Related Experiment Video

Updated: Sep 14, 2025

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

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The roles of mutant p53 in reprogramming and inflammation in breast cancers

Shivaani Kummar1, Marc Fellous2, Arnold J Levine3

  • 1Division of Hematology and Medical Oncology, Knight Cancer Institute, Oregon Health and Science University, Portland, OR, USA.

Cell Death and Differentiation
|July 22, 2025
PubMed

Insights

Rezatapopt, a p53 reactivator, shows promise in treating triple-negative breast cancer by stabilizing Y220C-mutant p53. This led to significant tumor reduction and inflammation resolution in a patient case study.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • p53 protein is a tumor suppressor.
  • Mutations in p53, such as Y220C, can lead to cancer.
  • Targeting mutant p53 is a therapeutic strategy.

Purpose of the Study:

  • To investigate the efficacy of rezatapopt, a novel p53 reactivator.
  • To explore the potential of rezatapopt in treating solid tumors, specifically triple-negative breast cancer.
  • To examine the impact of rezatapopt on tumor growth and cancer-related inflammation.

Main Methods:

  • Phase 1 PYNNACLE trial.
  • Administration of rezatapopt to a patient with triple-negative breast cancer.
  • Monitoring of tumor volume, skin inflammation, and lymphedema.

Main Results:

  • Rezatapopt specifically targets Y220C-mutant p53, stabilizing it to a wild-type conformation.
  • A patient with triple-negative breast cancer experienced rapid resolution of severe skin inflammation and lymphedema within one week.
  • Tumor volume decreased by 41% after six weeks of treatment, with sustained reduction and inflammation resolution for over 24 months.

Conclusions:

  • Rezatapopt demonstrates potential as a therapeutic agent for Y220C-mutant p53 solid tumors.
  • The drug may reverse cancer-mediated inflammation and reduce tumor burden.
  • Further investigation into wild-type TP53-regulated pathways is warranted to understand the observed effects.

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