WHO 2021 and beyond: new types, molecular markers and tools for brain tumor classification

Tran, Suzanne; Bielle, Franck

doi:10.1097/cco.0000000000000903

Cited by 6 publications

(3 citation statements)

References 47 publications

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“…In previous classification, CNS tumors received a grade assigned to each entity, and grades were used across different entities predicted to have similar survival. However, in WHO CNS5, the switch to within-tumor-type grading has been used to many tumor types ( Tran and Bielle, 2022 ). Moreover, based on the recommendations of the 2019 cIMPACT-NOW Utrecht meeting, WHO CNS5 has simplified tumor nomenclature for better clinical utility, for example, “anaplastic astrocytoma” and “anaplastic oligodendroglioma” are no longer used; instead, such tumors are simply referred to as grade 3.…”

Section: Introductionmentioning

confidence: 99%

Pediatric CNS tumors and 2021 WHO classification: what do oncologists need from pathologists?

d’Amati,

Bargiacchi,

Rossi

et al. 2024

Front. Mol. Neurosci.

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The fifth edition of the WHO Classification of Tumors of the Central Nervous System (CNS), published in 2021, established new approaches to both CNS tumor nomenclature and grading, emphasizing the importance of integrated diagnoses and layered reports. This edition increased the role of molecular diagnostics in CNS tumor classification while still relying on other established approaches such as histology and immunohistochemistry. Moreover, it introduced new tumor types and subtypes based on novel diagnostic technologies such as DNA methylome profiling. Over the past decade, molecular techniques identified numerous key genetic alterations in CSN tumors, with important implications regarding the understanding of pathogenesis but also for prognosis and the development and application of effective molecularly targeted therapies. This review summarizes the major changes in the 2021 fifth edition classification of pediatric CNS tumors, highlighting for each entity the molecular alterations and other information that are relevant for diagnostic, prognostic, or therapeutic purposes and that patients’ and oncologists’ need from a pathology report.

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Section: Introductionmentioning

confidence: 99%

Pediatric CNS tumors and 2021 WHO classification: what do oncologists need from pathologists?

d’Amati,

Bargiacchi,

Rossi

et al. 2024

Front. Mol. Neurosci.

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“…Tumor tissues were collected from a cohort of 52 pediatric patients with MB, classified according to WHO 2021 classification ( 38 ), at the Bambino Gesù Children's Hospital (OPBG), Rome, Italy. Patient tissues and blood samples of both patient and healthy donors were collected and evaluated by cytofluorimetric analysis for GD2 expression.…”

Section: Methodsmentioning

confidence: 99%

GD2-Targeting CAR T-cell Therapy for Patients with GD2+ Medulloblastoma

Ciccone,

Quintarelli,

Camera

et al. 2024

Clinical Cancer Research

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Purpose: Medulloblastoma (MB), the most common childhood malignant brain tumor, has a poor prognosis in about 30% of patients. The current standard of care, which includes surgery, radiation and chemotherapy, is often responsible for cognitive, neurologic and endocrine side effects. We investigated whether chimeric antigen receptor (CAR) T-cells directed towards the disialoganglioside GD2 can represent a potentially more effective treatment with reduced long-term side effects. Experimental Design: GD2 expression was evaluated on primary tumor biopsies of MB children by flow-cytometry. GD2 expression in MB cells was evaluated also in response to an EZH2 inhibitor (Tazemetostat). In in vitro, as well as in in vivo models, GD2+MB cells were targeted by a CAR-GD2.CD28.4-1BBζ (CAR.GD2)-T construct, including the suicide gene inducible-caspase-9. Results: GD2 was expressed in 73.17% of MB tumors. The SHH and G4 subtypes expressed the highest levels of GD2, while the WNT subtype the lowest. In in-vitro co-culture assays, CAR.GD2 T-cells were able to kill GD2+MB cells. Pre-treatment with Tazemetostat upregulated GD2 expression, sensitizing GD2dimMB cells to CAR.GD2 T-cells cytotoxic activity. In orthotopic mouse models of MB, intravenously injected CAR.GD2 T-cells significantly controlled tumor growth, prolonging overall survival of treated mice. Moreover, the dimerizing drug AP1903 was able to cross the murine blood brain barrier and to eliminate both blood circulating and tumor infiltrating CAR.GD2 T-cells. Conclusions: Our experimental data indicate the feasibility of CAR.GD2 T-cell therapy. A phase I/II clinical trial will be conducted to evaluate the safety and therapeutic efficacy of CAR.GD2 therapy in high-risk MB patients.

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“…Glioma, the most common primary intracranial malignant tumor, accounts for almost 80% of malignancies in the central nervous system (CNS) [7]. Although our previous research and numerous other attempts to develop effective prognostic markers and strati cations for glioma, glioma remains a type of malignant tumor with extremely poor prognosis due to genetic heterogeneity [8][9][10]. Therefore, it remains needful and urgent to identify well-de ned and effective biomarkers in glioma to comprehensively raise therapeutic effect.…”

Section: Introductionmentioning

confidence: 99%

Identification of NEK6 as a potential biomarker for prognosis in glioma

Wang,

et al. 2024

Preprint

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Never in mitosis gene A-related kinase 6 (NEK6) is involved in mitotic cell cycle. However, the characteristics and roles of NEK6 in pan-cancer remain incomplete. The objective of the present study is to comprehensively explore the prognostic value of NEK6 and its potential functions in multiple cancers, especially in gliomas. In this study, we conducted of comprehensive analyses of NEK6 in pan-cancer, including expression profile, immune characteristics and its relationship with clinical prognosis. We found that NEK6 was significantly upregulated in gliomas. And the increased level of NEK6 was significantly associated with poor clinical prognoses of tumor patients. Moreover, the single-cell analysis revealed that NEK6 overexpression was highly related to malignant cells and Mono/Macrophages in glioma tissue. spebrutinib and barasertib were identified to be targeted therapeutic drugs for gliomas. Then, the prognostic role of NEK6 was further validated using an independent glioma cohort, and confirmed that the highly expression of NEK6 in glioma was positively correlated with poor prognosis in patients with glioma. In vitro experiment demonstrated that knockdown of NEK6 hindered the growth and migration capacity of the glioma cells, leading to a halt in the G2/M phase of the cell cycle and triggering apoptosis in glioma cell lines. Taken together, our data uncovered the prognostic value, therapeutic potential, and molecular insight of NEK6 in glioma.

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WHO 2021 and beyond: new types, molecular markers and tools for brain tumor classification

Cited by 6 publications

References 47 publications

Pediatric CNS tumors and 2021 WHO classification: what do oncologists need from pathologists?

Pediatric CNS tumors and 2021 WHO classification: what do oncologists need from pathologists?

GD2-Targeting CAR T-cell Therapy for Patients with GD2+ Medulloblastoma

Identification of NEK6 as a potential biomarker for prognosis in glioma

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