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Updated: Sep 3, 2025

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Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
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P63 and P73 Activation in Cancers with p53 Mutation
Bi-He Cai1, Yun-Chien Hsu1, Fang-Yu Yeh1
1School of Medicine, I-Shou University, No. 8, Yida Rd., Jiaosu Village Yanchao District, Kaohsiung 82445, Taiwan.
Biomedicines
|July 27, 2022
Summary
This review explores drug therapies for p53 mutations, a key tumor suppressor. It discusses targeting p53, p63, and p73 for cancer treatment, focusing on missense and nonsense mutations.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The p53 family (p53, p63, p73) has tumor suppressor roles.
- p53 exhibits high mutation rates in cancers, losing its suppressor function.
- Missense and nonsense mutations are the most common p53 alterations.
Purpose of the Study:
- To review potential drug therapies for p53 missense and nonsense mutations.
- To explore the therapeutic potential of p63 and p73 activators as anti-cancer agents.
- To summarize p63 and p73 activators and strategies to enhance their efficacy, especially for p53 gain-of-function mutants.
Main Methods:
- Literature review of existing research on p53 family mutations.
- Analysis of drug therapies targeting specific p53 mutations (missense, nonsense).
- Summary of p63 and p73 activators and their mechanisms.
Main Results:
- p53 mutations impair tumor suppression, necessitating therapeutic interventions.
- p63 and p73 activators show promise as alternative anti-cancer strategies.
- Strategies for improving activator responses against p53 gain-of-function mutants are discussed.
Conclusions:
- Targeting p53 mutations and utilizing p63/p73 activators represent viable therapeutic avenues in oncology.
- Further research into enhancing p63/p73 activator efficacy is crucial for effective cancer treatment.
- Understanding p53 family dynamics is key to developing novel anti-cancer drugs.
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