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  1. Article ; Online: Reductionism that leads to manuscript rejection.

    Gronemeyer, Hinrich

    International journal of cancer

    2021  Volume 150, Issue 7, Page(s) 1075–1076

    MeSH term(s) Editorial Policies ; Manuscripts, Medical as Topic ; Medical Writing/standards ; Periodicals as Topic
    Language English
    Publishing date 2021-12-20
    Publishing country United States
    Document type Editorial
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.33899
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 478: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 576: Show issues

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  2. Article ; Online: Promising strategies: Combination of epigenetic inhibitors for cancer therapy.

    Gronemeyer, Hinrich

    International journal of cancer

    2020  Volume 147, Issue 10, Page(s) 2656–2657

    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; DNA Methylation/drug effects ; Epigenesis, Genetic/drug effects ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylase Inhibitors/therapeutic use ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics
    Chemical Substances Antineoplastic Agents ; Histone Deacetylase Inhibitors
    Language English
    Publishing date 2020-06-29
    Publishing country United States
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.33142
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    Zs.MO 576: Show issues

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  3. Article ; Online: Inference from RNA interference: Suggestions to our authors.

    Gronemeyer, Hinrich

    International journal of cancer

    2019  Volume 146, Issue 1, Page(s) 9

    MeSH term(s) Humans ; Publishing ; RNA Interference ; RNA, Small Interfering/genetics
    Chemical Substances RNA, Small Interfering
    Language English
    Publishing date 2019-09-06
    Publishing country United States
    Document type Editorial
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.32641
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  4. Article ; Online: Complexity against current cancer research: Are we on the wrong track?

    Kasikci, Yasenya / Gronemeyer, Hinrich

    International journal of cancer

    2022  Volume 150, Issue 10, Page(s) 1569–1578

    Abstract: Cancer genetics has led to major discoveries, including protooncogene and tumor-suppressor concepts, and cancer genomics generated concepts like driver and passenger genes, revealed tumor heterogeneity and clonal evolution. Reconstructing trajectories of ...

    Abstract Cancer genetics has led to major discoveries, including protooncogene and tumor-suppressor concepts, and cancer genomics generated concepts like driver and passenger genes, revealed tumor heterogeneity and clonal evolution. Reconstructing trajectories of tumorigenesis using spatial and single-cell genomics is possible. Patient stratification and prognostic parameters have been improved. Yet, despite these advances, successful translation into targeted therapies has been scarce and mostly limited to kinase inhibitors. Here, we argue that current cancer research may be on the wrong track, by considering cancer more as a "monogenic" disease, trying to extract common information from thousands of patients, while not properly considering complexity and individual diversity. We suggest to empower a systems cancer approach which reconstructs the information network that has been altered by the tumorigenic events, to analyze hierarchies and predict (druggable) key nodes that could interfere with/block the aberrant information transfer. We also argue that the interindividual variability between patients of similar cohorts is too high to extract common polygenic network information from large numbers of patients and argue in favor of an individualized approach. The analysis we propose would require a structured multinational and multidisciplinary effort, in which clinicians, and cancer, developmental, cell and computational biologists together with mathematicians and informaticians develop dynamic regulatory networks which integrate the entire information transfer in and between cells and organs in (patho)physiological conditions, revealing hierarchies and available drugs to interfere with key regulators. Based on this blueprint, the altered information transfer in individual cancers could be modeled and possible targeted (combo)therapies proposed.
    MeSH term(s) Carcinogenesis ; Genomics ; Humans ; Neoplasms/genetics ; Prognosis
    Language English
    Publishing date 2022-01-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.33912
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  5. Article ; Online: Big Data: The good, the bad and the ugly.

    Gronemeyer, Hinrich / Souren, Nicole Y

    International journal of cancer

    2021  Volume 148, Issue 12, Page(s) 2870–2871

    MeSH term(s) Big Data ; Chromatin Immunoprecipitation Sequencing ; Databases, Genetic/standards ; Deep Learning/ethics ; Humans ; Neural Networks, Computer ; Practice Guidelines as Topic ; Reproducibility of Results
    Language English
    Publishing date 2021-02-02
    Publishing country United States
    Document type Editorial
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.33466
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 478: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
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  6. Book: Affinity labelling and cloning of steroid and thyroid hormone receptors

    Gronemeyer, Hinrich

    (Ellis Horwood series in biomedicine)

    1988  

    Author's details ed. by H. Gronemeyer
    Series title Ellis Horwood series in biomedicine
    Keywords Affinity Labels ; Cloning, Molecular ; Receptors, Thyroid Hormone ; Receptors, Steroid ; Steroidhormonrezeptor ; Chemische Affinität ; Markierung ; Klonierung ; Schilddrüsenhormonrezeptor
    Subject Klonen ; Klonung ; Cloning ; Verklonung ; Klonierung ; Affinität ; Steroidhormon ; Steroidrezeptor ; Steroid-Rezeptoren
    Language English
    Size 322 S. : Ill., graph. Darst.
    Publisher VCH u.a.
    Publishing place Weinheim
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT003223126
    ISBN 0-89573-579-2 ; 3-527-26557-0 ; 978-0-89573-579-9 ; 978-3-527-26557-2
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    1988 A 5545 order for loan Magazin

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  7. Book: The nuclear receptor factsbook

    Laudet, Vincent / Gronemeyer, Hinrich

    (FactsBooks series)

    2002  

    Author's details Vincent Laudet ; Hinrich Gronemeyer
    Series title FactsBooks series
    Keywords Nuklearfaktor ; Methode
    Subject Methodik ; Verfahren ; Technik ; Methoden ; Nuklearer Faktor ; Nuclear factor ; NF ; Nuclearfaktor ; Nuklearer Transkriptionsfaktor
    Size XVII, 462 S. : Ill.
    Publisher Academic Press
    Publishing place London u.a.
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT012999620
    ISBN 0-12-437735-1 ; 978-0-12-437735-6
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2001 A 5718 order for loan Magazin

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  8. Article ; Online: Synergistic activation of RARβ and RARγ nuclear receptors restores cell specialization during stem cell differentiation by hijacking RARα-controlled programs.

    Koshy, Aysis / Mathieux, Elodie / Stüder, François / Bramoulle, Aude / Lieb, Michele / Colombo, Bruno Maria / Gronemeyer, Hinrich / Mendoza-Parra, Marco Antonio

    Life science alliance

    2022  Volume 6, Issue 2

    Abstract: How cells respond to different external cues to develop along defined cell lineages to form complex tissues is a major question in systems biology. Here, we investigated the potential of retinoic acid receptor (RAR)-selective synthetic agonists to ... ...

    Abstract How cells respond to different external cues to develop along defined cell lineages to form complex tissues is a major question in systems biology. Here, we investigated the potential of retinoic acid receptor (RAR)-selective synthetic agonists to activate the gene regulatory programs driving cell specialization during nervous tissue formation from embryonic carcinoma (P19) and mouse embryonic (E14) stem cells. Specifically, we found that the synergistic activation of the RARβ and RARγ by selective ligands (BMS641 or BMS961) induces cell maturation to specialized neuronal subtypes, and to astrocytes and oligodendrocyte precursors. Using RAR isotype knockout lines exposed to RAR-specific agonists, interrogated by global transcriptome landscaping and in silico modeling of transcription regulatory signal propagation, revealed major RARα-driven gene programs essential for optimal neuronal cell specialization and hijacked by the synergistic activation of the RARβ and RARγ receptors. Overall, this study provides a systems biology view of the gene programs accounting for the previously observed redundancy between RARs, paving the way toward their potential use for directing cell specialization during nervous tissue formation.
    MeSH term(s) Animals ; Mice ; Cell Differentiation/genetics ; Cell Lineage/genetics ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Retinoic Acid/genetics ; Stem Cells/physiology ; Retinoic Acid Receptor gamma
    Chemical Substances Receptors, Cytoplasmic and Nuclear ; Receptors, Retinoic Acid ; retinoic acid receptor beta ; Rara protein, mouse
    Language English
    Publishing date 2022-11-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2575-1077
    ISSN (online) 2575-1077
    DOI 10.26508/lsa.202201627
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  9. Article ; Online: Dual role of DR5 in death and survival signaling leads to TRAIL resistance in cancer cells.

    Shlyakhtina, Yelyzaveta / Pavet, Valeria / Gronemeyer, Hinrich

    Cell death & disease

    2017  Volume 8, Issue 8, Page(s) e3025

    Abstract: Besides its tumor-selective apoptotic activity, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) promotes pro-survival, proliferative or migratory signaling (NF-κB, PI3K/Akt, MAPK and JNK; referred to as 'non-apoptotic' cascades). Indeed, ... ...

    Abstract Besides its tumor-selective apoptotic activity, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) promotes pro-survival, proliferative or migratory signaling (NF-κB, PI3K/Akt, MAPK and JNK; referred to as 'non-apoptotic' cascades). Indeed, apoptosis and non-apoptotic signaling can be activated in clonal populations of cancer cells in response to treatment and, as a result, only a part of the initial cellular population dies while a fraction survives and develops resistance to TRAIL-induced apoptosis (referred to as 'fractional survival'). Notably, the molecular characterization of the protein platforms streaming into tumoricidal versus tumor-promoting cascades that control fractional survival remained elusive. Here we demonstrate that, in the context of DR4-DR5-DcR2 hetero-oligomeric complexes, a single death receptor (DR5) suffices to assemble composite plasma membrane-proximal pro-apoptotic/pro-survival platforms that propagate TRAIL signaling to both death and survival pathways in clonal populations of cancer cells. Moreover, we show that while all members of TRAIL-induced complexes support survival, none of them acted exclusively pro-apoptotic. Indeed, key apoptotic proteins as FADD and procaspase-8 were also involved in transducing non-apoptotic signaling in response to this cytokine. Collectively, this study reveals the Janus faces of DR5, and the contributions of other death complex components in fractional survival that foster the generation of resistance. Our data highlight a new level of complexity in TRAIL signaling and point to an improved therapeutic rationale in view of hitherto disappointing results.
    MeSH term(s) Apoptosis/drug effects ; Apoptosis/genetics ; Caspase 8/genetics ; Caspase 8/metabolism ; Cell Line, Transformed ; Cell Survival/drug effects ; Clone Cells ; Drug Resistance, Neoplasm/genetics ; Fas-Associated Death Domain Protein/genetics ; Fas-Associated Death Domain Protein/metabolism ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Gene Expression Regulation, Neoplastic ; Humans ; MAP Kinase Kinase 4/genetics ; MAP Kinase Kinase 4/metabolism ; Mitogen-Activated Protein Kinases/genetics ; Mitogen-Activated Protein Kinases/metabolism ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand/genetics ; Receptors, TNF-Related Apoptosis-Inducing Ligand/metabolism ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; TNF-Related Apoptosis-Inducing Ligand/genetics ; TNF-Related Apoptosis-Inducing Ligand/metabolism ; TNF-Related Apoptosis-Inducing Ligand/pharmacology ; Tumor Necrosis Factor Decoy Receptors/genetics ; Tumor Necrosis Factor Decoy Receptors/metabolism
    Chemical Substances FADD protein, human ; Fas-Associated Death Domain Protein ; NF-kappa B ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Recombinant Proteins ; TNF-Related Apoptosis-Inducing Ligand ; TNFRSF10A protein, human ; TNFRSF10B protein, human ; TNFRSF10D protein, human ; TNFSF10 protein, human ; Tumor Necrosis Factor Decoy Receptors ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; MAP Kinase Kinase 4 (EC 2.7.12.2) ; Caspase 8 (EC 3.4.22.-)
    Language English
    Publishing date 2017-08-31
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/cddis.2017.423
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Development of biotin-retinoid conjugates as chemical probes for analysis of retinoid function.

    Fujii, Shinya / Mori, Shuichi / Kagechika, Hiroyuki / Mendoza Parra, Marco Antonio / Gronemeyer, Hinrich

    Bioorganic & medicinal chemistry letters

    2018  Volume 28, Issue 14, Page(s) 2442–2445

    Abstract: Herein, we report the rational design, synthesis and biological evaluation of conjugates consisting of the synthetic retinoid Am580 and biotin connected via a linker moiety. We found that the linking substructure between the retinoid part and the biotin ... ...

    Abstract Herein, we report the rational design, synthesis and biological evaluation of conjugates consisting of the synthetic retinoid Am580 and biotin connected via a linker moiety. We found that the linking substructure between the retinoid part and the biotin part is critical for retaining the biological activity. Conjugate 4 with a shorter linker showed similar potency to endogenous retinoid ATRA (1) and the parent compound Am580 (2) for neural differentiation of mouse embryotic carcinoma P19 cells, and showed the same pattern of induction of gene expression. It is expected to be useful as a probe for investigations of retinoid function. The design rationale and structure-activity relationship of the linker moiety are expected to be helpful for developing biotin conjugates of other nuclear receptor ligands.
    MeSH term(s) Animals ; Biotin/chemistry ; Cell Differentiation/drug effects ; Cell Line, Tumor ; Ligands ; Mice ; Models, Molecular ; Molecular Probes/chemical synthesis ; Molecular Probes/chemistry ; Molecular Structure ; Neurons/drug effects ; Neurons/pathology ; RNA, Messenger/genetics ; Retinoids/analysis ; Retinoids/metabolism ; Structure-Activity Relationship
    Chemical Substances Ligands ; Molecular Probes ; RNA, Messenger ; Retinoids ; Biotin (6SO6U10H04)
    Language English
    Publishing date 2018-06-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1063195-1
    ISSN 1464-3405 ; 0960-894X
    ISSN (online) 1464-3405
    ISSN 0960-894X
    DOI 10.1016/j.bmcl.2018.06.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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