Oligodendroglioma overview: Difference between revisions

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==Classification==
==Classification==
Oligodendroglioma may be classified according to the WHO classification of the central nervous system tumors into five subtypes: oligodendroglioma (OII), [[anaplastic|anaplastic oligodendroglioma (OIII)]], oligoastrocytoma (OAII), [[oligoastrocytoma|anaplastic oligoastrocytoma (OAIII)]], and [[glioblastoma|glioblastoma with oligodendroglioma component (GBMo)]].<ref name="pmid17618441">{{cite journal| author=Louis DN, Ohgaki H, Wiestler OD, Cavenee WK, Burger PC, Jouvet A et al.| title=The 2007 WHO classification of tumours of the central nervous system. | journal=Acta Neuropathol | year= 2007 | volume= 114 | issue= 2 | pages= 97-109 | pmid=17618441 | doi=10.1007/s00401-007-0243-4 | pmc=PMC1929165 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17618441  }} </ref>
Oligodendroglioma may be classified according to the WHO classification of the central nervous system tumors into five subtypes: oligodendroglioma (OII), [[anaplastic|anaplastic oligodendroglioma (OIII)]], oligoastrocytoma (OAII), [[oligoastrocytoma|anaplastic oligoastrocytoma (OAIII)]], and [[glioblastoma|glioblastoma with oligodendroglioma component (GBMo)]].


==Pathophysiology==
==Pathophysiology==
Oligodendroglioma arises from the tripotential [[glial cell|glial precursor cells]] and ''not'' from the bipotential [[oligodendrocyte]]s.<ref name="pathogenesis">General features of oligodendroglioma. Libre Pathology. http://librepathology.org/wiki/index.php/Oligodendroglioma#cite_note-1</ref> Genes associated with the pathogenesis of oligodendroglioma include [[translocation|t(1;19)(q10;p10)]], ''[[mutation|NJDS]]'', ''[[Isocitrate dehydrogenase|IDH1]]'', ''[[IDH2]]'', ''CIC'', ''[[Far upstream element-binding protein 1|FUBP1]]'', ''[[p53]]'', ''[[CD57|Leu-7]]'', ''[[TCF12|TCF-12]]'', ''[[Ogt|MGMT]]'', ''[[P73|TP73]]'', ''[[EGFR]]'', and ''[[PTEN]]''.<ref name="transloc">Molecular genetics of oligodendroglioma. https://en.wikipedia.org/wiki/Oligodendroglioma</ref><ref name="pmid21817013">{{cite journal| author=Bettegowda C, Agrawal N, Jiao Y, Sausen M, Wood LD, Hruban RH et al.| title=Mutations in CIC and FUBP1 contribute to human oligodendroglioma. | journal=Science | year= 2011 | volume= 333 | issue= 6048 | pages= 1453-5 | pmid=21817013 | doi=10.1126/science.1210557 | pmc=PMC3170506 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21817013  }} </ref><ref name="prog">Prognosis and treatment of oligodendroglioma. Wikipedia 2015. https://en.wikipedia.org/wiki/Oligodendroglioma</ref><ref name="pmid22072542">{{cite journal| author=Yip S, Butterfield YS, Morozova O, Chittaranjan S, Blough MD, An J et al.| title=Concurrent CIC mutations, IDH mutations, and 1p/19q loss distinguish oligodendrogliomas from other cancers. | journal=J Pathol | year= 2012 | volume= 226 | issue= 1 | pages= 7-16 | pmid=22072542 | doi=10.1002/path.2995 | pmc=PMC3246739 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22072542  }} </ref><ref name="pmid26068201">{{cite journal| author=Labreche K, Simeonova I, Kamoun A, Gleize V, Chubb D, Letouzé E et al.| title=TCF12 is mutated in anaplastic oligodendroglioma. | journal=Nat Commun | year= 2015 | volume= 6 | issue=  | pages= 7207 | pmid=26068201 | doi=10.1038/ncomms8207 | pmc=PMC4490400 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26068201  }} </ref><ref name="pmid21937591">{{cite journal| author=Suri V, Jha P, Agarwal S, Pathak P, Sharma MC, Sharma V et al.| title=Molecular profile of oligodendrogliomas in young patients. | journal=Neuro Oncol | year= 2011 | volume= 13 | issue= 10 | pages= 1099-106 | pmid=21937591 | doi=10.1093/neuonc/nor146 | pmc=PMC3177666 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21937591  }} </ref><ref name="pmid9038605">{{cite journal| author=Hagel C, Laking G, Laas R, Scheil S, Jung R, Milde-Langosch K et al.| title=Demonstration of p53 protein and TP53 gene mutations in oligodendrogliomas. | journal=Eur J Cancer | year= 1996 | volume= 32A | issue= 13 | pages= 2242-8 | pmid=9038605 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9038605  }} </ref><ref name="von DeimlingHartmann2005">{{cite journal|last1=von Deimling|first1=A|last2=Hartmann|first2=C|title=Oligodendrogliomas: Impact of molecular genetics on treatment|journal=Neurology India|volume=53|issue=2|year=2005|pages=140|issn=0028-3886|doi=10.4103/0028-3886.16394}}</ref> On gross pathology, oligodendroglioma is characterized by a well-circumscribed, gelatinous, calcified, gray mass which may expand a [[gyrus]] and remodel the [[skull]].<ref name="grosspa">Gross appearance of oligodendroglioma. Dr Henry Knipe and Dr Frank Gaillard et al. http://radiopaedia.org/articles/oligodendroglioma</ref> On microscopic histopathological analysis, oligodendroglioma is characterized by diffuse growth pattern of highly cellular lesion with rounded nucleus with [[atypia]] and perinuclear halo resembling ''fried eggs'', distinct cell borders, clear cytoplasm, and abundant [[calcification]].<ref name="von DeimlingHartmann2005">{{cite journal|last1=von Deimling|first1=A|last2=Hartmann|first2=C|title=Oligodendrogliomas: Impact of molecular genetics on treatment|journal=Neurology India|volume=53|issue=2|year=2005|pages=140|issn=0028-3886|doi=10.4103/0028-3886.16394}}</ref><ref name="micro">Microscopic features of oligodendroglioma. Libre Pathology. http://librepathology.org/wiki/index.php/Oligodendroglioma</ref><ref name="turk">{{Citation |last=Ersen |first=Ayca|year=2008 |title=Pathology of malignant gliomas: Challenges of everyday practice and the WHO 2007 |publisher=Turkish Journal of Pathology |publication-place= |page= |url=http://www.turkjpath.org/text.php3?id=645 |accessdate=9 October, 2015 }}</ref><ref name="pmid15509821">{{cite journal| author=Eskandar EN, Loeffler JS, O'Neill AM, Hunter GJ, Louis DN| title=Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 33-2004. A 34-year-old man with a seizure and a frontal-lobe brain lesion. | journal=N Engl J Med | year= 2004 | volume= 351 | issue= 18 | pages= 1875-82 | pmid=15509821 | doi=10.1056/NEJMcpc049025 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15509821  }} </ref> Oligodendroglioma is demonstrated by positivity to tumor markers such as [[Microtubule-associated protein|MAP2]], [[GFAP]], [[S100 calcium binding protein A8|S-100]], EMA, [[isocitrate dehydrogenase|IDH1-R132H]], ATRX, [[Ki-67 (Biology)|Ki-67]], [[Neuron-Specific Enolase (NSE)|NSE]] , [[Synaptophysin]], [[OLIG1]], and [[OLIG2]].<ref name="IHC">IHC of oligodendroglioma. Libre Pathology. http://librepathology.org/wiki/index.php/Oligodendroglioma</ref><ref name="pmid16622556">{{cite journal| author=Hilbig A, Barbosa-Coutinho LM, Netto GC, Bleil CB, Toscani NV| title=[Immunohistochemistry in oligodendrogliomas]. | journal=Arq Neuropsiquiatr | year= 2006 | volume= 64 | issue= 1 | pages= 67-71 | pmid=16622556 | doi=/S0004-282X2006000100014 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16622556  }} </ref><ref name="von DeimlingHartmann2005">{{cite journal|last1=von Deimling|first1=A|last2=Hartmann|first2=C|title=Oligodendrogliomas: Impact of molecular genetics on treatment|journal=Neurology India|volume=53|issue=2|year=2005|pages=140|issn=0028-3886|doi=10.4103/0028-3886.16394}}</ref>
Oligodendroglioma arises from the tripotential [[glial cell|glial precursor cells]] and ''not'' from the bipotential [[oligodendrocyte]]s. Genes associated with the pathogenesis of oligodendroglioma include [[translocation|t(1;19)(q10;p10)]], ''[[mutation|NJDS]]'', ''[[Isocitrate dehydrogenase|IDH1]]'', ''[[IDH2]]'', ''CIC'', ''[[Far upstream element-binding protein 1|FUBP1]]'', ''[[p53]]'', ''[[CD57|Leu-7]]'', ''[[TCF12|TCF-12]]'', ''[[Ogt|MGMT]]'', ''[[P73|TP73]]'', ''[[EGFR]]'', and ''[[PTEN]]''. On gross pathology, oligodendroglioma is characterized by a well-circumscribed, gelatinous, calcified, gray mass which may expand a [[gyrus]] and remodel the [[skull]]. On microscopic histopathological analysis, oligodendroglioma is characterized by diffuse growth pattern of highly cellular lesion with rounded nucleus with [[atypia]] and perinuclear halo resembling ''fried eggs'', distinct cell borders, clear cytoplasm, and abundant [[calcification]]. Oligodendroglioma is demonstrated by positivity to tumor markers such as [[Microtubule-associated protein|MAP2]], [[GFAP]], [[S100 calcium binding protein A8|S-100]], EMA, [[isocitrate dehydrogenase|IDH1-R132H]], ATRX, [[Ki-67 (Biology)|Ki-67]], [[Neuron-Specific Enolase (NSE)|NSE]] , [[Synaptophysin]], [[OLIG1]], and [[OLIG2]].


==Causes==
==Causes==

Revision as of 22:47, 7 May 2019

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sara Mohsin, M.D.[2]Sujit Routray, M.D. [3]

Overview

Oligodendrogliomas are a type of glioma that are believed to originate from the tripotential glial precursor cells and not from the bipotential oligodendrocytes. The term "oligodendroglioma" was first coined by Bailey and Cushing in 1926 following the observation that the tumor cells are morphologically similar to oligodendrocytes. Oligodendroglioma may be classified according to the WHO classification of the central nervous system tumors into five subtypes: oligodendroglioma (OII), anaplastic oligodendroglioma (OIII), oligoastrocytoma (OAII), anaplastic oligoastrocytoma (OAIII), and glioblastoma with oligodendroglioma component (GBMo). Genes associated with the pathogenesis of oligodendroglioma include t(1;19)(q10;p10), NJDS, IDH1, IDH2, CIC, FUBP1, p53, Leu-7, TCF-12, MGMT, TP73, EGFR, and PTEN. On gross pathology, oligodendroglioma is characterized by a well-circumscribed, gelatinous, calcified, gray mass which may expand a gyrus and remodel the skull. On microscopic histopathological analysis, oligodendroglioma is characterized by diffuse growth pattern of highly cellular lesion with rounded nucleus with atypia and perinuclear halo resembling fried eggs, distinct cell borders, clear cytoplasm, and abundant calcification. Common causes of oligodendroglioma include genetic mutations. Oligodendroglioma must be differentiated from pilocytic astrocytoma, central neurocytoma, ependymoma, dysembryoplastic neuroepithelial tumor, and meningioma. Oligodendroglioma is a disease that tends to affect the middle-aged adult population. Oligodendroglioma most commonly occurs in the 4th and 5th decade of life. Males are more commonly affected with oligodendroglioma than females. The male to female ratio is approximately 2 to 1. Oligodendroglioma usually affects individuals of the Caucasian race. African American, Latin American, and Asian individuals are less likely to develop oligodendroglioma. The most potent risk factor in the development of oligodendroglioma is family history of brain tumors. If left untreated, patients with oligodendroglioma may progress to develop seizures, focal neurological deficits, hydrocephalus, brain herniation, intracranial hemorrhage, and ultimately death. When evaluating a patient for oligodendroglioma, you should take a detailed history of the presenting symptom (onset, duration, and progression), other associated symptoms, and a thorough past medical history review. Other specific areas of focus when obtaining the history include review of common risk factors such as family history of brain tumors. Symptoms associated with oligodendroglioma include seizure, headache, nausea, vomiting, vertigo, visual loss, diplopia, strabismus, muscle weakness, numbness, speech difficulties, mood disturbances, and personality changes. Common physical examination findings of oligodendroglioma include nystagmus, papilledema, esotropia, visual field loss, altered mental status, aphasia, ataxia, hemiparesis, tremors, and focal neurological deficits. Findings on CT scan suggestive of oligodendroglioma are round or oval, marginated, hypo- to isodense mass with hemorrhage, calcification, and ill-defined enhancement following intravenous contrast administration. On brain MRI, oligodendroglioma is characterized by a mass which is typically hypointense on T1-weighted images and hyperintense on T2-weighted images. Calcification is observed on T2* decay component of MRI. Other imaging studies for oligodendroglioma include MR spectroscopy (dominant N-acetyl aspartate peak, increased choline levels and decreased NAA levels with a myo-inositol peak), MR perfusion (increased "chicken wire" network of vascularity, which results in elevated relative cerebral blood volume), PET scan (to differentiate between oligodendroglioma from anaplastic oligodendroglioma and tumor recurrence from tumor necrosis), and bone scan (bone metastasis). The predominant therapy for oligodendroglioma is surgical resection. Adjunctive chemotherapy and radiation are required. Supportive therapy for oligodendroglioma includes anticonvulsants and corticosteroids.

Historical Perspective

The term "oligodendroglioma" was first coined by Bailey and Cushing in 1926 following the observation that the tumor cells are morphologically similar to oligodendrocytes. Oligodendroglioma was first described and published by W. E. Carnegie Dickson in 1926. In 2009, NJDS mutation was first identified in the pathogenesis of oligodendroglioma by Kevin Smith. Irradiation of pituitary adenoma was also discovered to be associated with oligodendroglioma by Kevin Smith et al.

Classification

Oligodendroglioma may be classified according to the WHO classification of the central nervous system tumors into five subtypes: oligodendroglioma (OII), anaplastic oligodendroglioma (OIII), oligoastrocytoma (OAII), anaplastic oligoastrocytoma (OAIII), and glioblastoma with oligodendroglioma component (GBMo).

Pathophysiology

Oligodendroglioma arises from the tripotential glial precursor cells and not from the bipotential oligodendrocytes. Genes associated with the pathogenesis of oligodendroglioma include t(1;19)(q10;p10), NJDS, IDH1, IDH2, CIC, FUBP1, p53, Leu-7, TCF-12, MGMT, TP73, EGFR, and PTEN. On gross pathology, oligodendroglioma is characterized by a well-circumscribed, gelatinous, calcified, gray mass which may expand a gyrus and remodel the skull. On microscopic histopathological analysis, oligodendroglioma is characterized by diffuse growth pattern of highly cellular lesion with rounded nucleus with atypia and perinuclear halo resembling fried eggs, distinct cell borders, clear cytoplasm, and abundant calcification. Oligodendroglioma is demonstrated by positivity to tumor markers such as MAP2, GFAP, S-100, EMA, IDH1-R132H, ATRX, Ki-67, NSE , Synaptophysin, OLIG1, and OLIG2.

Causes

Common causes of oligodendroglioma include genetic mutations. Common genetic mutations involved in the development of oligodendroglioma can be found here.[1][2][3][4][5][6][7][8]

Differentiating Oligodendroglioma from other diseases

Oligodendroglioma must be differentiated from pilocytic astrocytoma, central neurocytoma, ependymoma, dysembryoplastic neuroepithelial tumor, and meningioma.[9][10][11][12]

Epidemiology and Demographics

Oligodendroglioma, although rare, is the third most common glioma.[13] The incidence of oligodendroglioma and anaplastic oligodendroglioma is estimated to be 0.32 and 0.17 cases per 100,000 individuals in the United States, respectively.[14] Oligodendroglioma is a disease that tends to affect the middle-aged adult population.[13] Oligodendroglioma most commonly occurs in the 4th and 5th decade of life. Males are more commonly affected with oligodendroglioma than females. The male to female ratio is approximately 2 to 1.[15] Oligodendroglioma usually affects individuals of the Caucasian race. African American, Latin American, and Asian individuals are less likely to develop oligodendroglioma.[16]

Risk factors

The most potent risk factor in the development of oligodendroglioma is family history of brain tumors.[14]

Screening

There is insufficient evidence to recommend routine screening for oligodendroglioma.[17]

Natural History, Complications and Prognosis

If left untreated, patients with oligodendroglioma may progress to develop seizures, focal neurological deficits, hydrocephalus, brain herniation, intracranial hemorrhage, and ultimately death.[18] Common complications associated with oligodendroglioma include hydrocephalus, intracranial hemorrhage, coma, bone marrow metastasis, recurrence, venous thromboembolism, parkinsonism, and side effects of chemotherapy and radiotherapy.[15][19][20][21][22][23][24] Depending on the extent and grade of the tumor at the time of diagnosis, the prognosis of oligodendroglioma may vary. However, the prognosis is generally regarded as good. The median survival time for oligodendroglioma is 11.6 years for grade II and 3.5 years for grade III.[25]

Diagnosis

  • CT or MRI scan is necessary to characterize the anatomy of oligodendroglial tumors such as:
    • Tumor size
    • Tumor location
    • Heter/homogeneity
  • However, the confirmation of final diagnosis is dependent on histopathologic examination of the biopsy specimen

Staging

There is no established system for the staging of oligodendroglioma.

History and Symptoms

When evaluating a patient for oligodendroglioma, you should take a detailed history of the presenting symptom (onset, duration, and progression), other associated symptoms, and a thorough past medical history review. Other specific areas of focus when obtaining the history include review of common risk factors such as family history of brain tumors.[14] Symptoms associated with oligodendroglioma include seizure, headache, nausea, vomiting, vertigo, visual loss, diplopia, strabismus, muscle weakness, numbness, speech difficulties, mood disturbances, and personality changes.[12][26][27][28]

Physical examination

Common physical examination findings of oligodendroglioma include nystagmus, papilledema, esotropia, visual field loss, altered mental status, and focal neurological deficits.[28][12][29][30][24]

Laboratory Findings

Some patients with oligodendroglioma may have elevated protein and cell count with normal glucose and lactate on CSF analysis, which is usually suggestive of hydrocephalus.[31]

Chest X Ray

Chest x-ray may be performed to detect metastases of anaplastic oligodendroglioma to the lungs.[32]

CT

Head CT scan may be helpful in the diagnosis of oligodendroglioma. Findings on CT scan suggestive of oligodendroglioma are round or oval, marginated, hypo- to isodense mass with hemorrhage, calcification, and ill-defined enhancement following intravenous contrast administration.[33][31]

MRI

Brain MRI is helpful in the diagnosis of oligodendroglioma. On brain MRI, oligodendroglioma is characterized by a mass which is typically hypointense on T1-weighted images and hyperintense on T2-weighted images. Calcification is observed on T2* decay component of MRI.[34][31]

Ultrasound

There are no ultrasound findings associated with oligodendroglioma.

Other Imaging Findings

Other imaging studies for oligodendroglioma include MR spectroscopy (dominant N-acetyl aspartate peak, increased choline levels and decreased NAA levels with a myo-inositol peak), MR perfusion (increased "chicken wire" network of vascularity, which results in elevated relative cerebral blood volume), PET scan (to differentiate between oligodendroglioma from anaplastic oligodendroglioma and tumor recurrence from tumor necrosis), and bone scan (bone metastasis).[29][35][36][37][38][39][40][41][42]

Other Diagnostic Studies

Other diagnostic studies for oligodendroglioma include biopsy (homogeneous, compact, rounded cells with distinct borders and clear cytoplasm surrounding a dense central nucleus and perinuclear halo) and fluorescent in-situ hybridization (FISH) technique (deletions of chromosome 1p and 19q).[43][29][44]

Treatment

Medical Therapy

The predominant therapy for oligodendroglioma is surgical resection. Adjunctive chemotherapy and radiation are required.[45][46][47] Supportive therapy for oligodendroglioma includes anticonvulsants and corticosteroids.[45]

Surgery

Surgery is the first-line treatment option for patients with oligodendroglioma.[45] CSF shunting is usually reserved for patients with hydrocephalus.[31]

Primary Prevention

There is no established method for prevention of oligodendroglioma.

Secondary Prevention

There are no secondary preventive measures available for oligodendroglioma.

References

  1. Molecular genetics of oligodendroglioma. https://en.wikipedia.org/wiki/Oligodendroglioma
  2. Bettegowda C, Agrawal N, Jiao Y, Sausen M, Wood LD, Hruban RH; et al. (2011). "Mutations in CIC and FUBP1 contribute to human oligodendroglioma". Science. 333 (6048): 1453–5. doi:10.1126/science.1210557. PMC 3170506. PMID 21817013.
  3. Prognosis and treatment of oligodendroglioma. Wikipedia 2015. https://en.wikipedia.org/wiki/Oligodendroglioma
  4. Yip S, Butterfield YS, Morozova O, Chittaranjan S, Blough MD, An J; et al. (2012). "Concurrent CIC mutations, IDH mutations, and 1p/19q loss distinguish oligodendrogliomas from other cancers". J Pathol. 226 (1): 7–16. doi:10.1002/path.2995. PMC 3246739. PMID 22072542.
  5. Labreche K, Simeonova I, Kamoun A, Gleize V, Chubb D, Letouzé E; et al. (2015). "TCF12 is mutated in anaplastic oligodendroglioma". Nat Commun. 6: 7207. doi:10.1038/ncomms8207. PMC 4490400. PMID 26068201.
  6. Suri V, Jha P, Agarwal S, Pathak P, Sharma MC, Sharma V; et al. (2011). "Molecular profile of oligodendrogliomas in young patients". Neuro Oncol. 13 (10): 1099–106. doi:10.1093/neuonc/nor146. PMC 3177666. PMID 21937591.
  7. Hagel C, Laking G, Laas R, Scheil S, Jung R, Milde-Langosch K; et al. (1996). "Demonstration of p53 protein and TP53 gene mutations in oligodendrogliomas". Eur J Cancer. 32A (13): 2242–8. PMID 9038605.
  8. von Deimling, A; Hartmann, C (2005). "Oligodendrogliomas: Impact of molecular genetics on treatment". Neurology India. 53 (2): 140. doi:10.4103/0028-3886.16394. ISSN 0028-3886.
  9. DDx of oligodendroglioma. Libre Pathology 2015. http://librepathology.org/wiki/index.php/Oligodendroglioma
  10. Differential diagnosis of oligodendroglioma. Dr Henry Knipe and Dr Frank Gaillard et al. Radiopaedia 2015. http://radiopaedia.org/articles/oligodendroglioma
  11. Herholz K, Langen KJ, Schiepers C, Mountz JM (2012). "Brain tumors". Semin Nucl Med. 42 (6): 356–70. doi:10.1053/j.semnuclmed.2012.06.001. PMC 3925448. PMID 23026359.
  12. 12.0 12.1 12.2 Douay X, Daems-Monpeurt C, Labalette P, Blond S, Petit H (1997). "[Bilateral 3rd cranial nerve palsy disclosing oligodendroglioma]". Rev Neurol (Paris). 153 (6–7): 430–2. PMID 9684012.
  13. 13.0 13.1 Epidemiology of oligodendroglioma. Dr Henry Knipe and Dr. Frank Gaillard et al. http://radiopaedia.org/articles/oligodendroglioma
  14. 14.0 14.1 14.2 McCarthy BJ, Rankin KM, Aldape K, Bondy ML, Brännström T, Broholm H; et al. (2011). "Risk factors for oligodendroglial tumors: a pooled international study". Neuro Oncol. 13 (2): 242–50. doi:10.1093/neuonc/noq173. PMC 3064625. PMID 21149253.
  15. 15.0 15.1 Simonetti G, Gaviani P, Botturi A, Innocenti A, Lamperti E, Silvani A (2015). "Clinical management of grade III oligodendroglioma". Cancer Manag Res. 7: 213–23. doi:10.2147/CMAR.S56975. PMC 4524382. PMID 26251628.
  16. Patterns by Gender for Selected Histologies CBTRUS Statistical Report: NPCR and SEER Data from 2004-2006. CBTRUS.org 2015. http://www.cbtrus.org/2010-NPCR-SEER/CBTRUS-WEBREPORT-Final-3-2-10.pdf
  17. Early detection, diagnosis, and staging of brain tumors. American cancer society. http://www.cancer.org/cancer/braincnstumorsinadults/detailedguide/brain-and-spinal-cord-tumors-in-adults-detection
  18. Manousaki M, Papadaki H, Papavdi A, Kranioti EF, Mylonakis P, Varakis J; et al. (2011). "Sudden unexpected death from oligodendroglioma: a case report and review of the literature". Am J Forensic Med Pathol. 32 (4): 336–40. doi:10.1097/PAF.0b013e3181d3dc86. PMID 20375839.
  19. Guppy KH, Akins PT, Moes GS, Prados MD (2009). "Spinal cord oligodendroglioma with 1p and 19q deletions presenting with cerebral oligodendrogliomatosis". J Neurosurg Spine. 10 (6): 557–63. doi:10.3171/2009.2.SPINE08853. PMID 19558288.
  20. Sharma A, Agarwal A, Sharma MC, Anand M, Agarwal S, Raina V (2003). "Bone marrow metastasis in anaplastic oligodendroglioma". Int J Clin Pract. 57 (4): 351–2. PMID 12800473.
  21. Solitare GB, Robinson F, Lamarche JB (1967). "Oligodendroglioma: recurrence following an exceptionally long postoperative symptom-free interval". Can Med Assoc J. 97 (14): 862–5. PMC 1923454. PMID 6051252.
  22. Harada K, Kiya K, Matsumura S, Mori S, Uozumi T (1982). "Spontaneous intracranial hemorrhage caused by oligodendroglioma--a case report and review of the literature". Neurol Med Chir (Tokyo). 22 (1): 81–4. PMID 6176898.
  23. Hentschel S, Toyota B (2003). "Intracranial malignant glioma presenting as subarachnoid hemorrhage". Can J Neurol Sci. 30 (1): 63–6. PMID 12619787.
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