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Antiangiogenic Therapies and Extracranial Metastasis in Glioblastoma: A Case Report and Review of the Literature.

Khattab MH, Marciscano AE, Lo SS, Lim M, Laterra JJ, Kleinberg LR, Redmond KJ - Case Rep Oncol Med (2015)

Bottom Line: We present a case report of a patient with glioblastoma multiforme (GBM) complicated by extracranial metastasis (ECM) whose survival of nearly four years surpassed the anticipated life expectancy given numerous negative prognostic factors including EGFRvIII-mutation, unmethylated MGMT promoter status, and ECM.Interestingly, while this patient suffered from locally aggressive disease with multiple intracranial recurrences, the proximal cause of death was progressive extracranial disease and complications related to pulmonary metastases.Herein, we review potential mechanisms of ECM with an emphasis upon glioblastoma molecular and genetic profiles and the potential implications of targeted agents such as bevacizumab.

View Article: PubMed Central - PubMed

Affiliation: Department of Radiation Oncology & Molecular Radiation Sciences, Johns Hopkins University, 401 North Broadway, Suite 1440, Baltimore, MD 21231-5678, USA.

ABSTRACT
We present a case report of a patient with glioblastoma multiforme (GBM) complicated by extracranial metastasis (ECM) whose survival of nearly four years surpassed the anticipated life expectancy given numerous negative prognostic factors including EGFRvIII-mutation, unmethylated MGMT promoter status, and ECM. Interestingly, while this patient suffered from locally aggressive disease with multiple intracranial recurrences, the proximal cause of death was progressive extracranial disease and complications related to pulmonary metastases. Herein, we review potential mechanisms of ECM with an emphasis upon glioblastoma molecular and genetic profiles and the potential implications of targeted agents such as bevacizumab.

No MeSH data available.


Related in: MedlinePlus

Surgical pathological specimens from (a) initial craniotomy and (b-c) repeat craniotomy for recurrent intracranial disease. Histopathological analysis of the initial (a) right temporal lobe specimen demonstrated glioblastoma with small cell features. The pathological specimen after second resection (b) demonstrated active glioblastoma, almost entirely viable with <5% necrosis. Following the third and final (c) craniotomy for locally recurrent disease, predominantly viable (approximately 15% necrosis) active glioblastoma was identified. Molecular studies were negative for MGMT methylation and EGFR amplification was detected by FISH.
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fig1: Surgical pathological specimens from (a) initial craniotomy and (b-c) repeat craniotomy for recurrent intracranial disease. Histopathological analysis of the initial (a) right temporal lobe specimen demonstrated glioblastoma with small cell features. The pathological specimen after second resection (b) demonstrated active glioblastoma, almost entirely viable with <5% necrosis. Following the third and final (c) craniotomy for locally recurrent disease, predominantly viable (approximately 15% necrosis) active glioblastoma was identified. Molecular studies were negative for MGMT methylation and EGFR amplification was detected by FISH.

Mentions: A previously healthy 51-year-old right-handed African American gentleman initially presented following an unwitnessed seizure. MRI revealed focal enhancement in the posterior temporal lobe measuring approximately 9 mm as well as T2 hyperintensity within the right insular cortex and right temporal lobe. He was empirically treated for HSV encephalitis until CSF HSV PCR assay returned negative. Given persistent mental status changes, MR imaging at 4 and 9 months after initial presentation revealed an enhancing temporoparietal mass with interval enlargement between scans. He underwent right temporal craniotomy with postoperative pathology consistent with WHO grade IV astrocytoma (GBM) with small cell features (Figure 1(a)). Specific histopathological findings of cellular atypia with variable morphology ranging from packed cells with relatively homogeneous ovoid nuclei to less cellular areas with a whorled configuration, foci of necrosis with scattered calcifications, numerous mitoses, and endothelial proliferation were noted. Immunohistochemical staining demonstrated strong staining for vimentin and negative staining for EMA. Additional tumor analysis revealed an unmethylated MGMT gene promoter and EGFR amplification, later confirmed to be EGFRvIII positive.


Antiangiogenic Therapies and Extracranial Metastasis in Glioblastoma: A Case Report and Review of the Literature.

Khattab MH, Marciscano AE, Lo SS, Lim M, Laterra JJ, Kleinberg LR, Redmond KJ - Case Rep Oncol Med (2015)

Surgical pathological specimens from (a) initial craniotomy and (b-c) repeat craniotomy for recurrent intracranial disease. Histopathological analysis of the initial (a) right temporal lobe specimen demonstrated glioblastoma with small cell features. The pathological specimen after second resection (b) demonstrated active glioblastoma, almost entirely viable with <5% necrosis. Following the third and final (c) craniotomy for locally recurrent disease, predominantly viable (approximately 15% necrosis) active glioblastoma was identified. Molecular studies were negative for MGMT methylation and EGFR amplification was detected by FISH.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4493308&req=5

fig1: Surgical pathological specimens from (a) initial craniotomy and (b-c) repeat craniotomy for recurrent intracranial disease. Histopathological analysis of the initial (a) right temporal lobe specimen demonstrated glioblastoma with small cell features. The pathological specimen after second resection (b) demonstrated active glioblastoma, almost entirely viable with <5% necrosis. Following the third and final (c) craniotomy for locally recurrent disease, predominantly viable (approximately 15% necrosis) active glioblastoma was identified. Molecular studies were negative for MGMT methylation and EGFR amplification was detected by FISH.
Mentions: A previously healthy 51-year-old right-handed African American gentleman initially presented following an unwitnessed seizure. MRI revealed focal enhancement in the posterior temporal lobe measuring approximately 9 mm as well as T2 hyperintensity within the right insular cortex and right temporal lobe. He was empirically treated for HSV encephalitis until CSF HSV PCR assay returned negative. Given persistent mental status changes, MR imaging at 4 and 9 months after initial presentation revealed an enhancing temporoparietal mass with interval enlargement between scans. He underwent right temporal craniotomy with postoperative pathology consistent with WHO grade IV astrocytoma (GBM) with small cell features (Figure 1(a)). Specific histopathological findings of cellular atypia with variable morphology ranging from packed cells with relatively homogeneous ovoid nuclei to less cellular areas with a whorled configuration, foci of necrosis with scattered calcifications, numerous mitoses, and endothelial proliferation were noted. Immunohistochemical staining demonstrated strong staining for vimentin and negative staining for EMA. Additional tumor analysis revealed an unmethylated MGMT gene promoter and EGFR amplification, later confirmed to be EGFRvIII positive.

Bottom Line: We present a case report of a patient with glioblastoma multiforme (GBM) complicated by extracranial metastasis (ECM) whose survival of nearly four years surpassed the anticipated life expectancy given numerous negative prognostic factors including EGFRvIII-mutation, unmethylated MGMT promoter status, and ECM.Interestingly, while this patient suffered from locally aggressive disease with multiple intracranial recurrences, the proximal cause of death was progressive extracranial disease and complications related to pulmonary metastases.Herein, we review potential mechanisms of ECM with an emphasis upon glioblastoma molecular and genetic profiles and the potential implications of targeted agents such as bevacizumab.

View Article: PubMed Central - PubMed

Affiliation: Department of Radiation Oncology & Molecular Radiation Sciences, Johns Hopkins University, 401 North Broadway, Suite 1440, Baltimore, MD 21231-5678, USA.

ABSTRACT
We present a case report of a patient with glioblastoma multiforme (GBM) complicated by extracranial metastasis (ECM) whose survival of nearly four years surpassed the anticipated life expectancy given numerous negative prognostic factors including EGFRvIII-mutation, unmethylated MGMT promoter status, and ECM. Interestingly, while this patient suffered from locally aggressive disease with multiple intracranial recurrences, the proximal cause of death was progressive extracranial disease and complications related to pulmonary metastases. Herein, we review potential mechanisms of ECM with an emphasis upon glioblastoma molecular and genetic profiles and the potential implications of targeted agents such as bevacizumab.

No MeSH data available.


Related in: MedlinePlus