Artikel
Increased KIR4.1 immunoreactivity in human glioma tissue
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Autoren
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Lucas Schirmer
- Neurologische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universität München
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Florian Ringel
- Neurochirurgische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universität München
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Vicki Marie Butenschön
- Neurochirurgische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universität München
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Rajneesh Srivastava
- Neurologische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universität München
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Bernhard Hemmer
- Neurologische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universität München
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Jens Gempt
- Neurochirurgische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universität München
| Veröffentlicht: | 2. Juni 2015 |
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Gliederung
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Objective: KIR4.1 (KCNJ10) is a major inward rectifying potassium channel in glial cells that shows a differential expression and regulation under several pathological conditions like multiple sclerosis. Redistribution and mislocalization of the channel have been suggested to take place in glioma cells as well. We aimed to determine the immunoreactivity (IR) of KIR4.1 in human glioma tissue in relation to other pathological analysis (mitosis rate, MGMT methylation status, IDH1/2 mutation, WHO grading) and clinical data.
Method: We analyzed the expression of KIR4.1 and the presence of Ki67+ nuclei (mitosis rate) in snap frozen samples including glioma infiltration zone and tumor core tissue obtained from surgery. KIR4.1 and Ki67 IR was supplemented by related glial markers and MGMT methylation status, presence of IDH1/2 mutation and 1p19q co-deletion. WHO grading as well as clinical data with previous therapy were available for all included samples.
Results: 21 patients harboring cerebral gliomas were included (WHO IV, n = 14; WHO III, n = 3; WHO II, n = 3; WHO I, n = 1). Mean age was 56 years (25 to 80 years), 7 patients were female, 15 male. 5 patients underwent surgery previously, and 3 had previous radiotherapy. In 16 patients, tumor was resected completely; the remaining patients underwent partial resection. 6/12 patients had a MGMT methylation, 2/6 patients had a 1p19q co-deletion, 3/8 were IDH1/2 mutated. In general, we observed a higher expression of KIR4.1 in glioma center as compared to infiltration zone areas. In glioma core areas, an enhanced KIR4.1 IR was linked to higher numbers of Ki67+ nuclei. KIR4.1+ cells were usually clustered around vessels, and those KIR4.1+ clusters were surrounded by Ki67+ cells. Moreover, increased KIR4.1 IR tended to be associated with IDH1/2 mutation but not with MGMT methylation.
Conclusions: Overall, KIR4.1 IR is enhanced in human glioma tissue and shows an association with numbers of Ki67+ cells. Differential expression and regulation of KIR4.1 is assumed to take place in glioma lesions.
