| REVIEW ARTICLE |
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| Year : 2022 | Volume
: 65
| Issue : 5 | Page : 24-32 |
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Glioblastoma: Changing concepts in the WHO CNS5 classification
Jie Chen1, Pengcheng Han2, Sonika Dahiya2
1 Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, USA
2 Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri, USA
Correspondence Address:
Sonika Dahiya
Division of Neuropathology, Department of Pathology and Immunology, Washington University School of Medicine. 425 Euclid Avenue, Campus Box 8118, St Louis, MO - 63110
USA
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijpm.ijpm_1109_21
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Glioblastoma is the most common malignant central nervous system (CNS) tumor in adults. Acute common clinical symptoms include headache, seizure, behavior changes, focal neurological deficits, and signs of increased intracranial pressure. The classic MRI finding of glioblastoma is an irregularly shaped, rim-enhancing or ring-enhancing lesion with a central dark area of necrosis. This constellation of features correlates with microscopic findings of tumor necrosis and microvascular proliferation. Besides these common features, several well-recognized histological subtypes include giant cell glioblastoma, granular cell glioblastoma, gliosarcoma, glioblastoma with a primitive neuronal component, small cell glioblastoma, and epithelioid glioblastoma. While glioblastoma was historically classified as isocitrate dehydrogenase (IDH)-wildtype and IDH-mutant groups, the Consortium to Inform Molecular and Practical Approaches to CNS Tumor Taxonomy (cIMPACT-NOW) and the fifth edition of the WHO Classification of Tumors of the Central Nervous System clearly updated the nomenclature to reflect glioblastoma to be compatible with wildtype IDH status only. Therefore, glioblastoma is now defined as “a diffuse, astrocytic glioma that is IDH-wildtype and H3-wildtype and has one or more of the following histological or genetic features: microvascular proliferation, necrosis, Telomerase reverse transcriptase promoter mutation, Epidermal growth factor receptor gene amplification, +7/−10 chromosome copy-number changes (CNS WHO grade 4).”
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