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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Related Experiment Video

Updated: May 1, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
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The TP53 gene network in a postgenomic era.

Thierry Soussi

    Human Mutation
    |April 23, 2014
    PubMed
    Summary

    TP53 pathway inactivation is common in cancer, with mutations or network member dysfunction contributing to disease. This review covers TP53 gene features, models, and clinical care, advocating for standardized variant data.

    Area of Science:

    • Oncology
    • Genetics
    • Molecular Biology

    Background:

    • TP53 pathway inactivation is a hallmark of human cancers.
    • While TP53 gene mutations are frequent, alterations in network members like MDM2, MDM4 (mdmX), and miR-125b also disrupt its function.
    • Understanding these complex interactions is crucial for cancer research and treatment.

    Purpose of the Study:

    • To review the fundamental features of wild-type and mutant TP53 proteins.
    • To discuss animal models and clinical aspects, including patient care recommendations.
    • To highlight the need for innovative strategies and standardized guidelines for TP53 variant reporting and annotation.

    Main Methods:

    • Review of existing literature on TP53 gene, proteins, and associated network members.

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  • Analysis of animal models relevant to TP53 research.
  • Examination of clinical data and patient care guidelines related to TP53 alterations.
  • Discussion of data standardization and annotation strategies for TP53 variants.
  • Main Results:

    • The TP53 network is complex, with multiple mechanisms leading to pathway inactivation.
    • Wild-type and mutant TP53 proteins exhibit diverse modifications and functions.
    • Standardized reporting of TP53 variants is essential for data exchange and analysis across cancer databases.

    Conclusions:

    • The TP53 gene and its network are central to cancer development and progression.
    • Innovative approaches and standardized data are necessary for accurate tumor profiling and improved patient care.
    • This special issue provides a comprehensive overview to advance TP53 research in the post-genomic era.