Comparative molecular analysis of primary and recurrent oligodendroglioma that acquired imbalanced 1p/19q codeletion andTP53mutation: a case report

被引：4

作者：

Ono, Takahiro ^{[1
]}

Reinhardt, Annekathrin ^{[2
,3
,4
]}

Takahashi, Masataka ^{[1
]}

Nanjo, Hiroshi ^{[5
]}

Kamataki, Akihisa ^{[6
]}

von Deimling, Andreas ^{[2
,3
,4
]}

Shimizu, Hiroaki ^{[1
]}

机构：

[1] Akita Univ, Dept Neurosurg, Grad Sch Med, 1-1-1 Hondo, Akita, Akita 0108543, Japan

[2] Heidelberg Univ, Dept Neuropathol, Neuenheimer Feld 224, D-69120 Heidelberg, Germany

[3] Heidelberg Univ, CCU Neuropathol, Neuenheimer Feld 224, D-69120 Heidelberg, Germany

[4] DKFZ, Neuenheimer Feld 224, D-69120 Heidelberg, Germany

[5] Akita Univ Hosp, Dept Clin Pathol, 1-1-1 Hondo, Akita, Akita 0108543, Japan

[6] Hirosaki Univ, Dept Anat Pathol, Grad Sch Med, 5 Zaifu Cho, Hirosaki, Aomori 0368562, Japan

来源：

ACTA NEUROCHIRURGICA | 2020年 / 162卷 / 12期

基金：

日本学术振兴会;

关键词：

Case report; Oligodendroglioma; 1p; 19q codeletion; Methylation profile; TP53mutation; Copy-neutral loss of heterozygosity; TUMORS; PROGRESSION; IDH;

D O I：

10.1007/s00701-020-04514-3

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Oligodendroglioma is defined byIDHmutation and 1p/19q codeletion. NormalTP53status is also its molecular feature. We report a case of oligodendroglioma that acquired imbalanced 1p/19q codeletion andTP53mutation at recurrence after temozolomide therapy. The primary and recurrent tumors sharedIDH1andTERTpromoter mutations. Although 1p/19q was codeleted in the primary tumor, it was imbalanced in the recurrent tumor harboringTP53mutation. The copy-neutral loss of heterozygosity might have imbalanced the 1p/19q codeletion, while temozolomide therapy possibly caused theTP53mutation. Such phenomena, although rare, should be noted during the clinical treatment of oligodendrogliomas.

引用

页码：3019 / 3024

页数：6

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