Glioblastoma in natalizumab-treated multiple sclerosis patients

Fabian Sierra Morales; Robert B. Wright; Jorge Novo; Leonidas D. Arvanitis; Dusan Stefoski; Igor J. Koralnik

doi:10.1002/acn3.428

Glioblastoma in natalizumab-treated multiple sclerosis patients

Fabian Sierra Morales, Robert B. Wright, Jorge Novo, Leonidas D. Arvanitis, Dusan Stefoski, Igor J. Koralnik^*

^*Corresponding author for this work

Pathology

Research output: Contribution to journal › Article › peer-review

3 Scopus citations

Abstract

We present two natalizumab-treated multiple sclerosis patients who developed glioblastoma multiforme (GBM) with variable outcomes. One patient had an isocitrate dehydrogenase (IDH)-wildtype GBM with aggressive behavior, who declined treatment and died 13 weeks after symptoms onset. The other patient underwent resection of an IDH-mutant secondary GBM that arose from a previously diagnosed grade II astrocytoma. He is still alive 5 years after the diagnosis of GBM. JC virus was not detected in either case. Whether natalizumab played a role in the development of GBM in those patients deserves further investigation.

Original language	English (US)
Pages (from-to)	512-516
Number of pages	5
Journal	Annals of clinical and translational neurology
Volume	4
Issue number	7
DOIs	https://doi.org/10.1002/acn3.428
State	Published - Jul 1 2017

ASJC Scopus subject areas

Neuroscience(all)
Clinical Neurology

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title = "Glioblastoma in natalizumab-treated multiple sclerosis patients",

abstract = "We present two natalizumab-treated multiple sclerosis patients who developed glioblastoma multiforme (GBM) with variable outcomes. One patient had an isocitrate dehydrogenase (IDH)-wildtype GBM with aggressive behavior, who declined treatment and died 13 weeks after symptoms onset. The other patient underwent resection of an IDH-mutant secondary GBM that arose from a previously diagnosed grade II astrocytoma. He is still alive 5 years after the diagnosis of GBM. JC virus was not detected in either case. Whether natalizumab played a role in the development of GBM in those patients deserves further investigation.",

author = "{Sierra Morales}, Fabian and Wright, {Robert B.} and Jorge Novo and Arvanitis, {Leonidas D.} and Dusan Stefoski and Koralnik, {Igor J.}",

note = "Funding Information: We thank Dr. Eugene Major from NINDS for performing JC Virus PCR testing in brain sample from patient one. This work was supported in part by grants of the National Institutes of Health R01 NS 047029 and R01 NS 074995 to IJK. Publisher Copyright: {\textcopyright} 2017 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.",

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AU - Wright, Robert B.

AU - Novo, Jorge

AU - Arvanitis, Leonidas D.

AU - Stefoski, Dusan

AU - Koralnik, Igor J.

N1 - Funding Information: We thank Dr. Eugene Major from NINDS for performing JC Virus PCR testing in brain sample from patient one. This work was supported in part by grants of the National Institutes of Health R01 NS 047029 and R01 NS 074995 to IJK. Publisher Copyright: © 2017 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.

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N2 - We present two natalizumab-treated multiple sclerosis patients who developed glioblastoma multiforme (GBM) with variable outcomes. One patient had an isocitrate dehydrogenase (IDH)-wildtype GBM with aggressive behavior, who declined treatment and died 13 weeks after symptoms onset. The other patient underwent resection of an IDH-mutant secondary GBM that arose from a previously diagnosed grade II astrocytoma. He is still alive 5 years after the diagnosis of GBM. JC virus was not detected in either case. Whether natalizumab played a role in the development of GBM in those patients deserves further investigation.

AB - We present two natalizumab-treated multiple sclerosis patients who developed glioblastoma multiforme (GBM) with variable outcomes. One patient had an isocitrate dehydrogenase (IDH)-wildtype GBM with aggressive behavior, who declined treatment and died 13 weeks after symptoms onset. The other patient underwent resection of an IDH-mutant secondary GBM that arose from a previously diagnosed grade II astrocytoma. He is still alive 5 years after the diagnosis of GBM. JC virus was not detected in either case. Whether natalizumab played a role in the development of GBM in those patients deserves further investigation.

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Glioblastoma in natalizumab-treated multiple sclerosis patients

Abstract

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