Nonhematogenic circulating aneuploid cells confer inferior prognosis and therapeutic resistance in gliomas

Aneuploidy is the hallmark of malignancy. Our previous study successfully detected nonhematogenic circulating aneuploidy cells (CACs) in types of gliomas. The current prospective clinical study aims to further precisely subcategorize aneuploid CACs, including CD31− circulating tumor cells (CTCs) and...

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Published in:Cancer science 2022-10, Vol.113 (10), p.3535-3546
Main Authors: Li, Mingxiao, Gao, Faliang, Ren, Xiaohui, Dong, Gehong, Chen, Hongyan, Lin, Alexander Y., Wang, Daisy Dandan, Liu, Mingyang, Lin, Peter Ping, Shen, Shaoping, Jiang, Haihui, Yang, Chuanwei, Zhang, Xiaokang, Zhao, Xuzhe, Zhu, Qinghui, Li, Ming, Cui, Yong, Lin, Song
Format: Article
Language:English
Subjects:
Aneuploidy
Blood-brain barrier
blood–brain‐barrier, CD31‐CTC
Brain cancer
Brain tumors
CD31 + CTEC
CD45 antigen
Development and progression
Endothelial cells
Epidermal growth factor
Fluorescence in situ hybridization
Glial fibrillary acidic protein
Glioma
Gliomas
Hybridization
Laboratories
Lesions
Malignancy
Medical prognosis
Metastasis
Original
Patients
Prognosis
Statistical analysis
therapy resistance
Tumor cells
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Summary:Aneuploidy is the hallmark of malignancy. Our previous study successfully detected nonhematogenic circulating aneuploidy cells (CACs) in types of gliomas. The current prospective clinical study aims to further precisely subcategorize aneuploid CACs, including CD31− circulating tumor cells (CTCs) and CD31+ circulating tumor endothelial cells, and thoroughly investigate the clinical utilities of these different subtypes of cells. Co‐detection and analysis of CTCs and circulating tumor‐derived endothelial cells (CTECs) expressing CD133, glial fibrillary acidic protein (GFAP), or epidermal growth factor receptor variant III (EGFR vIII) were performed by integrated subtraction enrichment and immunostaining fluorescence in situ hybridization (SE‐iFISH) in 111 preoperative primary diffuse glioma patients. Aneuploid CACs could be detected in most de novo glioma patients. Among detected CACs, 45.6% were CD31−/CD45− aneuploid CTCs and the remaining 54.4% were CD31+/CD45− aneuploid CTECs. Positive detection of CTECs significantly correlated with disruption of the blood–brain barrier. The median number of large CTCs (LCTCs, >5 μm, 2) in low‐grade glioma (WHO grade 2) was less than high‐grade glioma (WHO grades 3 and 4) (3, p = 0.044), but this difference was not observed in small CTCs (SCTCs, ≤5 μm), CTECs or CACs (CTCs + CTECs). The numbers of CTCs, CTECs, or CACs in patients with contrast‐enhancing (CE) lesions considerably exceeded that of non‐CE lesions (p 
ISSN:1347-9032
1349-7006
DOI:10.1111/cas.15516