Evidence map›Paper›PMID 30508182›Full record

ReviewJournal of molecular cell biology2019

Mutant p53 in cancer therapy-the barrier or the path.

Xiang Zhou, Qian Hao, Hua Lu

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of molecular cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 1% of its field
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

160 citing papers in PubMed, 2 syntheses or guidelines pooled it, 244 citations in OpenAlex.

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  18. Targeting the p53/xCT/GSH Axis with PRIMA-1International journal of molecular sciences · 2025
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100 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 2 countries.

Xiang ZhouFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, and Key Laboratory of Medical Epigenetics and Metabolism, Fudan University, Shanghai, China.
Qian HaoFudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Hua LuDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA, USA.
Fudan University Shanghai Cancer Center · CNTulane University · US

Funding

The Role of Ribosomal Proteins in the P53-MDM2 PathwayR01CA095441 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2002 to 2021
$5.1M
Role of the AMPK-MDMX-p53 pathway in cancerR01CA127724 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2007 to 2019
$3.0M
NCI NIH HHS R01 CA095441NCI NIH HHS R01 CA127724
6 · The paper itself

Abstract

Since wild-type p53 is central for maintaining genomic stability and preventing oncogenesis, its coding gene TP53 is highly mutated in ~50% of human cancers, and its activity is almost abrogated in the rest of cancers. Approximately 80% of p53 mutations are single point mutations with several hotspot mutations. Besides loss of function and dominant-negative effect on the wild-type p53 activity, the hotspot p53 mutants also acquire new oncogenic functions, so-called 'gain-of-functions' (GOF). Because the GOF of mutant p53 is highly associated with late-stage malignance and drug resistance, these p53 mutants have become hot targets for developing novel cancer therapies. In this essay, we review some recent progresses in better understanding of the role of mutant p53 GOF in chemoresistance and the underlying mechanisms, and discuss the pros and cons of targeting mutant p53 for the development of anti-cancer therapies.

Indexed as

Antineoplastic Agents, AlkylatingApoptosisATP Binding Cassette Transporter, Subfamily B, Member 1Drug Resistance, NeoplasmGain of Function MutationGenomic InstabilityHumansNeoplasm MetastasisNeoplasmsTumor Suppressor Protein p53Antineoplastic Agents, AlkylatingATP Binding Cassette Transporter, Subfamily B, Member 1Tumor Suppressor Protein p53cancer therapychemoresistancegain-of-functionmutant p53synthetic lethality

Identifiers

PMID30508182
PMCPMC6487791
OpenAlexW2902556019

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

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.