Abstract

Abstract BACKGROUND After the new molecular-based classification was reported to be useful for predicting prognosis, the T2-fluid-attenuated inversion recovery (FLAIR) mismatch sign has gained interest as one of the promising methods for detecting lower-grade gliomas (LGGs) with isocitrate dehydrogenase (IDH) mutations and chromosome 1p/19q non-codeletion (IDH mut-Noncodel) with high specificity. Although all institutions could use T2-FLAIR mismatch sign without any obstacles, this sign was not completely helpful because of its low sensitivity. In this study, we attempted to uncover the mechanism of T2-FLAIR mismatch sign for clarifying the cause of this sign’s low sensitivity. MATERIAL AND METHODS In this study, data on 101 consecutive and unselected patients with LGGs (WHO grades 2 and 3) admitted to Miyazaki University Hospital between November 2005 and January 2021 were collected. The inclusion criteria were as follows: (1) obtained molecular information on IDH mutation and chromosome 1p/19q codeletion status and (2) obtained preoperative MRI data, including T2-weighted imaging and FLAIR sequences. In this study, 99 patients were enrolled and then classified into three groups based on IDH mutation and chromosome 1p/19q codeletion status: (1) IDH-mutant, 1p/19q-codeleted LGGs (IDH mut-codel); (2) IDH-mutant, 1p/19q-noncodeleted LGGs (IDH mut-Noncodel); and (3) IDH wild-type LGGs (IDH wt). RESULTS Among 99 patients with LGGs, 22 were T2-FLAIR mismatch sign-positive (22%), and this sign as a marker of IDH mut-Noncodel showed a sensitivity of 55.6% and specificity of 96.8%. Via pathological analyses, we could provide evidence that not only microcystic changes but the enlarged intercellular space was associated with T2-FLAIR mismatch sign (p =0.017). As per the molecular analyses, overexpression of mTOR-related genes (m-TOR, RICTOR) were detected as the molecular events correlated with T2-FLAIR mismatch sign (p = 0.020, 0.030. respectively). CONCLUSION We suggested that T2-FLAIR mismatch sign could pick up the IDH mut-Noncodel LGGs with enlarged intercellular space or that with overexpression of mTOR-related genes.

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