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  1. Article ; Online: Mutant p53 Gain-of-Function in the Spotlight: Are We Suffering a GOF Delusion?

    Lane, David P

    Cancer discovery

    2024  Volume 14, Issue 2, Page(s) 211–213

    Abstract: Mutant p53 proteins are often highly expressed in human cancers and have been thought to have oncogenic driver gain-of-function (GOF) properties. Wang and colleagues show, surprisingly, that this is not the case because removing the TP53-mutant gene from ...

    Abstract Mutant p53 proteins are often highly expressed in human cancers and have been thought to have oncogenic driver gain-of-function (GOF) properties. Wang and colleagues show, surprisingly, that this is not the case because removing the TP53-mutant gene from human and mouse cancer cells using CRISPR technology has no effect on cancer cell growth in vitro or in vivo. See related article by Wang et al., p. 362 (10) .
    MeSH term(s) Humans ; Mice ; Animals ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Gain of Function Mutation ; Delusions ; Cell Line, Tumor ; Genes, p53 ; Mutation
    Chemical Substances Tumor Suppressor Protein p53
    Language English
    Publishing date 2024-02-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2159-8290.CD-23-1362
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6916: Show issues Location:
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  2. Article ; Online: Covalent Rescue of Mutant p53.

    Lane, David P / Verma, Chandra S

    Cancer discovery

    2022  Volume 13, Issue 1, Page(s) 14–16

    Abstract: Summary: p53 mutant proteins are widely expressed in human cancer. In this issue, Guiley and Shokat describe the development of compounds that rescue the function of the Y220C mutant p53 protein by forming covalent complexes with the target protein. See ...

    Abstract Summary: p53 mutant proteins are widely expressed in human cancer. In this issue, Guiley and Shokat describe the development of compounds that rescue the function of the Y220C mutant p53 protein by forming covalent complexes with the target protein. See related article by Guiley and Shokat, p. 56 (3).
    MeSH term(s) Humans ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Neoplasms/drug therapy ; Neoplasms/genetics
    Chemical Substances Tumor Suppressor Protein p53
    Language English
    Publishing date 2022-12-23
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2159-8290.CD-22-1212
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6916: Show issues Location:
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  3. Article: An Automated Quantification Tool for Angiogenic Sprouting From Endothelial Spheroids.

    Kannan, Pavitra / Schain, Martin / Lane, David P

    Frontiers in pharmacology

    2022  Volume 13, Page(s) 883083

    Abstract: The process of sprouting angiogenesis can be ... ...

    Abstract The process of sprouting angiogenesis can be measured
    Language English
    Publishing date 2022-04-27
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2022.883083
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: p53 stabilisation potentiates [

    Berglund, Hanna / Salomonsson, Sara Lundsten / Mohajershojai, Tabassom / Gago, Fernando Jose Ferrer / Lane, David P / Nestor, Marika

    European journal of nuclear medicine and molecular imaging

    2023  Volume 51, Issue 3, Page(s) 768–778

    Abstract: Purpose: Molecular radiotherapy is a treatment modality that is highly suitable for targeting micrometastases and [: Methods: This study investigated the use of the p53 stabilising peptide VIP116 and [: Results: The results demonstrated that ... ...

    Abstract Purpose: Molecular radiotherapy is a treatment modality that is highly suitable for targeting micrometastases and [
    Methods: This study investigated the use of the p53 stabilising peptide VIP116 and [
    Results: The results demonstrated that monotherapy with either VIP116 or [
    Conclusion: In conclusion, the combination of VIP116 and [
    MeSH term(s) Humans ; Mice ; Animals ; Tumor Suppressor Protein p53 ; Octreotide/therapeutic use ; Organometallic Compounds/therapeutic use ; Heterografts ; Neuroblastoma/radiotherapy ; Neuroendocrine Tumors/radiotherapy ; Radionuclide Imaging ; Positron-Emission Tomography
    Chemical Substances copper dotatate CU-64 ; Tumor Suppressor Protein p53 ; Octreotide (RWM8CCW8GP) ; Organometallic Compounds
    Language English
    Publishing date 2023-10-12
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 8236-3
    ISSN 1619-7089 ; 0340-6997 ; 1619-7070
    ISSN (online) 1619-7089
    ISSN 0340-6997 ; 1619-7070
    DOI 10.1007/s00259-023-06462-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1227: Show issues Location:
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  5. Article ; Online: Guardian of Genome Editing.

    Ho, Teresa / Lane, David P

    The CRISPR journal

    2019  Volume 1, Page(s) 258–260

    Language English
    Publishing date 2019-05-11
    Publishing country United States
    Document type Journal Article
    ISSN 2573-1602
    ISSN (online) 2573-1602
    DOI 10.1089/crispr.2018.29021.dal
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Understanding p53 functions through p53 antibodies.

    Sabapathy, Kanaga / Lane, David P

    Journal of molecular cell biology

    2019  Volume 11, Issue 4, Page(s) 317–329

    Abstract: TP53 is the most frequently mutated gene across all cancer types. Our understanding of its functions has evolved since its discovery four decades ago. Initially thought to be an oncogene, it was later realized to be a critical tumour suppressor. A ... ...

    Abstract TP53 is the most frequently mutated gene across all cancer types. Our understanding of its functions has evolved since its discovery four decades ago. Initially thought to be an oncogene, it was later realized to be a critical tumour suppressor. A significant amount of our knowledge about p53 functions have come from the use of antibodies against its various forms. The early anti-p53 antibodies contributed to the recognition of p53 accumulation as a common feature of cancer cells and to our understanding of p53 DNA-binding and transcription activities. They led to the concept that conformational changes can facilitate p53's activity as a growth inhibitory protein. The ensuing p53 conformational-specific antibodies further underlined p53's conformational flexibility, collectively forming the basis for current efforts to generate therapeutic molecules capable of altering the conformation of mutant p53. A subsequent barrage of antibodies against post-translational modifications on p53 has clarified p53's roles further, especially with respect to the mechanistic details and context-dependence of its activity. More recently, the generation of p53 mutation-specific antibodies have highlighted the possibility to go beyond the general framework of our comprehension of mutant p53-and promises to provide insights into the specific properties of individual p53 mutants. This review summarizes our current knowledge of p53 functions derived through the major classes of anti-p53 antibodies, which could be a paradigm for understanding other molecular events in health and disease.
    MeSH term(s) Antibodies, Monoclonal/immunology ; Epitopes/immunology ; Humans ; Mutation ; Neoplasms/metabolism ; Neoplasms/pathology ; Protein Processing, Post-Translational ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/immunology ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Antibodies, Monoclonal ; Epitopes ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2019-03-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2500949-7
    ISSN 1759-4685 ; 1674-2788
    ISSN (online) 1759-4685
    ISSN 1674-2788
    DOI 10.1093/jmcb/mjz010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Corrigendum to 'Understanding p53 functions through p53 antibodies'.

    Sabapathy, Kanaga / Lane, David P

    Journal of molecular cell biology

    2019  Volume 11, Issue 12, Page(s) 1105

    Language English
    Publishing date 2019-12-24
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ZDB-ID 2500949-7
    ISSN 1759-4685 ; 1674-2788
    ISSN (online) 1759-4685
    ISSN 1674-2788
    DOI 10.1093/jmcb/mjz110
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: p53: updates on mechanisms, biology and therapy (II).

    Lane, David P / Verma, Chandra S

    Journal of molecular cell biology

    2019  Volume 11, Issue 4, Page(s) 265–266

    MeSH term(s) Animals ; Gain of Function Mutation ; Humans ; Models, Animal ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Tumor Suppressor Protein p53
    Language English
    Publishing date 2019-06-20
    Publishing country United States
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 2500949-7
    ISSN 1759-4685 ; 1674-2788
    ISSN (online) 1759-4685
    ISSN 1674-2788
    DOI 10.1093/jmcb/mjz018
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: p53: updates on mechanisms, biology and therapy (I).

    Lane, David P / Verma, Chandra S

    Journal of molecular cell biology

    2019  Volume 11, Issue 3, Page(s) 185–186

    MeSH term(s) Humans ; Mutation ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/therapy ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Tumor Suppressor Protein p53
    Language English
    Publishing date 2019-06-20
    Publishing country United States
    Document type Editorial
    ZDB-ID 2500949-7
    ISSN 1759-4685 ; 1674-2788
    ISSN (online) 1759-4685
    ISSN 1674-2788
    DOI 10.1093/jmcb/mjz017
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Can Glycosylation Mask the Detection of MHC Expressing p53 Peptides by T Cell Receptors?

    Nguyen, Thanh Binh / Lane, David P / Verma, Chandra S

    Biomolecules

    2021  Volume 11, Issue 7

    Abstract: Proteins of the major histocompatibility complex (MHC) class I, or human leukocyte antigen (HLA) in humans interact with endogenous peptides and present them to T cell receptors (TCR), which in turn tune the immune system to recognize and discriminate ... ...

    Abstract Proteins of the major histocompatibility complex (MHC) class I, or human leukocyte antigen (HLA) in humans interact with endogenous peptides and present them to T cell receptors (TCR), which in turn tune the immune system to recognize and discriminate between self and foreign (non-self) peptides. Of especial importance are peptides derived from tumor-associated antigens. T cells recognizing these peptides are found in cancer patients, but not in cancer-free individuals. What stimulates this recognition, which is vital for the success of checkpoint based therapy? A peptide derived from the protein p53 (residues 161-169 or p161) was reported to show this behavior. T cells recognizing this unmodified peptide could be further stimulated in vitro to create effective cancer killing CTLs (cytotoxic T lymphocytes). We hypothesize that the underlying difference may arise from post-translational glycosylation of p161 in normal individuals, likely masking it against recognition by TCR. Defects in glycosylation in cancer cells may allow the presentation of the native peptide. We investigate the structural consequences of such peptide glycosylation by investigating the associated structural dynamics.
    MeSH term(s) Acetylglucosamine/metabolism ; Glycosylation ; HLA-A24 Antigen/chemistry ; HLA-A24 Antigen/metabolism ; Human Immunodeficiency Virus Proteins/chemistry ; Human Immunodeficiency Virus Proteins/metabolism ; Humans ; Hydrogen Bonding ; Models, Molecular ; Molecular Dynamics Simulation ; Peptide Fragments/chemistry ; Peptide Fragments/metabolism ; Protein Conformation ; Receptors, Antigen, T-Cell/chemistry ; Receptors, Antigen, T-Cell/metabolism ; Tumor Suppressor Protein p53/chemistry ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances HLA-A24 Antigen ; Human Immunodeficiency Virus Proteins ; Peptide Fragments ; Receptors, Antigen, T-Cell ; Tumor Suppressor Protein p53 ; Acetylglucosamine (V956696549)
    Language English
    Publishing date 2021-07-19
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701262-1
    ISSN 2218-273X ; 2218-273X
    ISSN (online) 2218-273X
    ISSN 2218-273X
    DOI 10.3390/biom11071056
    Database MEDical Literature Analysis and Retrieval System OnLINE

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