Updating the grading criteria for adult diffuse gliomas: beyond the WHO2016CNS classification

[...]the WHO has never specified the actual cut-off number for differentiating grade II and III due to the non-reproducibility and inter-observer variability of the mitotic count, which may be caused by the following: discriminating mitoses, particularly granular ones, from apoptosis is often challe...

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Published inBrain tumor pathology Vol. 37; no. 1; pp. 1 - 4
Main Author Komori, Takashi
Format Journal Article
LanguageEnglish
Published Singapore Springer Singapore 2020
Springer Nature B.V
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Summary:[...]the WHO has never specified the actual cut-off number for differentiating grade II and III due to the non-reproducibility and inter-observer variability of the mitotic count, which may be caused by the following: discriminating mitoses, particularly granular ones, from apoptosis is often challenging; the specimen size varies; the diameter of the microscopic fields differs depending on the manufacturer; and the evaluation area may be different, whether evaluating 10 consecutive high-powered fields or an entire specimen. Since the discovery of IDH mutations, it has been suggested that the legacy grading scheme depending on the mitotic count may not be a strong predictor of the outcome of WHO grade II and III astrocytomas with IDH-mutant, although it is still considered valid for IDH-wildtype gliomas [12]. Standardization as well as optimization of the antigen retrieval protocol for Ki-67 across every institution is generally much more challenging than standardizing the mitotic counting approach. Interestingly enough, Shirahata et al. found that the overall survival of IDH-mutant diffuse astrocytic tumors was associated with the CDKN2A/B homozygous deletion status and the presence of necrosis; patients with CDKN2A/B homozygous deletion without necrosis, graded as WHO grade III anaplastic astrocytoma according to the current criteria, exhibited an equivalent survival rate to those with WHO grade IV glioblastoma, IDH-mutant with CDKN2A/B homozygous deletion and necrosis [13].
Bibliography:SourceType-Other Sources-1
content type line 63
ObjectType-Editorial-2
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ISSN:1433-7398
1861-387X
DOI:10.1007/s10014-020-00358-y