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Case Study
- Meningioma harboring IDH1 R132H mutation: a case report
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Soyeon Ahn, Chung Lee, Jong-Pil Park, Se Hoon Kim
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Received June 24, 2026 Accepted August 19, 2026 Published online November 3, 2026
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DOI: https://doi.org/10.4132/jptm.2026.08.19
[Epub ahead of print]
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Abstract
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- Meningiomas are the most common primary central nervous system tumors. Monosomy of chromosome 22 is the most frequently reported genetic abnormality in meningioma and the occurrence of IDH1 mutations in meningioma is exceedingly rare. We report an uncommon case of IDH1 R132H-mutant meningioma. A 69-year-old man presented with two intracranial masses, one of which was identified as an IDH1 R132H-mutant meningioma by next-generation sequencing and further confirmed by pyrosequencing and immunohistochemistry. The rarity of this molecular finding and the potentially favorable prognosis observed in previously reported cases highlight the need for its recognition as a distinct molecular subset. Isocitrate dehydrogenase–targeted therapy may represent a future therapeutic option, pending validation through prospective studies and larger case series.
Original Article
- Expression of Interleukin-6 in Induced Viral Myocarditis in Mice.
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Soo Yeon Cho, Hye Kyung Jin, Min Sun Cho, Sung Sook Kim, Woon Sup Han, Dong Sun Han, Hak Chung Lee
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Korean J Pathol. 1995;29(2):212-220.
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Abstract
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- Viral myocarditis is considered an important cause of dilated cardiomyopathy. At preseent, two mechanisms are known to be involved in the pathogenesis of viral myocarditis and subse-quent cardiomyopathy: viral direct toxicity and immune mediated toxicity. Some authors have reported that IL-6 influences the immunologic mechanism and the virus-induced tissue damage in myocarditis. We injected encephalomyocarditis(EMC) virus to induce viral myocarditis in ICR mice. In order to study the lymphocyte subset and IL-6 expression to clarify the immune mechanism and to demonstrate the role of IL-6 in viral induced myocardial damage. The following results were obtained: 1) In virus inoculated mice, inflammation was severest at 10 days, and some serious complications developed, indicating a possible transition to dilated cardiomyopathy. 2) On analysis of the lymphocyte subset, CD4 cells were most prevalent at 5 days and CD8 cells were most prevalent at 10 and 20 days. 3) IL-6 was significantly increased and expression of IL-6 was constant, but its intensity was strongest at 5 days. In conclusion, IL-6, produced by inflammatory cells, fibroblasts, and endothelial cells, might play an important role in myocardial damage in experimentally induced EMC viral myocarditis by its direct cytotoxicity or cytokine mediated activation of cytotoxic cells.
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