The gene is mutated in 50% of human tumors. Oncogenic functions of mutant maintain tumor cell proliferation and tumor growth also in osteosarcomas. We collected data on mutations in patients to indicate which are more common and describe their role in in vitro and animal models. We also describe animal models with dysfunction, which provide a good platform for testing the potential therapeutic approaches. Finally, we have indicated a whole range of pharmacological compounds that modulate the action of p53, stabilize its mutated versions or lead to its degradation, cause silencing or, on the contrary, induce the expression of its functional version in genetic therapy. Although many of the described therapies are at the preclinical testing stage, they offer hope for a change in the approach to osteosarcoma treatment based on targeting in the future.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8428337 | PMC |
http://dx.doi.org/10.3390/cancers13174284 | DOI Listing |
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