Evidence map›Paper›PMID 42352266›Full record

ReviewBiomolecules2026

The Enigmatic Tumor Suppressor p53 Biomolecule: Its Role and Prognostic and Predictive Values in Cancer Therapy and Precision Medicine.

Zahid Hussain Siddik

Abstract readReview
In one paragraph

Review in Biomolecules, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Zahid Hussain SiddikDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX 77096, USA.ORCID 0000-0002-6832-834X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p53 biomolecule is critical for facile antitumor response in cancer therapy. Once fully activated, p53 will kill tumor cells by activating programmed cell death (PCD), such as apoptosis and ferroptosis, and inducing immunogenic cell death. It is not surprising, therefore, that in about 50% of cancers p53 is mutated and non-functional, which induces drug resistance. Paradoxically, many cancers harboring the wild-type

Indexed as

NeoplasmsPrecision MedicineTumor Suppressor Protein p53AnimalsApoptosisDrug Resistance, NeoplasmHumansMutationPrognosisTumor Suppressor Protein p53cancer therapyMDM2MDM4p53 activationpost-translational phosphorylationprecision medicineresistance mechanisms

Identifiers

PMID42352266
PMCPMC13297438

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.