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  1. Article ; Online: Neurons as stromal drivers of nervous system cancer formation and progression.

    Anastasaki, Corina / Gao, Yunqing / Gutmann, David H

    Developmental cell

    2023  Volume 58, Issue 2, Page(s) 81–93

    Abstract: Similar to their pivotal roles in nervous system development, neurons have emerged as critical regulators of cancer initiation, maintenance, and progression. Focusing on nervous system tumors, we describe the normal relationships between neurons and ... ...

    Abstract Similar to their pivotal roles in nervous system development, neurons have emerged as critical regulators of cancer initiation, maintenance, and progression. Focusing on nervous system tumors, we describe the normal relationships between neurons and other cell types relevant to normal nerve function, and discuss how disruptions of these interactions promote tumor evolution, focusing on electrical (gap junctions) and chemical (synaptic) coupling, as well as the establishment of new paracrine relationships. We also review how neuron-tumor communication contributes to some of the complications of cancer, including neuropathy, chemobrain, seizures, and pain. Finally, we consider the implications of cancer neuroscience in establishing risk for tumor penetrance and in the design of future anti-tumoral treatments.
    MeSH term(s) Humans ; Neurons/metabolism ; Gap Junctions/metabolism ; Nervous System Neoplasms/metabolism
    Language English
    Publishing date 2023-01-21
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2022.12.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: RAS and beyond: the many faces of the neurofibromatosis type 1 protein.

    Anastasaki, Corina / Orozco, Paola / Gutmann, David H

    Disease models & mechanisms

    2022  Volume 15, Issue 2

    Abstract: Neurofibromatosis type 1 is a rare neurogenetic syndrome, characterized by pigmentary abnormalities, learning and social deficits, and a predisposition for benign and malignant tumor formation caused by germline mutations in the NF1 gene. With the ... ...

    Abstract Neurofibromatosis type 1 is a rare neurogenetic syndrome, characterized by pigmentary abnormalities, learning and social deficits, and a predisposition for benign and malignant tumor formation caused by germline mutations in the NF1 gene. With the cloning of the NF1 gene and the recognition that the encoded protein, neurofibromin, largely functions as a negative regulator of RAS activity, attention has mainly focused on RAS and canonical RAS effector pathway signaling relevant to disease pathogenesis and treatment. However, as neurofibromin is a large cytoplasmic protein the RAS regulatory domain of which occupies only 10% of its entire coding sequence, both canonical and non-canonical RAS pathway modulation, as well as the existence of potential non-RAS functions, are becoming apparent. In this Special article, we discuss our current understanding of neurofibromin function.
    MeSH term(s) Genes, Neurofibromatosis 1 ; Humans ; Neurofibromatosis 1/genetics ; Neurofibromin 1/genetics ; Proteins ; Signal Transduction/genetics
    Chemical Substances Neurofibromin 1 ; Proteins
    Language English
    Publishing date 2022-02-21
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.049362
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: RAS and beyond

    Corina Anastasaki / Paola Orozco / David H. Gutmann

    Disease Models & Mechanisms, Vol 15, Iss

    the many faces of the neurofibromatosis type 1 protein

    2022  Volume 2

    Abstract: Neurofibromatosis type 1 is a rare neurogenetic syndrome, characterized by pigmentary abnormalities, learning and social deficits, and a predisposition for benign and malignant tumor formation caused by germline mutations in the NF1 gene. With the ... ...

    Abstract Neurofibromatosis type 1 is a rare neurogenetic syndrome, characterized by pigmentary abnormalities, learning and social deficits, and a predisposition for benign and malignant tumor formation caused by germline mutations in the NF1 gene. With the cloning of the NF1 gene and the recognition that the encoded protein, neurofibromin, largely functions as a negative regulator of RAS activity, attention has mainly focused on RAS and canonical RAS effector pathway signaling relevant to disease pathogenesis and treatment. However, as neurofibromin is a large cytoplasmic protein the RAS regulatory domain of which occupies only 10% of its entire coding sequence, both canonical and non-canonical RAS pathway modulation, as well as the existence of potential non-RAS functions, are becoming apparent. In this Special article, we discuss our current understanding of neurofibromin function.
    Keywords neurofibromin ; ras ; cyclic amp ; tumor suppressor ; Medicine ; R ; Pathology ; RB1-214
    Subject code 610
    Language English
    Publishing date 2022-02-01T00:00:00Z
    Publisher The Company of Biologists
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Stem cell modeling of nervous system tumors.

    Furnari, Frank B / Anastasaki, Corina / Bian, Shan / Fine, Howard A / Koga, Tomoyuki / Le, Lu Q / Rodriguez, Fausto J / Gutmann, David H

    Disease models & mechanisms

    2024  Volume 17, Issue 2

    Abstract: Nervous system tumors, particularly brain tumors, represent the most common tumors in children and one of the most lethal tumors in adults. Despite decades of research, there are few effective therapies for these cancers. Although human nervous system ... ...

    Abstract Nervous system tumors, particularly brain tumors, represent the most common tumors in children and one of the most lethal tumors in adults. Despite decades of research, there are few effective therapies for these cancers. Although human nervous system tumor cells and genetically engineered mouse models have served as excellent platforms for drug discovery and preclinical testing, they have limitations with respect to accurately recapitulating important aspects of the pathobiology of spontaneously arising human tumors. For this reason, attention has turned to the deployment of human stem cell engineering involving human embryonic or induced pluripotent stem cells, in which genetic alterations associated with nervous system cancers can be introduced. These stem cells can be used to create self-assembling three-dimensional cerebral organoids that preserve key features of the developing human brain. Moreover, stem cell-engineered lines are amenable to xenotransplantation into mice as a platform to investigate the tumor cell of origin, discover cancer evolutionary trajectories and identify therapeutic vulnerabilities. In this article, we review the current state of human stem cell models of nervous system tumors, discuss their advantages and disadvantages, and provide consensus recommendations for future research.
    MeSH term(s) Child ; Humans ; Animals ; Mice ; Cell Differentiation ; Induced Pluripotent Stem Cells/pathology ; Brain Neoplasms/pathology ; Brain/pathology ; Mutation
    Language English
    Publishing date 2024-02-14
    Publishing country England
    Document type Review ; Journal Article
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.050533
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Commentary: Identification of Mutation Regions on

    Anastasaki, Corina / Gao, Feng / Gutmann, David H

    Frontiers in genetics

    2019  Volume 10, Page(s) 115

    Language English
    Publishing date 2019-03-01
    Publishing country Switzerland
    Document type Journal Article ; Comment
    ZDB-ID 2606823-0
    ISSN 1664-8021
    ISSN 1664-8021
    DOI 10.3389/fgene.2019.00115
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Generation of human induced pluripotent stem cell-derived cerebral organoids for cellular and molecular characterization.

    Anastasaki, Corina / Wilson, Anna F / Chen, Alexander S / Wegscheid, Michelle L / Gutmann, David H

    STAR protocols

    2022  Volume 3, Issue 1, Page(s) 101173

    Abstract: Human induced pluripotent stem cell (hiPSC)-derived cerebral organoids (COs) can serve as ... ...

    Abstract Human induced pluripotent stem cell (hiPSC)-derived cerebral organoids (COs) can serve as an
    MeSH term(s) Cell Differentiation/genetics ; Humans ; Induced Pluripotent Stem Cells ; Neurodevelopmental Disorders ; Organoids
    Language English
    Publishing date 2022-02-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2022.101173
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Independent

    Freret, Morgan E / Anastasaki, Corina / Gutmann, David H

    Neurology. Genetics

    2018  Volume 4, Issue 4, Page(s) e261

    Language English
    Publishing date 2018-07-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2818607-2
    ISSN 2376-7839
    ISSN 2376-7839
    DOI 10.1212/NXG.0000000000000261
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  8. Article ; Online: Generation of human induced pluripotent stem cell-derived cerebral organoids for cellular and molecular characterization

    Corina Anastasaki / Anna F. Wilson / Alexander S. Chen / Michelle L. Wegscheid / David H. Gutmann

    STAR Protocols, Vol 3, Iss 1, Pp 101173- (2022)

    2022  

    Abstract: ... of this profile, please refer to Anastasaki et al. (2020) and Wegscheid et al. (2021). ...

    Abstract Summary: Human induced pluripotent stem cell (hiPSC)-derived cerebral organoids (COs) can serve as an in vitro model for studying normal and pathologic human brain development. Here, we optimized existing protocols to streamline the generation of forebrain COs from hiPSCs. We employ these COs to define the impact of disease-causing mutations on cell fate, differentiation, maturation, and morphology relevant to neurodevelopmental disorders. Although limited to forebrain CO identity, this schema requires minimal external interference and is amenable to low-throughput biochemical assays.For complete details on the use and execution of this profile, please refer to Anastasaki et al. (2020) and Wegscheid et al. (2021).
    Keywords Cell Biology ; Cell culture ; Developmental biology ; Health Sciences ; Neuroscience ; Stem Cells ; Science (General) ; Q1-390
    Language English
    Publishing date 2022-03-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: NF1 mutation-driven neuronal hyperexcitability sets a threshold for tumorigenesis and therapeutic targeting of murine optic glioma.

    Anastasaki, Corina / Chatterjee, Jit / Koleske, Joshua P / Gao, Yunqing / Bozeman, Stephanie L / Kernan, Chloe M / Marco Y Marquez, Lara I / Chen, Ji-Kang / Kelly, Caitlin E / Blair, Connor J / Dietzen, Dennis J / Kesterson, Robert A / Gutmann, David H

    Neuro-oncology

    2024  

    Abstract: Background: With the recognition that noncancerous cells function as critical regulators of brain tumor growth, we recently demonstrated that neurons drive low-grade glioma initiation and progression. Using mouse models of neurofibromatosis type 1 (NF1)- ...

    Abstract Background: With the recognition that noncancerous cells function as critical regulators of brain tumor growth, we recently demonstrated that neurons drive low-grade glioma initiation and progression. Using mouse models of neurofibromatosis type 1 (NF1)-associated optic pathway glioma (OPG), we showed that Nf1 mutation induces neuronal hyperexcitability and midkine expression, which activates an immune axis to support tumor growth, such that high-dose lamotrigine treatment reduces Nf1-OPG proliferation. Herein, we execute a series of complementary experiments to address several key knowledge gaps relevant to future clinical translation.
    Methods: We leverage a collection of Nf1-mutant mice that spontaneously develop OPGs to alter both germline and retinal neuron-specific midkine expression. Nf1-mutant mice harboring several different NF1 patient-derived germline mutations were employed to evaluate neuronal excitability and midkine expression. Two distinct Nf1-OPG preclinical mouse models were used to assess lamotrigine effects on tumor progression and growth in vivo.
    Results: We establish that neuronal midkine is both necessary and sufficient for Nf1-OPG growth, demonstrating an obligate relationship between germline Nf1 mutation, neuronal excitability, midkine production, and Nf1-OPG proliferation. We show anti-epileptic drug (lamotrigine) specificity in suppressing neuronal midkine production. Relevant to clinical translation, lamotrigine prevents Nf1-OPG progression and suppresses the growth of existing tumors for months following drug cessation. Importantly, lamotrigine abrogates tumor growth in two Nf1-OPG strains using pediatric epilepsy clinical dosing.
    Conclusions: Together, these findings establish midkine and neuronal hyperexcitability as targetable drivers of Nf1-OPG growth and support the use of lamotrigine as a potential chemoprevention or chemotherapy agent for children with NF1-OPG.
    Language English
    Publishing date 2024-04-12
    Publishing country England
    Document type Journal Article
    ZDB-ID 2028601-6
    ISSN 1523-5866 ; 1522-8517
    ISSN (online) 1523-5866
    ISSN 1522-8517
    DOI 10.1093/neuonc/noae054
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    Zs.A 5307: Show issues Location:
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  10. Article ; Online: A common single nucleotide variant in the cytokine receptor-like factor-3 (CRLF3) gene causes neuronal deficits in human and mouse cells.

    Wilson, Anna F / Barakat, Rasha / Mu, Rui / Karush, Leah L / Gao, Yunqing / Hartigan, Kelly A / Chen, Ji-Kang / Shu, Hongjin / Turner, Tychele N / Maloney, Susan E / Mennerick, Steven J / Gutmann, David H / Anastasaki, Corina

    Human molecular genetics

    2023  Volume 32, Issue 24, Page(s) 3342–3352

    Abstract: Single nucleotide variants in the general population are common genomic alterations, where the majority are presumed to be silent polymorphisms without known clinical significance. Using human induced pluripotent stem cell (hiPSC) cerebral organoid ... ...

    Abstract Single nucleotide variants in the general population are common genomic alterations, where the majority are presumed to be silent polymorphisms without known clinical significance. Using human induced pluripotent stem cell (hiPSC) cerebral organoid modeling of the 1.4 megabase Neurofibromatosis type 1 (NF1) deletion syndrome, we previously discovered that the cytokine receptor-like factor-3 (CRLF3) gene, which is co-deleted with the NF1 gene, functions as a major regulator of neuronal maturation. Moreover, children with NF1 and the CRLF3L389P variant have greater autism burden, suggesting that this gene might be important for neurologic function. To explore the functional consequences of this variant, we generated CRLF3L389P-mutant hiPSC lines and Crlf3L389P-mutant genetically engineered mice. While this variant does not impair protein expression, brain structure, or mouse behavior, CRLF3L389P-mutant human cerebral organoids and mouse brains exhibit impaired neuronal maturation and dendrite formation. In addition, Crlf3L389P-mutant mouse neurons have reduced dendrite lengths and branching, without any axonal deficits. Moreover, Crlf3L389P-mutant mouse hippocampal neurons have decreased firing rates and synaptic current amplitudes relative to wild type controls. Taken together, these findings establish the CRLF3L389P variant as functionally deleterious and suggest that it may be a neurodevelopmental disease modifier.
    MeSH term(s) Child ; Humans ; Animals ; Mice ; Induced Pluripotent Stem Cells/metabolism ; Neurons/metabolism ; Brain/metabolism ; Receptors, Cytokine/metabolism ; Nucleotides/metabolism
    Chemical Substances Receptors, Cytokine ; Nucleotides ; CRLF3 protein, human
    Language English
    Publishing date 2023-09-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 1108742-0
    ISSN 1460-2083 ; 0964-6906
    ISSN (online) 1460-2083
    ISSN 0964-6906
    DOI 10.1093/hmg/ddad155
    Database MEDical Literature Analysis and Retrieval System OnLINE

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