Histopathological malignant progression of grade II and III gliomas correlated with IDH1/2 mutation status |
| |
Authors: | Makoto Ohno Yoshitaka Narita Yasuji Miyakita Yoshiko Okita Yuko Matsushita Akihiko Yoshida Shintaro Fukushima Koichi Ichimura Takamasa Kayama Soichiro Shibui |
| |
Institution: | 1. Department of Neurosurgery and Neuro-Oncology, National Cancer Center Hospital, 5-1-1, Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan 2. Department of Pathology and Clinical Laboratories, National Cancer Center Hospital, 5-1-1, Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan 3. Division of Brain Tumor Translational Research, National Cancer Center Research Institute, 5-1-1, Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan
|
| |
Abstract: | The impact of isocitrate dehydrogenase (IDH1/2) mutations on the malignant progression of gliomas was investigated by comparing the histopathological features of 53 grade II and III gliomas after recurrence according to the IDH1/2 status. We identified IDH1/2 mutations in 44.4?% (16 of 36) of astrocytic tumors and 70.6?% (12 of 17) of oligodendroglial tumors. Histopathological malignant progression was observed in 68.8?% (11 in 16) and 55?% (11 in 20) of astrocytic tumors with and without IDH1/2 mutations, respectively. There were 8 secondary glioblastomas (GBM) that had progressed from 5 diffuse astrocytomas (DA) and 3 anaplastic astrocytomas (AA) with IDH1/2 mutations. Seven secondary GBMs were derived from 3 DAs and 4 AAs with wild-type IDH1/2. Malignant progression was observed in 47.1?% (8 of 17) of oligodendroglial tumors. All 12 oligodendroglial tumors with IDH1/2 mutations remained as such without progressing to GBM, whereas 3 of the 5 oligodendroglial tumors without IDH1/2 mutations progressed to GBM at recurrence. In conclusion, grade II and III gliomas developed to more malignant histological types, irrespective of the IDH1/2 mutation status, and the monitoring of the IDH1/2 status could be of value to predict the development of GBM in patients with oligodendroglial tumors. |
| |
Keywords: | |
本文献已被 SpringerLink 等数据库收录! |
|