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  1. Article ; Online: Correction to: Wig-1 regulates cell cycle arrest and cell death through the p53 targets FAS and 14-3-3s.

    Bersani, C / Xu, L -D / Vilborg, A / Lui, W -O / Wiman, K G

    Oncogene

    2023  Volume 42, Issue 9, Page(s) 709

    Language English
    Publishing date 2023-01-25
    Publishing country England
    Document type Published Erratum
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-023-02601-0
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  2. Article ; Online: p53 talks to PARP: the increasing complexity of p53-induced cell death.

    Wiman, K G

    Cell death and differentiation

    2013  Volume 20, Issue 11, Page(s) 1438–1439

    MeSH term(s) Apoptosis/physiology ; Humans ; Reactive Oxygen Species/metabolism ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Reactive Oxygen Species ; TP53 protein, human ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2013-10-07
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/cdd.2013.111
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  3. Article ; Online: Introduction to Nobel Conference: 'The Cell Cycle and Cell Death in Disease'.

    Wiman, K G / Zhivotovsky, B

    Journal of internal medicine

    2017  Volume 281, Issue 5, Page(s) 418–421

    MeSH term(s) Cell Cycle/physiology ; Cell Cycle Proteins/physiology ; Cell Death/physiology ; Congresses as Topic ; Disease ; Drug Discovery ; Humans ; Nobel Prize ; Signal Transduction
    Chemical Substances Cell Cycle Proteins
    Language English
    Publishing date 2017-05-12
    Publishing country England
    Document type Introductory Journal Article
    ZDB-ID 96274-0
    ISSN 1365-2796 ; 0954-6820
    ISSN (online) 1365-2796
    ISSN 0954-6820
    DOI 10.1111/joim.12618
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  4. Article ; Online: Understanding cell cycle and cell death regulation provides novel weapons against human diseases.

    Wiman, K G / Zhivotovsky, B

    Journal of internal medicine

    2017  Volume 281, Issue 5, Page(s) 483–495

    Abstract: Cell division, cell differentiation and cell death are the three principal physiological processes that regulate tissue homoeostasis in multicellular organisms. The growth and survival of cells as well as the integrity of the genome are regulated by a ... ...

    Abstract Cell division, cell differentiation and cell death are the three principal physiological processes that regulate tissue homoeostasis in multicellular organisms. The growth and survival of cells as well as the integrity of the genome are regulated by a complex network of pathways, in which cell cycle checkpoints, DNA repair and programmed cell death have critical roles. Disruption of genomic integrity and impaired regulation of cell death may both lead to uncontrolled cell growth. Compromised cell death can also favour genomic instability. It is becoming increasingly clear that dysregulation of cell cycle and cell death processes plays an important role in the development of major disorders such as cancer, cardiovascular disease, infection, inflammation and neurodegenerative diseases. Research achievements in these fields have led to the development of novel approaches for treatment of various conditions associated with abnormalities in the regulation of cell cycle progression or cell death. A better understanding of how cellular life-and-death processes are regulated is essential for this development. To highlight these important advances, the Third Nobel Conference entitled 'The Cell Cycle and Cell Death in Disease' was organized at Karolinska Institutet in 2016. In this review we will summarize current understanding of cell cycle progression and cell death and discuss some of the recent advances in therapeutic applications in pathological conditions such as cancer, neurological disorders and inflammation.
    MeSH term(s) Caspases/metabolism ; Cell Cycle/physiology ; Cell Death/physiology ; Genome, Human/physiology ; Humans ; Inflammasomes/physiology ; Inflammation/drug therapy ; Neoplasms/drug therapy ; Neoplasms/pathology ; Nervous System Diseases/drug therapy ; Nervous System Diseases/metabolism
    Chemical Substances Inflammasomes ; Caspases (EC 3.4.22.-)
    Language English
    Publishing date 2017-05
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 96274-0
    ISSN 1365-2796 ; 0954-6820
    ISSN (online) 1365-2796
    ISSN 0954-6820
    DOI 10.1111/joim.12609
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Pharmacological reactivation of mutant p53: from protein structure to the cancer patient.

    Wiman, K G

    Oncogene

    2010  Volume 29, Issue 30, Page(s) 4245–4252

    Abstract: The p53 tumor suppressor pathway blocks tumor development by triggering apoptosis or cellular senescence in response to oncogenic stress. A large fraction of human tumors carry p53 mutations that disrupt DNA binding of p53 and transcriptional regulation ... ...

    Abstract The p53 tumor suppressor pathway blocks tumor development by triggering apoptosis or cellular senescence in response to oncogenic stress. A large fraction of human tumors carry p53 mutations that disrupt DNA binding of p53 and transcriptional regulation of target genes. Reconstitution of wild-type p53 in vivo triggers rapid elimination of tumors. Therefore, pharmacological reactivation of mutant p53 is a promising strategy for novel cancer therapy. Several approaches for identification of small molecules that target mutant p53 have been applied, including rational design and screening of chemical libraries. The compound PhiKan083 binds with high affinity to a crevice created by the Y220C mutation in p53 and stabilizes the mutant protein. The compound PRIMA-1 (p53 reactivation and induction of massive apoptosis) restores wild-type conformation to mutant p53 by binding to the core and induces apoptosis in human tumor cells. The PRIMA-1 analog APR-246 is currently tested in a clinical trial. Successful development of mutant p53-reactivating anticancer drugs should have a major impact on the treatment of cancer.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Aza Compounds/pharmacology ; Bridged Bicyclo Compounds, Heterocyclic/pharmacology ; Drug Design ; Drug Screening Assays, Antitumor ; Genes, p53 ; Humans ; Mutation ; Neoplasms/drug therapy ; Neoplasms/genetics ; Tumor Suppressor Protein p53/chemistry
    Chemical Substances Antineoplastic Agents ; Aza Compounds ; Bridged Bicyclo Compounds, Heterocyclic ; Tumor Suppressor Protein p53 ; 2,2-bis(hydroxymethyl)-1-azabicyclo(2,2,2,)octan-3-one (GHC34M30BG)
    Language English
    Publishing date 2010-05-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/onc.2010.188
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  6. Article ; Online: TP53: an oncogene in disguise.

    Soussi, T / Wiman, K G

    Cell death and differentiation

    2015  Volume 22, Issue 8, Page(s) 1239–1249

    Abstract: The standard classification used to define the various cancer genes confines tumor protein p53 (TP53) to the role of a tumor suppressor gene. However, it is now an indisputable fact that many p53 mutants act as oncogenic proteins. This statement is based ...

    Abstract The standard classification used to define the various cancer genes confines tumor protein p53 (TP53) to the role of a tumor suppressor gene. However, it is now an indisputable fact that many p53 mutants act as oncogenic proteins. This statement is based on multiple arguments including the mutation signature of the TP53 gene in human cancer, the various gains-of-function (GOFs) of the different p53 mutants and the heterogeneous phenotypes developed by knock-in mouse strains modeling several human TP53 mutations. In this review, we will shatter the classical and traditional image of tumor protein p53 (TP53) as a tumor suppressor gene by emphasizing its multiple oncogenic properties that make it a potential therapeutic target that should not be underestimated. Analysis of the data generated by the various cancer genome projects highlights the high frequency of TP53 mutations and reveals that several p53 hotspot mutants are the most common oncoprotein variants expressed in several types of tumors. The use of Muller's classical definition of mutations based on quantitative and qualitative consequences on the protein product, such as 'amorph', 'hypomorph', 'hypermorph' 'neomorph' or 'antimorph', allows a more meaningful assessment of the consequences of cancer gene modifications, their potential clinical significance, and clearly demonstrates that the TP53 gene is an atypical cancer gene.
    MeSH term(s) Animals ; Aza Compounds/metabolism ; Bridged Bicyclo Compounds, Heterocyclic/metabolism ; Humans ; Maleimides/metabolism ; Mutation/genetics ; Phenotype ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances 1-(propoxymethyl)maleimide ; Aza Compounds ; Bridged Bicyclo Compounds, Heterocyclic ; Maleimides ; Tumor Suppressor Protein p53 ; 2,2-bis(hydroxymethyl)-1-azabicyclo(2,2,2,)octan-3-one (GHC34M30BG)
    Language English
    Publishing date 2015-05-29
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/cdd.2015.53
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  7. Article: Strategies for therapeutic targeting of the p53 pathway in cancer.

    Wiman, K G

    Cell death and differentiation

    2006  Volume 13, Issue 6, Page(s) 921–926

    MeSH term(s) Adenoviridae/genetics ; Animals ; Antibodies, Monoclonal/therapeutic use ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Apoptosis/drug effects ; Aza Compounds/pharmacology ; Bridged Bicyclo Compounds, Heterocyclic/pharmacology ; Clinical Trials as Topic ; Genetic Therapy/trends ; Head and Neck Neoplasms/genetics ; Head and Neck Neoplasms/metabolism ; Head and Neck Neoplasms/therapy ; Humans ; Imidazoles/pharmacology ; Mutation ; Piperazines/pharmacology ; Proto-Oncogene Proteins c-mdm2/antagonists & inhibitors ; Proto-Oncogene Proteins c-mdm2/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/immunology ; Tumor Suppressor Protein p53/metabolism ; Viral Vaccines
    Chemical Substances Antibodies, Monoclonal ; Antineoplastic Agents ; Aza Compounds ; Bridged Bicyclo Compounds, Heterocyclic ; Imidazoles ; Piperazines ; Tumor Suppressor Protein p53 ; Viral Vaccines ; dl1520 ; nutlin 1 ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27) ; 2,2-bis(hydroxymethyl)-1-azabicyclo(2,2,2,)octan-3-one (GHC34M30BG)
    Language English
    Publishing date 2006-03-11
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1225672-9
    ISSN 1350-9047
    ISSN 1350-9047
    DOI 10.1038/sj.cdd.4401921
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  8. Article ; Online: PRIMA-1

    Shen, J / Vakifahmetoglu, H / Stridh, H / Zhivotovsky, B / Wiman, K G

    Oncogene

    2017  Volume 36, Issue 25, Page(s) 3650

    Abstract: This corrects the article DOI: 10.1038/onc.2016.210. ...

    Abstract This corrects the article DOI: 10.1038/onc.2016.210.
    Language English
    Publishing date 2017-06-22
    Publishing country England
    Document type Published Erratum
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/onc.2017.9
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  9. Article ; Online: PRIMA-1Met induces mitochondrial apoptosis through activation of caspase-2.

    Shen, J / Vakifahmetoglu, H / Stridh, H / Zhivotovsky, B / Wiman, K G

    Oncogene

    2016  Volume 35, Issue 50, Page(s) 6446

    Language English
    Publishing date 2016-12-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/onc.2016.210
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  10. Article: Reactivation of mutant p53: molecular mechanisms and therapeutic potential.

    Selivanova, G / Wiman, K G

    Oncogene

    2007  Volume 26, Issue 15, Page(s) 2243–2254

    Abstract: The p53 tumor suppressor gene is the most frequently mutated gene in cancer. Most p53 mutations are missense point mutations that cluster in the DNA-binding core domain. This results in distortion of core domain folding and disruption of DNA binding and ... ...

    Abstract The p53 tumor suppressor gene is the most frequently mutated gene in cancer. Most p53 mutations are missense point mutations that cluster in the DNA-binding core domain. This results in distortion of core domain folding and disruption of DNA binding and transcriptional transactivation of p53 target genes. Structural studies have demonstrated that mutant p53 core domain unfolding is not irreversible. Mutant p53 is expressed at high levels in many tumors. Therefore, mutant p53 is a promising target for novel cancer therapy. Mutant p53 reactivation will restore p53-dependent apoptosis, resulting in efficient removal of tumor cells. A number of strategies for targeting mutant p53 have been designed, including peptides and small molecules that restore the active conformation and DNA binding to mutant p53 and induce p53-dependent suppression of tumor cell growth in vitro and in vivo. This opens possibilities for the clinical application of mutant p53 reactivation in the treatment of cancer.
    MeSH term(s) Humans ; Mutation ; Neoplasms/drug therapy ; Neoplasms/genetics ; Protein Conformation/drug effects ; Tumor Suppressor Protein p53/agonists ; Tumor Suppressor Protein p53/chemistry ; Tumor Suppressor Protein p53/genetics
    Chemical Substances Tumor Suppressor Protein p53
    Language English
    Publishing date 2007-04-02
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/sj.onc.1210295
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