Neurosurg Psychiatry. 1994 Oct. 57(10):1245-8. [Medline].
Yokota T, Tachizawa T, Fukino K, Teramoto A, Kouno J, Matsumoto K. A family with spinal anaplastic ependymoma: evidence of loss of chromosome 22q in tumor. J Hum Genet. 2003. 48(11):598-602. [Medline].
Ebert C, von Haken M, Meyer-Puttlitz B, et al. Molecular genetic analysis of ependymal tumors. NF2 mutations and chromosome 22q loss occur preferentially in intramedullary spinal ependymomas. Am J Pathol. 1999 Aug. 155(2):627-32. [Medline].
Hulsebos TJ, Oskam NT, Bijleveld EH, Westerveld A, Hermsen MA, van den Ouweland AM. Evidence for an ependymoma tumour suppressor gene in chromosome region 22pter-22q11.2. Br J Cancer. 1999 Dec. 81(7):1150-4. [Medline].
James CD, He J, Carlbom E, et al. Loss of genetic information in central nervous system tumors common to children and young adults. Genes Chromosomes Cancer. 1990 Jul. 2(2):94-102. [Medline].
Yao Y, Mack SC, Taylor MD. Molecular genetics of ependymoma. Chin J Cancer. 2011 Oct. 30(10):669-81. [Medline].
McGuire CS, Sainani KL, Fisher PG. Incidence patterns for ependymoma: a Surveillance, Epidemiology, and End Results study. J Neurosurg. 2008 Dec 5. [Medline].
Bouffet E, Perilongo G, Canete A, Massimino M. Intracranial ependymomas in children: a critical review of prognostic factors and a plea for cooperation. Med Pediatr Oncol. 1998 Jun. 30(6):319-29; discussion 329-31. [Medline].
Polednak AP, Flannery JT. Brain, other central nervous system, and eye cancer. Cancer. 1995 Jan 1. 75(1 Suppl):330-7. [Medline].
Macdonald J. Advances in imaging techniques in neuroendocrine tumors: miscellaneous papers of interest. Curr Opin Oncol. 1990 Feb. 2(1):117-8. [Medline].
Rogers L, Pueschel J, Spetzler R, et al. Is gross-total resection sufficient treatment for posterior fossa ependymomas?. J Neurosurg. 2005 Apr. 102(4):629-36. [Medline].
Merchant TE, Li C, Xiong X, Gaber MW. Cytokine and Growth Factor Responses After Radiotherapy for Localized Ependymoma. Int J Radiat Oncol Biol Phys. 2008 Nov 17. [Medline].
Goldwein JW, Glauser TA, Packer RJ, et al. Recurrent intracranial ependymomas in children. Survival, patterns of failure, and prognostic factors. Cancer. 1990 Aug 1. 66(3):557-63. [Medline].
Chiu JK, Woo SY, Ater J, et al. Intracranial ependymoma in children: analysis of prognostic factors. J Neurooncol. 1992 Jul. 13(3):283-90. [Medline].
Stafford SL, Pollock BE, Foote RL, Gorman DA, Nelson DF, Schomberg PJ. Stereotactic radiosurgery for recurrent ependymoma. Cancer. 2000 Feb 15. 88(4):870-5. [Medline].
Partap S, Fisher PG. Update on new treatments and developments in childhood brain tumors. Curr Opin Pediatr. 2007 Dec. 19(6):670-4. [Medline].
Reni M, Gatta G, Mazza E, Vecht C. Ependymoma. Crit Rev Oncol Hematol. 2007 Jul. 63(1):81-9. [Medline].
Tabori U, Ma J, Carter M, Zielenska M, Rutka J, Bouffet E, et al. Human telomere reverse transcriptase expression predicts progression and survival in pediatric intracranial ependymoma. J Clin Oncol. 2006 Apr 1. 24(10):1522-8. [Medline].
Sowar K, Straessle J, Donson AM, Handler M, Foreman NK. Predicting which children are at risk for ependymoma relapse. J Neurooncol. 2006 May. 78(1):41-6. [Medline].
Modena P, Lualdi E, Facchinetti F, Veltman J, Reid JF, Minardi S, et al. Identification of tumor-specific molecular signatures in intracranial ependymoma and association with clinical characteristics. J Clin Oncol. 2006 Nov 20. 24(33):5223-33. [Medline].
Catsman-Berrevoets CE, Van Dongen HR, Mulder PG, et al. Tumour type and size are high risk factors for the syndrome of "cerebellar" mutism and subsequent dysarthria. J Neurol Neurosurg Psychiatry. 1999 Dec. 67(6):755-7. [Medline].
Doxey D, Bruce D, Sklar F, et al. Posterior fossa syndrome: identifiable risk factors and irreversible complications. Pediatr Neurosurg. 1999 Sep. 31(3):131-6. [Medline].
Healey EA, Barnes PD, Kupsky WJ, Scott RM, Sallan SE, Black PM. The prognostic significance of postoperative residual tumor in ependymoma. Neurosurgery. 1991 May. 28(5):666-71; discussion 671-2. [Medline].
Carrie C, Mottolese C, Bouffet E, Negrier S, Bachelot TH, Lasset C. Non-metastatic childhood ependymomas. Radiother Oncol. 1995 Aug. 36(2):101-6. [Medline].
McGuire CS, Sainani KL, Fisher PG. Both location and age predict survival in ependymoma: a SEER study. Pediatr Blood Cancer. 2009 Jan. 52(1):65-9. [Medline].
Amirian ES, Armstrong TS, Gilbert MR, Scheurer ME. Predictors of survival among older adults with ependymoma. J Neurooncol. 2011 Sep 28. [Medline].
Tomita T, McLone DG, Das L, Brand WN. Benign ependymomas of the posterior fossa in childhood. Pediatr Neurosci. 1988. 14(6):277-85. [Medline].
Sutton LN, Goldwein J, Perilongo G, Lang B, Schut L, Rorke L. Prognostic factors in childhood ependymomas. Pediatr Neurosurg. 1990-1991. 16(2):57-65. [Medline].
Jayawickreme DP, Hayward RD, Harkness WF. Intracranial ependymomas in childhood: a report of 24 cases followed for 5 years. Childs Nerv Syst. 1995 Jul. 11(7):409-13. [Medline].
Pollack IF, Gerszten PC, Martinez AJ, et al. Intracranial ependymomas of childhood: long-term outcome and prognostic factors. Neurosurgery. 1995 Oct. 37(4):655-66; discussion 666-7. [Medline].
Robertson PL, Zeltzer PM, Boyett JM, et al. Survival and prognostic factors following radiation therapy and chemotherapy for ependymomas in children: a report of the Children's Cancer Group. J Neurosurg. 1998 Apr. 88(4):695-703. [Medline].
Horn B, Heideman R, Geyer R, Pollack I, Packer R, Goldwein J. A multi-institutional retrospective study of intracranial ependymoma in children: identification of risk factors. J Pediatr Hematol Oncol. 1999 May-Jun. 21(3):203-11. [Medline].
Merchant TE, Mulhern RK, Krasin MJ, Kun LE, Williams T, Li C. Preliminary results from a phase II trial of conformal radiation therapy and evaluation of radiation-related CNS effects for pediatric patients with localized ependymoma. J Clin Oncol. 2004 Aug 1. 22(15):3156-62. [Medline].
Agbahiwe HC, Wharam M, Batra S, Cohen K, Terezakis SA. Management of pediatric myxopapillary ependymoma: the role of adjuvant radiation. Int J Radiat Oncol Biol Phys. 2013 Feb 1. 85(2):421-7. [Medline].
Bailey P. Tumors arising from ependymal cells. Arch Neurol Psychiatr. 1924. 11:1-27.
Barnholtz-Sloan JS, Severson RK, Stanton B, Hamre M, Sloan AE. Pediatric brain tumors in non-Hispanics, Hispanics, African Americans and Asians: differences in survival after diagnosis. Cancer Causes Control. 2005 Jun. 16(5):587-92. [Medline].
Bijlsma EK, Voesten AM, Bijleveld EH, et al. Molecular analysis of genetic changes in ependymomas. Genes Chromosomes Cancer. 1995 Aug. 13(4):272-7. [Medline].
Birch BD, Johnson JP, Parsa A, et al. Frequent type 2 neurofibromatosis gene transcript mutations in sporadic intramedullary spinal cord ependymomas. Neurosurgery. 1996 Jul. 39(1):135-40. [Medline].
Duffner PK, Krischer JP, Sanford RA, Horowitz ME, Burger PC, Cohen ME. Prognostic factors in infants and very young children with intracranial ependymomas. Pediatr Neurosurg. 1998 Apr. 28(4):215-22. [Medline].
Goldwein JW, Leahy JM, Packer RJ, et al. Intracranial ependymomas in children. Int J Radiat Oncol Biol Phys. 1990 Dec. 19(6):1497-502. [Medline].
Guyotat J, Signorelli F, Desme S, Frappaz D, Madarassy G, Montange MF. Intracranial ependymomas in adult patients: analyses of prognostic factors. J Neurooncol. 2002 Dec. 60(3):255-68. [Medline].
Kramer DL, Parmiter AH, Rorke LB, et al. Molecular cytogenetic studies of pediatric ependymomas. J Neurooncol. 1998 Mar. 37(1):25-33. [Medline].
Lyons MK, Kelly PJ. Posterior fossa ependymomas: report of 30 cases and review of the literature. Neurosurgery. 1991 May. 28(5):659-64; discussion 664-5. [Medline].
Neumann E, Kalousek DK, Norman MG, et al. Cytogenetic analysis of 109 pediatric central nervous system tumors. Cancer Genet Cytogenet. 1993 Nov. 71(1):40-9. [Medline].
Ransom DT, Ritland SR, Kimmel DW, et al. Cytogenetic and loss of heterozygosity studies in ependymomas, pilocytic astrocytomas, and oligodendrogliomas. Genes Chromosomes Cancer. 1992 Nov. 5(4):348-56. [Medline].
Rogatto SR, Casartelli C, Rainho CA, Barbieri-Neto J. Chromosomes in the genesis and progression of ependymomas. Cancer Genet Cytogenet. 1993 Sep. 69(2):146-52. [Medline].
Ross GW, Rubinstein LJ. Lack of histopathological correlation of malignant ependymomas with postoperative survival. J Neurosurg. 1989 Jan. 70(1):31-6. [Medline].
Rubio MP, Correa KM, Ramesh V, et al. Analysis of the neurofibromatosis 2 gene in human ependymomas and astrocytomas. Cancer Res. 1994 Jan 1. 54(1):45-7. [Medline].
Slavc I, MacCollin MM, Dunn M, et al. Exon scanning for mutations of the NF2 gene in pediatric ependymomas, rhabdoid tumors and meningiomas. Int J Cancer. 1995 Aug 22. 64(4):243-7. [Medline].
Stratton MR, Darling J, Lantos PL, et al. Cytogenetic abnormalities in human ependymomas. Int J Cancer. 1989 Oct 15. 44(4):579-81. [Medline].
Stüben G, Stuschke M, Kroll M, Havers W, Sack H. Postoperative radiotherapy of spinal and intracranial ependymomas: analysis of prognostic factors. Radiother Oncol. 1997 Oct. 45(1):3-10. [Medline].
Tominaga T, Kayama T, Kumabe T, et al. Anaplastic ependymomas: clinical features and tumour suppressor gene p53 analysis. Acta Neurochir (Wien). 1995. 135(3-4):163-70. [Medline].
Vagner-Capodano AM, Gentet JC, Gambarelli D, et al. Cytogenetic studies in 45 pediatric brain tumors. Pediatr Hematol Oncol. 1992 Jul-Sep. 9(3):223-35. [Medline].
Vanuytsel L, Brada M. The role of prophylactic spinal irradiation in localized intracranial ependymoma. Int J Radiat Oncol Biol Phys. 1991 Aug. 21(3):825-30. [Medline].
von Haken MS, White EC, Daneshvar-Shyesther L, et al. Molecular genetic analysis of chromosome arm 17p and chromosome arm 22q DNA sequences in sporadic pediatric ependymomas. Genes Chromosomes Cancer. 1996 Sep. 17(1):37-44. [Medline].
Weremowicz S, Kupsky WJ, Morton CC, Fletcher JA. Cytogenetic evidence for a chromosome 22 tumor suppressor gene in ependymoma. Cancer Genet Cytogenet. 1992 Jul 15. 61(2):193-6. [Medline].
Wernicke C, Thiel G, Lozanova T, et al. Involvement of chromosome 22 in ependymomas. Cancer Genet Cytogenet. 1995 Feb. 79(2):173-6. [Medline].
Yates AJ. An overview of principles for classifying brain tumors. Mol Chem Neuropathol. 1992 Oct. 17(2):103-20. [Medline].