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      Molecular characteristics of meningiomas

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Meningioma is the most common primary intracranial tumor in adults. The grading of meningioma is based on World Health Organization criteria, which rely on histopathological features alone. This grading system is unable to conclusively predict the clinical behavior of these tumors (i.e., recurrence or prognosis in benign or atypical grades). Advances in molecular techniques over the last decade that include genomic and epigenomic data associated with meningiomas have been used to identify genetic biomarkers that can predict tumor behavior. This review summarizes the molecular characteristics of meningioma using genetic and epigenetic biomarkers. Molecular alterations that can predict meningioma behavior may be integrated into the upcoming World Health Organization grading system.

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          Convergence of Wnt, beta-catenin, and cadherin pathways.

          W Nelson (2004)
          The specification and proper arrangements of new cell types during tissue differentiation require the coordinated regulation of gene expression and precise interactions between neighboring cells. Of the many growth factors involved in these events, Wnts are particularly interesting regulators, because a key component of their signaling pathway, beta-catenin, also functions as a component of the cadherin complex, which controls cell-cell adhesion and influences cell migration. Here, we assemble evidence of possible interrelations between Wnt and other growth factor signaling, beta-catenin functions, and cadherin-mediated adhesion.
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            The recurrence of intracranial meningiomas after surgical treatment.

            D. Simpson (1957)
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              Epigenetic modulators, modifiers and mediators in cancer aetiology and progression.

              Andrew Feinberg, Michael Koldobskiy, Anita Göndör (2016)
              This year is the tenth anniversary of the publication in this journal of a model suggesting the existence of 'tumour progenitor genes'. These genes are epigenetically disrupted at the earliest stages of malignancies, even before mutations, and thus cause altered differentiation throughout tumour evolution. The past decade of discovery in cancer epigenetics has revealed a number of similarities between cancer genes and stem cell reprogramming genes, widespread mutations in epigenetic regulators, and the part played by chromatin structure in cellular plasticity in both development and cancer. In the light of these discoveries, we suggest here a framework for cancer epigenetics involving three types of genes: 'epigenetic mediators', corresponding to the tumour progenitor genes suggested earlier; 'epigenetic modifiers' of the mediators, which are frequently mutated in cancer; and 'epigenetic modulators' upstream of the modifiers, which are responsive to changes in the cellular environment and often linked to the nuclear architecture. We suggest that this classification is helpful in framing new diagnostic and therapeutic approaches to cancer.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Pathol Transl Med
                Journal ID (iso-abbrev): J Pathol Transl Med
                Journal ID (publisher-id): JPTM
                Title: Journal of Pathology and Translational Medicine
                Publisher: The Korean Society of Pathologists and the Korean Society for Cytopathology
                ISSN (Print): 2383-7837
                ISSN (Electronic): 2383-7845
                Publication date (Print): January 2020
                Publication date (Electronic): 15 January 2020
                Volume: 54
                Issue: 1
                Pages: 45-63
                Affiliations
                Department of Hospital Pathology, College of Medicine, The Catholic University of Korea, Seoul, Korea
                Author notes
                Corresponding Author: Youn Soo Lee, MD, PhD, Department of Hospital Pathology, College of Medicine, The Catholic University of Korea, 222 Banpo-daero, Seocho-gu, Seoul 06591, Korea Tel: +82-2-2258-1626, Fax: +82-2-2258-1628, E-mail: lys9908@ 123456catholic.ac.kr
                Author information
                http://orcid.org/0000-0003-4794-639X
                http://orcid.org/0000-0002-1653-6315
                Article
                Publisher ID: jptm-2019-11-05
                DOI: 10.4132/jptm.2019.11.05
                PMC ID: 6986967
                PubMed ID: 31964111
                SO-VID: 9882d038-77a9-4a61-81b4-612a744b44e1
                Copyright © © 2020 The Korean Society of Pathologists/The Korean Society for Cytopathology
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 30 August 2019
                Date revision received : 22 October 2019
                Date accepted : 5 November 2019
                Categories
                Subject: Review

                Keywords: meningioma,molecular diagnosis,pathological diagnosis
                Data availability:
                Keywords: meningioma, molecular diagnosis, pathological diagnosis

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