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  1. Article: WNT-mediated gene gating: a novel principle connecting oncogenic super-enhancers with the nuclear pore to drive pathological expression of MYC.

    Göndör, Anita

    Molecular & cellular oncology

    2020  Volume 7, Issue 2, Page(s) 1710992

    Abstract: WNT signaling ... ...

    Abstract WNT signaling enhances
    Language English
    Publishing date 2020-01-27
    Publishing country United States
    Document type Journal Article
    ISSN 2372-3556
    ISSN 2372-3556
    DOI 10.1080/23723556.2019.1710992
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  2. Article ; Online: Nuclear architecture and chromatin structure on the path to cancer.

    Göndör, Anita

    Seminars in cancer biology

    2013  Volume 23, Issue 2, Page(s) 63–64

    MeSH term(s) Animals ; Cell Cycle/genetics ; Cell Cycle/physiology ; Cell Nucleus/genetics ; Cell Nucleus/pathology ; Cell Nucleus/physiology ; Cell Nucleus/ultrastructure ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Chromatin/chemistry ; Chromatin/ultrastructure ; Chromatin Assembly and Disassembly/genetics ; Chromatin Assembly and Disassembly/physiology ; DNA Replication/genetics ; DNA Replication/physiology ; Humans ; Neoplasms/genetics ; Neoplasms/pathology ; Nucleic Acid Conformation ; Telomere/genetics ; Telomere/metabolism ; Telomere/physiology
    Chemical Substances Chromatin
    Language English
    Publishing date 2013-04
    Publishing country England
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 1033980-2
    ISSN 1096-3650 ; 1044-579X
    ISSN (online) 1096-3650
    ISSN 1044-579X
    DOI 10.1016/j.semcancer.2013.02.006
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  3. Article ; Online: Dynamic chromatin loops bridge health and disease in the nuclear landscape.

    Göndör, Anita

    Seminars in cancer biology

    2013  Volume 23, Issue 2, Page(s) 90–98

    Abstract: The genome is dynamically organized in the nuclear space in a manner that reflects and influences nuclear functions. Developmental processes that govern the formation and maintenance of epigenetic memories are also tightly linked to adaptive changes in ... ...

    Abstract The genome is dynamically organized in the nuclear space in a manner that reflects and influences nuclear functions. Developmental processes that govern the formation and maintenance of epigenetic memories are also tightly linked to adaptive changes in the physical and functional landscape of the nuclear architecture. Biological and biophysical principles governing the three-dimensional folding of chromatin are therefore central to our understanding of epigenetic regulation during adaptive responses and in complex diseases, such as cancer. Accumulating evidence points to the direction that global alterations in nuclear architecture and chromatin folding conspire with unstable epigenetic states of the primary chromatin fiber to drive the phenotypic plasticity of cancer cells.
    MeSH term(s) Animals ; Cell Nucleus/genetics ; Cell Nucleus/metabolism ; Cell Nucleus/pathology ; Cell Nucleus/physiology ; Chromatin/chemistry ; Chromatin/metabolism ; Chromatin/physiology ; Chromatin Assembly and Disassembly/genetics ; Chromatin Assembly and Disassembly/physiology ; Genomic Instability/genetics ; Humans ; Models, Biological ; Neoplasms/genetics ; Nucleic Acid Conformation
    Chemical Substances Chromatin
    Language English
    Publishing date 2013-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1033980-2
    ISSN 1096-3650 ; 1044-579X
    ISSN (online) 1096-3650
    ISSN 1044-579X
    DOI 10.1016/j.semcancer.2013.01.002
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  4. Article: Enhancer functions in three dimensions: beyond the flat world perspective.

    Göndör, Anita / Ohlsson, Rolf

    F1000Research

    2018  Volume 7

    Abstract: Transcriptional enhancers constitute a subclass of regulatory elements that facilitate transcription. Such regions are generally organized by short stretches of DNA enriched in transcription factor-binding sites but also can include very large regions ... ...

    Abstract Transcriptional enhancers constitute a subclass of regulatory elements that facilitate transcription. Such regions are generally organized by short stretches of DNA enriched in transcription factor-binding sites but also can include very large regions containing clusters of enhancers, termed super-enhancers. These regions increase the probability or the rate (or both) of transcription generally in
    Language English
    Publishing date 2018
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2699932-8
    ISSN 2046-1402
    ISSN 2046-1402
    DOI 10.12688/f1000research.13842.1
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  5. Article ; Online: The Nodewalk assay to quantitate chromatin fiber interactomes in very small cell populations.

    Vestlund, Johanna / Sumida, Noriyuki / Mehmood, Rashid / Bhartiya, Deeksha / Wu, Shuangyang / Göndör, Anita

    Nature protocols

    2022  Volume 18, Issue 3, Page(s) 755–782

    Abstract: The chromosome conformation capture method and its derivatives, such as circularized chromosome conformation capture, carbon copy chromosome conformation capture, high-throughput chromosome conformation capture and capture high-throughput chromosome ... ...

    Abstract The chromosome conformation capture method and its derivatives, such as circularized chromosome conformation capture, carbon copy chromosome conformation capture, high-throughput chromosome conformation capture and capture high-throughput chromosome conformation capture, have pioneered our understanding of the principles of chromosome folding in the nucleus. These technical advances, however, cannot precisely quantitate interaction frequency in very small input samples. Here we describe a protocol for the Nodewalk assay, which is based on converting chromosome conformation capture DNA samples to RNA and subsequently to cDNA using strategically placed primers. This pipeline enables the quantitative analyses of chromatin fiber interactions without compromising its sensitivity down to <300 cells, making it suitable for MiSeq analyses of higher-order chromatin structures in biopsies, circulating tumor cells and transitional cell states, for example. Importantly, the quality of the Nodewalk sample can be assessed before sequencing to avoid unnecessary costs. Moreover, it enables analyses from hundreds of different restriction enzyme fragment viewpoints within the same initial small input sample to uncover complex, genome-wide networks. Following optimization of the different steps, the entire protocol can be completed within 2 weeks.
    MeSH term(s) Nucleic Acid Conformation ; Chromatin/genetics ; Chromosomes ; Genome ; DNA ; High-Throughput Nucleotide Sequencing/methods
    Chemical Substances Chromatin ; DNA (9007-49-2)
    Language English
    Publishing date 2022-11-25
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2244966-8
    ISSN 1750-2799 ; 1754-2189
    ISSN (online) 1750-2799
    ISSN 1754-2189
    DOI 10.1038/s41596-022-00774-8
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  6. Article ; Online: Circadian organization of the genome.

    Mallet de Lima, Carolina Diettrich / Göndör, Anita

    Science (New York, N.Y.)

    2018  Volume 359, Issue 6381, Page(s) 1212–1213

    MeSH term(s) Circadian Rhythm ; Genome ; Humans
    Language English
    Publishing date 2018--16
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.aat0934
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  7. Article ; Online: Enhancer functions in three dimensions

    Anita Göndör / Rolf Ohlsson

    F1000Research, Vol

    beyond the flat world perspective [version 1; referees: 3 approved]

    2018  Volume 7

    Abstract: Transcriptional enhancers constitute a subclass of regulatory elements that facilitate transcription. Such regions are generally organized by short stretches of DNA enriched in transcription factor-binding sites but also can include very large regions ... ...

    Abstract Transcriptional enhancers constitute a subclass of regulatory elements that facilitate transcription. Such regions are generally organized by short stretches of DNA enriched in transcription factor-binding sites but also can include very large regions containing clusters of enhancers, termed super-enhancers. These regions increase the probability or the rate (or both) of transcription generally in cis and sometimes over very long distances by altering chromatin states and the activity of Pol II machinery at promoters. Although enhancers were discovered almost four decades ago, their inner workings remain enigmatic. One important opening into the underlying principle has been provided by observations that enhancers make physical contacts with their target promoters to facilitate the loading of the RNA polymerase complex. However, very little is known about how such chromatin loops are regulated and how they govern transcription in the three-dimensional context of the nuclear architecture. Here, we present current themes of how enhancers may boost gene expression in three dimensions and we identify currently unresolved key questions.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2018-05-01T00:00:00Z
    Publisher F1000 Research Ltd
    Document type Article ; Online
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  8. Article ; Online: A phenotypic screening approach to target p60AmotL2-expressing invasive cancer cells.

    Fonseca, Pedro / Cui, Weiyingqi / Struyf, Nona / Tong, Le / Chaurasiya, Ayushi / Casagrande, Felipe / Zhao, Honglei / Fernando, Dinura / Chen, Xinsong / Tobin, Nicholas P / Seashore-Ludlow, Brinton / Lundqvist, Andreas / Hartman, Johan / Göndör, Anita / Östling, Päivi / Holmgren, Lars

    Journal of experimental & clinical cancer research : CR

    2024  Volume 43, Issue 1, Page(s) 107

    Abstract: Background: Tumor cells have the ability to invade and form small clusters that protrude into adjacent tissues, a phenomenon that is frequently observed at the periphery of a tumor as it expands into healthy tissues. The presence of these clusters is ... ...

    Abstract Background: Tumor cells have the ability to invade and form small clusters that protrude into adjacent tissues, a phenomenon that is frequently observed at the periphery of a tumor as it expands into healthy tissues. The presence of these clusters is linked to poor prognosis and has proven challenging to treat using conventional therapies. We previously reported that p60AmotL2 expression is localized to invasive colon and breast cancer cells. In vitro, p60AmotL2 promotes epithelial cell invasion by negatively impacting E-cadherin/AmotL2-related mechanotransduction.
    Methods: Using epithelial cells transfected with inducible p60AmotL2, we employed a phenotypic drug screening approach to find compounds that specifically target invasive cells. The phenotypic screen was performed by treating cells for 72 h with a library of compounds with known antitumor activities in a dose-dependent manner. After assessing cell viability using CellTiter-Glo, drug sensitivity scores for each compound were calculated. Candidate hit compounds with a higher drug sensitivity score for p60AmotL2-expressing cells were then validated on lung and colon cell models, both in 2D and in 3D, and on colon cancer patient-derived organoids. Nascent RNA sequencing was performed after BET inhibition to analyse BET-dependent pathways in p60AmotL2-expressing cells.
    Results: We identified 60 compounds that selectively targeted p60AmotL2-expressing cells. Intriguingly, these compounds were classified into two major categories: Epidermal Growth Factor Receptor (EGFR) inhibitors and Bromodomain and Extra-Terminal motif (BET) inhibitors. The latter consistently demonstrated antitumor activity in human cancer cell models, as well as in organoids derived from colon cancer patients. BET inhibition led to a shift towards the upregulation of pro-apoptotic pathways specifically in p60AmotL2-expressing cells.
    Conclusions: BET inhibitors specifically target p60AmotL2-expressing invasive cancer cells, likely by exploiting differences in chromatin accessibility, leading to cell death. Additionally, our findings support the use of this phenotypic strategy to discover novel compounds that can exploit vulnerabilities and specifically target invasive cancer cells.
    MeSH term(s) Humans ; Cell Line, Tumor ; Mechanotransduction, Cellular ; Early Detection of Cancer ; Colonic Neoplasms/drug therapy ; Colonic Neoplasms/genetics
    Language English
    Publishing date 2024-04-09
    Publishing country England
    Document type Journal Article
    ZDB-ID 803138-1
    ISSN 1756-9966 ; 0392-9078
    ISSN (online) 1756-9966
    ISSN 0392-9078
    DOI 10.1186/s13046-024-03031-w
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    Zs.A 2065: Show issues Location:
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  9. Article ; Online: Epigenetic modulators, modifiers and mediators in cancer aetiology and progression.

    Feinberg, Andrew P / Koldobskiy, Michael A / Göndör, Anita

    Nature reviews. Genetics

    2016  Volume 17, Issue 5, Page(s) 284–299

    Abstract: 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 ...

    Abstract 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.
    MeSH term(s) Animals ; DNA Methylation ; Disease Progression ; Epigenesis, Genetic ; Humans ; Mutation/genetics ; Neoplasms/etiology ; Neoplasms/pathology ; Stem Cells/pathology
    Language English
    Publishing date 2016-05
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2035157-4
    ISSN 1471-0064 ; 1471-0056
    ISSN (online) 1471-0064
    ISSN 1471-0056
    DOI 10.1038/nrg.2016.13
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  10. Article ; Online: Canonical WNT signaling-dependent gating of MYC requires a noncanonical CTCF function at a distal binding site.

    Chachoua, Ilyas / Tzelepis, Ilias / Dai, Hao / Lim, Jia Pei / Lewandowska-Ronnegren, Anna / Casagrande, Felipe Beccaria / Wu, Shuangyang / Vestlund, Johanna / Mallet de Lima, Carolina Diettrich / Bhartiya, Deeksha / Scholz, Barbara A / Martino, Mirco / Mehmood, Rashid / Göndör, Anita

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 204

    Abstract: Abnormal WNT signaling increases MYC expression in colon cancer cells in part via oncogenic super-enhancer-(OSE)-mediated gating of the active MYC to the nuclear pore in a poorly understood process. We show here that the principal tenet of the WNT- ... ...

    Abstract Abnormal WNT signaling increases MYC expression in colon cancer cells in part via oncogenic super-enhancer-(OSE)-mediated gating of the active MYC to the nuclear pore in a poorly understood process. We show here that the principal tenet of the WNT-regulated MYC gating, facilitating nuclear export of the MYC mRNA, is regulated by a CTCF binding site (CTCFBS) within the OSE to confer growth advantage in HCT-116 cells. To achieve this, the CTCFBS directs the WNT-dependent trafficking of the OSE to the nuclear pore from intra-nucleoplasmic positions in a stepwise manner. Once the OSE reaches a peripheral position, which is triggered by a CTCFBS-mediated CCAT1 eRNA activation, its final stretch (≤0.7 μm) to the nuclear pore requires the recruitment of AHCTF1, a key nucleoporin, to the CTCFBS. Thus, a WNT/ß-catenin-AHCTF1-CTCF-eRNA circuit enables the OSE to promote pathological cell growth by coordinating the trafficking of the active MYC gene within the 3D nuclear architecture.
    MeSH term(s) Active Transport, Cell Nucleus ; Binding Sites ; CCCTC-Binding Factor/genetics ; CCCTC-Binding Factor/metabolism ; Cell Nucleus/metabolism ; Colon/metabolism ; Colon/pathology ; Cytosol/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Enhancer Elements, Genetic ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Gene Expression Regulation, Neoplastic ; Genome, Human ; HCT116 Cells ; Humans ; Protein Binding ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Whole Genome Sequencing ; Wnt Signaling Pathway/genetics
    Chemical Substances AHCTF1 protein, human ; CCAT1 long noncoding RNA, human ; CCCTC-Binding Factor ; CTCF protein, human ; DNA-Binding Proteins ; MYC protein, human ; Proto-Oncogene Proteins c-myc ; RNA, Long Noncoding ; RNA, Messenger ; Transcription Factors
    Language English
    Publishing date 2022-01-11
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-021-27868-3
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