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Abstract

Objective

Noninvasive detection of molecular status of astrocytoma is of great clinical significance for predicting therapeutic response and prognosis. We aimed to evaluate whether morphological MRI (mMRI), SWI, DWI, and DSC-PWI could predict Ki-67 labeling index (LI), ATRX mutation, and MGMT promoter methylation status in IDH mutant (IDH-mut) astrocytoma.

Methods

We retrospectively analyzed mMRI, SWI, DWI, and DSC-PWI in 136 patients with IDH-mut astrocytoma.The features of mMRI and intratumoral susceptibility signals (ITSS) were compared using Fisher exact test or chi-square tests. Wilcoxon rank sum test was used to compare the minimum ADC (ADCmin), and minimum relative ADC (rADCmin) of IDH-mut astrocytoma in different molecular markers status. Mann–Whitney U test was used to compare the rCBVmax of IDH-mut astrocytoma with different molecular markers status. Receiver operating characteristic curves was performed to evaluate their diagnostic performances.

Results

ITSS, ADCmin, rADCmin, and rCBVmax were significantly different between high and low Ki-67 LI groups. ITSS, ADCmin, and rADCmin were significantly different between ATRX mutant and wild-type groups. Necrosis, edema, enhancement, and margin pattern were significantly different between low and high Ki-67 LI groups. Peritumoral edema was significantly different between ATRX mutant and wild-type groups. Grade 3 IDH-mut astrocytoma with unmethylated MGMT promoter was more likely to show enhancement compared to the methylated group.

Conclusions

mMRI, SWI, DWI, and DSC-PWI were shown to have the potential to predict Ki-67 LI and ATRX mutation status in IDH-mut astrocytoma. A combination of mMRI and SWI may improve diagnostic performance for predicting Ki-67 LI and ATRX mutation status.

Clinical relevance statement

Conventional MRI and functional MRI (SWI, DWI, and DSC-PWI) can predict Ki-67 expression and ATRX mutation status of IDH mutant astrocytoma, which may help clinicians determine personalized treatment plans and predict patient outcomes.

Key Points

• A combination of multimodal MRI may improve the diagnostic performance to predict Ki-67 LI and ATRX mutation status.

• Compared with IDH-mutant astrocytoma with low Ki-67 LI, IDH-mutant astrocytoma with high Ki-67 LI was more likely to show necrosis, edema, enhancement, poorly defined margin, higher ITSS levels, lower ADC, and higher rCBV.

• ATRX wild-type IDH-mutant astrocytoma was more likely to show edema, higher ITSS levels, and lower ADC compared to ATRX mutant IDH-mutant astrocytoma.

Details

Title
Prediction of Ki-67 labeling index, ATRX mutation, and MGMT promoter methylation status in IDH-mutant astrocytoma by morphological MRI, SWI, DWI, and DSC-PWI
Author
Yang, Xiefeng 1 ; Hu, Chengcong 2 ; Xing, Zhen 1 ; Lin, Yu 1 ; Su, Yan 1 ; Wang, Xingfu 2 ; Cao, Dairong 3   VIAFID ORCID Logo 

 First Affiliated Hospital of Fujian Medical University, Department of Radiology, Fuzhou, People’s Republic of China (GRID:grid.412683.a) (ISNI:0000 0004 1758 0400) 
 First Affiliated Hospital of Fujian Medical University, Department of Pathology, Fuzhou, People’s Republic of China (GRID:grid.412683.a) (ISNI:0000 0004 1758 0400) 
 First Affiliated Hospital of Fujian Medical University, Department of Radiology, Fuzhou, People’s Republic of China (GRID:grid.412683.a) (ISNI:0000 0004 1758 0400); The First Affiliated Hospital, Fujian Medical University, Fujian Key Laboratory of Precision Medicine for Cancer, Fuzhou, People’s Republic of China (GRID:grid.256112.3) (ISNI:0000 0004 1797 9307); The First Affiliated Hospital, Fujian Medical University, Key Laboratory of Radiation Biology of Fujian Higher Education Institutions, Fuzhou, People’s Republic of China (GRID:grid.412683.a) (ISNI:0000 0004 1758 0400) 
Pages
7003-7014
Publication year
2023
Publication date
Oct 2023
Publisher
Springer Nature B.V.
ISSN
09387994
e-ISSN
14321084
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2866634759
Copyright
© The Author(s), under exclusive licence to European Society of Radiology 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.