Evidence map›Paper›PMID 40696138›Full record

ReviewCell death and differentiation2025

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

Shivaani Kummar, Marc Fellous, Arnold J Levine

Abstract readReview
In one paragraph

Review in Cell death and differentiation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Shivaani KummarDivision of Hematology and Medical Oncology, Knight Cancer Institute, Oregon Health and Science University, Portland, OR, USA.
Marc FellousPMV Pharmaceuticals Inc, Princeton, NJ, USA.
Arnold J LevineThe Simons Center for Systems Biology, Institute for Advanced Study, Princeton, NJ, USA. alevine@ias.edu.ORCID 0000-0002-1871-6387

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rezatapopt is an investigational small molecule p53 reactivator that binds specifically to the Y220C-mutant p53 protein without interacting with wild-type or other mutant p53 proteins. Upon binding, rezatapopt stabilizes the Y220C-mutant p53 protein in the wild-type conformation, reactivating p53 functions. The Phase 1 PYNNACLE trial assessed rezatapopt in solid tumors. One study participant with triple-negative breast cancer experiencing severe inflammation of the skin overlying the breast and left arm edema saw inflammation improve within 1 week of receiving rezatapopt and completely resolve shortly after. After 6 weeks of treatment, tumor volume had reduced 41%. The patient remains on study, with continued resolution of the skin inflammation and reduced tumor burden for greater than 24 months. There are several wild type Tp53 regulated pathways that could play a role in reversing the inflammatory response and tumor growth observed in this patient case. This perspective explores the signal transduction pathways involved in this cancer mediated inflammation and the extensive reduction of detectable tumor tissue.

Indexed as

Breast NeoplasmsInflammationTumor Suppressor Protein p53FemaleHumansMutationSignal TransductionTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID40696138
PMCPMC12572242

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.