Intraventricular Gliosarcomas: Literature Review and a Case Description

Doddamani, Ramesh; Meena, Rajesh Kumar; Selvam, Murli M.; Venkataramanaa, Neelam K; Tophkhane, Madhvi; Garg, Sharat K.

doi:10.1016/j.wneu.2016.03.033

Cited by 11 publications

(28 citation statements)

References 19 publications

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“…14,21 Multiple rare primary locations for these lesions have been described, including the cerebellum, pineal region, cerebellopontine angle, intraventricular, and within the spinal cord. 11,[22][23][24][25][26] While distant metastases were not reported in this group of patients, extracranial local extension was seen in three cases, with one involving the masticator space. The more commonly seen finding of temporal lobe involvement was noted in the majority of our studies, concordant with a study of 353 GSC through the Surveillance, Epidemiology, and End Results (SEER) database which demonstrated that GSC had a higher propensity for temporal lobe involvement than GBM.…”

Section: Discussionmentioning

confidence: 60%

“…Another unique feature of GSC is its ability to metastasize to multiple sites outside of the CNS . Multiple rare primary locations for these lesions have been described, including the cerebellum, pineal region, cerebellopontine angle, intraventricular, and within the spinal cord . While distant metastases were not reported in this group of patients, extracranial local extension was seen in three cases, with one involving the masticator space.…”

Section: Discussionmentioning

confidence: 68%

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Gliosarcoma: Neuroimaging and Immunohistochemical Findings

Peckham

Osborn

Palmer

et al. 2018

Journal of Neuroimaging

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BACKGROUND AND PURPOSE Gliosarcoma (GSC) is an intra‐axial lesion which often abuts a dural margin and is composed of glial and mesenchymal elements. This lesion is considered a variant of isocitrate dehydrogenase (IDH)‐wild type glioblastoma (GBM). The purpose of this study is to evaluate the imaging and molecular features of GSC in a large patient cohort. METHODS Pathology‐proved GSC cases were collected from our quaternary care center spanning the last 16 years and IDH status was documented. Older GSC cases without prior immunohistochemical testing underwent tissue block staining to obtain IDH status. When available, p53, phosphate and tensin (PTEN), MIB‐1, EGFR amplification, and MGMT methylation were recorded and imaging findings tabulated. Logistic regression analyses were performed to determine correlation of molecular markers and imaging characteristics. RESULTS A total of 25 cases were identified (21 de novo, 4 post‐treatment). All lesions contacted a dural, pial, or ependymal surface and were negative for an IDH R132H mutation, including postradiation GSC. In total, 16 of 16 cases showed nonamplification of EGFR/CEP7, 2 of 16 demonstrated MGMT methylation, and multiple lesions demonstrated p53 and PTEN mutations. Imaging features included areas of nodular thickening in necrotic lesions which appeared to abut the site of dural contact. There was no significant correlation of molecular markers with imaging characteristics. CONCLUSION GSC was IDH(–) in all cases, supporting the current understanding of this lesion being a wild‐type GBM variant. Additional molecular markers demonstrated no significant correlation with imaging findings in this cohort.

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Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 68%

Gliosarcoma: Neuroimaging and Immunohistochemical Findings

Peckham

Osborn

Palmer

et al. 2018

Journal of Neuroimaging

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“…[ 15 , 16 , 20 - 24 , 26 , 29 , 45 - 48 ] They are classified as IDH-wildtype variant[ 2 , 29 ] with two different components: gliomatous part (i.e., astrocytic with areas of necrosis, and fulfilling the criteria for glioblastoma [GBM]) determined by the identification of GFAP; and a sarcomatous part that resemble a spindle cell sarcoma determined by the presence of the reticulin element. [ 15 , 16 , 31 , 24 , 45 , 46 , 48 ] The exact pathogenesis is unknown, one theory suggests that sarcomatous components originated from the malignant transformation of hyperplastic blood vessels. [ 15 , 16 , 24 , 31 , 45 , 46 , 48 ]…”

Section: Introductionmentioning

confidence: 99%

“…[ 15 , 16 , 31 , 24 , 45 , 46 , 48 ] The exact pathogenesis is unknown, one theory suggests that sarcomatous components originated from the malignant transformation of hyperplastic blood vessels. [ 15 , 16 , 24 , 31 , 45 , 46 , 48 ]…”

Section: Introductionmentioning

confidence: 99%

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IDH1-mutant primary intraventricular gliosarcoma: Case report and systematic review of a rare location and molecular profile

Filho

Barreto

Martins

et al. 2020

Surgical Neurology International

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Background: Gliosarcoma (GS) is classified as an IDH-wild-type variant of glioblastoma (GBM). While GS is already an unusual presentation of GBM, IDH1-mutant cases are especially rare. We present an IDH1-mutant primary intraventricular GS case report and a systematic review of the molecular profile in GS correlating to the prognostic and pathogenesis of IDH1/2 mutations. Case Description: A 44-years-old man presented with ongoing fatigue symptoms and a new-onset intense occipital headache. The patient complained of memory loss, dyscalculia, and concentration difficulties. An MRI revealed a bihemispheric intraventricular mass crossing the midline through the corpus callosum and infiltrating the trigone of the lateral ventricles, hypointense, and hyperintense on the T1- and T2-weighted image. We performed a microsurgical resection with a transparietal transsulcal approach; however, the contralateral mass was attached to vascular structures and we decided to reoperate the patient in another moment. The histopathological study showed a Grade IV tumor and the immunohistochemistry confirmed the diagnosis of GS. The patient presented progressive neurologic decline and died 45 days after the surgical approach. Conclusion: We did two systematic reviews studies from PubMed, EMBASE, MEDLINE, Cochrane, and SCOPUS databases, and included molecular and intraventricular studies of GS. We performed further meta-analysis using OpenMetaAnalyst™ software. We conducted a forest plot with the molecular profile of GS. When correlated IDH1 mutation versus tp53 mutation, we found an odds ratio (OR) of 0.018 (0.005–0.064) and P < 0.001. Moreover, we compared IDH1 mutation versus MGMT methylation (P = 0.006; OR = 0.138 [0.034–0.562]). The studies evaluating the molecular profile in GS prognostics are often extended from all GBMs despite specifics GBM variants (i.e., GS). We found a correlation between IDH1 mutation expression with tp53 and MGMT expression in GS, and future studies exploring this molecular profile in GS are strongly encouraged.

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