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The 2016 World Health Organization Classification of Tumors of the Central Nervous System: a summary
The 2016 World Health Organization Classification of Tumors of the Central Nervous System is both a conceptual and practical advance over its 2007 predecessor and is hoped that it will facilitate clinical, experimental and epidemiological studies that will lead to improvements in the lives of patients with brain tumors.
The 2007 WHO Classification of Tumours of the Central Nervous System
The fourth edition of the World Health Organization (WHO) classification of tumours of the central nervous system, published in 2007, lists several new entities, including angiocentric glioma,
Genetic pathways to primary and secondary glioblastoma.
Primary and secondary glioblastomas constitute distinct disease subtypes, affecting patients of different age and developing through different genetic pathways, and differ significantly in their pattern of promoter methylation and in expression profiles at RNA and protein levels.
Population-based studies on incidence, survival rates, and genetic alterations in astrocytic and oligodendroglial gliomas.
Data is summarized on incidence rates, survival, and genetic alterations from population-based studies of astrocytic and oligodendrogliomas that were carried out in the Canton of Zurich, Switzerland to suggest that the acquisition of TP53 mutations in these glioblastoma subtypes may occur through different mechanisms.
The Definition of Primary and Secondary Glioblastoma
IDH1 mutations are the earliest detectable genetic alteration in precursor low-grade diffuse astrocytomas and in oligodendrogliomas, indicating that these tumors are derived from neural precursor cells that differ from those of primary glioblastomas.
Genetic Pathways to Glioblastoma
A population-based study on glioblastomas in the Canton of Zurich, Switzerland, suggests that the acquisition of TP53 mutations in these glooblastoma subtypes occurs through different mechanisms.
IDH1 mutations are early events in the development of astrocytomas and oligodendrogliomas.
The frequent presence of IDH1 mutations in secondary glioblastomas and their near-complete absence in primary gliOBlastomas reinforce the concept that despite their histological similarities, these subtypes are genetically and clinically distinct entities.
Epidemiology and etiology of gliomas
TP53 mutations are significantly more frequent in low-grade astrocytomas with promoter methylation of the O6-methylguanine-DNA methyltransferase repair gene, suggesting that, in addition to deamination of 5-methylcytosine, exogenous or endogenous alkylation in the O 6 position of guanine may contribute to the formation of these mutations.
IDH1 Mutations as Molecular Signature and Predictive Factor of Secondary Glioblastomas
IDH1 mutations are a strong predictor of a more favorable prognosis and a highly selective molecular marker of secondary glioblastomas that complements clinical criteria for distinguishing them from primary gliOBlastomas.
Primary and secondary glioblastomas: from concept to clinical diagnosis.
Current available data are insufficient for a substitution of histologic classification and grading of astrocytic tumors by genetic typing alone, and future research should aim at the identification of criteria for a combined clinical, histologic, and genetic classification of astroscopic tumors.