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Comparative molecular analysis of primary and recurrent oligodendroglioma that acquired imbalanced 1p/19q codeletion and TP53 mutation: a case report

  • Case Report - Tumor - Glioma
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Abstract

Oligodendroglioma is defined by IDH mutation and 1p/19q codeletion. Normal TP53 status is also its molecular feature. We report a case of oligodendroglioma that acquired imbalanced 1p/19q codeletion and TP53 mutation at recurrence after temozolomide therapy. The primary and recurrent tumors shared IDH1 and TERT promoter mutations. Although 1p/19q was codeleted in the primary tumor, it was imbalanced in the recurrent tumor harboring TP53 mutation. The copy-neutral loss of heterozygosity might have imbalanced the 1p/19q codeletion, while temozolomide therapy possibly caused the TP53 mutation. Such phenomena, although rare, should be noted during the clinical treatment of oligodendrogliomas.

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Acknowledgments

We thank Dr. Susumu Fushimi, Dr. Kenichi Shibata, Dr. Rui Kondo, and Dr. Satsuki Takahashi at the Hiraka General Hospital for providing clinical data and samples of the primary case. We also thank Dr. Akira Kurose at the Department of Anatomic Pathology, Hirosaki University Graduate School of Medicine for his practical advice.

Molecular diagnoses in this study were funded by a grant from the Japan Society for the Promotion of Science (JSPS) KAKENHI, Grant Number JP19K16823; Dr. Takahiro Ono received this grant.

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This manuscript has not been published or presented elsewhere in part or in entirety and is not under consideration by another journal.

Funding

Molecular diagnoses in this study were funded by a grant from the Japan Society for the Promotion of Science (JSPS) KAKENHI, Grant Number JP19K16823; Dr. Takahiro Ono received this grant.

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Correspondence to Takahiro Ono.

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Ono, T., Reinhardt, A., Takahashi, M. et al. Comparative molecular analysis of primary and recurrent oligodendroglioma that acquired imbalanced 1p/19q codeletion and TP53 mutation: a case report. Acta Neurochir 162, 3019–3024 (2020). https://doi.org/10.1007/s00701-020-04514-3

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  • DOI: https://doi.org/10.1007/s00701-020-04514-3

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