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      Neurodevelopmental disorders, like cancer, are connected to impaired chromatin remodelers, PI3K/mTOR, and PAK1-regulated MAPK

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          Abstract

          Neurodevelopmental disorders (NDDs) and cancer share proteins, pathways, and mutations. Their clinical symptoms are different. However, individuals with NDDs have higher probabilities of eventually developing cancer. Here, we review the literature and ask how the shared features can lead to different medical conditions and why having an NDD first can increase the chances of malignancy. To explore these vital questions, we focus on dysregulated PI3K/mTOR, a major brain cell growth pathway in differentiation, and MAPK, a critical pathway in proliferation, a hallmark of cancer. Differentiation is governed by chromatin organization, making aberrant chromatin remodelers highly likely agents in NDDs. Dysregulated chromatin organization and accessibility influence the lineage of specific cell brain types at specific embryonic development stages. PAK1, with pivotal roles in brain development and in cancer, also regulates MAPK. We review, clarify, and connect dysregulated pathways with dysregulated proliferation and differentiation in cancer and NDDs and highlight PAK1 role in brain development and MAPK regulation. Exactly how PAK1 activation controls brain development, and why specific chromatin remodeler components, e.g., BAF170 encoded by SMARCC2 in autism, await clarification.

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          Most cited references214

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          Hallmarks of Cancer: The Next Generation

          The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
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            Cell signaling by receptor tyrosine kinases.

            Recent structural studies of receptor tyrosine kinases (RTKs) have revealed unexpected diversity in the mechanisms of their activation by growth factor ligands. Strategies for inducing dimerization by ligand binding are surprisingly diverse, as are mechanisms that couple this event to activation of the intracellular tyrosine kinase domains. As our understanding of these details becomes increasingly sophisticated, it provides an important context for therapeutically countering the effects of pathogenic RTK mutations in cancer and other diseases. Much remains to be learned, however, about the complex signaling networks downstream from RTKs and how alterations in these networks are translated into cellular responses.
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              The PI3K Pathway in Human Disease.

              Phosphoinositide 3-kinase (PI3K) activity is stimulated by diverse oncogenes and growth factor receptors, and elevated PI3K signaling is considered a hallmark of cancer. Many PI3K pathway-targeted therapies have been tested in oncology trials, resulting in regulatory approval of one isoform-selective inhibitor (idelalisib) for treatment of certain blood cancers and a variety of other agents at different stages of development. In parallel to PI3K research by cancer biologists, investigations in other fields have uncovered exciting and often unpredicted roles for PI3K catalytic and regulatory subunits in normal cell function and in disease. Many of these functions impinge upon oncology by influencing the efficacy and toxicity of PI3K-targeted therapies. Here we provide a perspective on the roles of class I PI3Ks in the regulation of cellular metabolism and in immune system functions, two topics closely intertwined with cancer biology. We also discuss recent progress developing PI3K-targeted therapies for treatment of cancer and other diseases.
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                Author and article information

                Contributors
                NussinoR@mail.nih.gov
                Journal
                Biophys Rev
                Biophys Rev
                Biophysical Reviews
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                1867-2450
                1867-2469
                1 April 2023
                1 April 2023
                April 2023
                : 15
                : 2
                : 163-181
                Affiliations
                [1 ]GRID grid.418021.e, ISNI 0000 0004 0535 8394, Computational Structural Biology Section, , Frederick National Laboratory for Cancer Research, ; Frederick, MD 21702 USA
                [2 ]GRID grid.12136.37, ISNI 0000 0004 1937 0546, Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, , Tel Aviv University, ; 69978 Tel Aviv, Israel
                [3 ]GRID grid.6935.9, ISNI 0000 0001 1881 7391, Graduate School of Informatics, , Middle East Technical University, ; Ankara, Turkey
                [4 ]GRID grid.15876.3d, ISNI 0000000106887552, Department of Chemical and Biological Engineering, College of Engineering, , Koc University, ; 34450 Istanbul, Turkey
                [5 ]GRID grid.48336.3a, ISNI 0000 0004 1936 8075, Cancer Innovation Laboratory, , National Cancer Institute, ; Frederick, MD 21702 USA
                [6 ]GRID grid.15876.3d, ISNI 0000000106887552, School of Medicine, , Koc University, ; 34450 Istanbul, Turkey
                Author information
                http://orcid.org/0000-0002-8115-6415
                Article
                1054
                10.1007/s12551-023-01054-9
                10133437
                37124926
                af728fb7-5088-4ce4-9edd-6b5584f6b0c8
                © The Author(s) 2023

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 8 March 2023
                : 21 March 2023
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000054, National Cancer Institute;
                Award ID: HHSN261201500003I
                Categories
                Review
                Custom metadata
                © International Union for Pure and Applied Biophysics (IUPAB) and Springer-Verlag GmbH Germany, part of Springer Nature 2023

                Biophysics
                chromatin,cell cycle,autism,rasopathies,asd
                Biophysics
                chromatin, cell cycle, autism, rasopathies, asd

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