Evidence map›Paper›PMID 32722796›Full record

ReviewJournal of molecular cell biology2020

Gain-of-function mutant p53 in cancer progression and therapy.

Cen Zhang, Juan Liu, Dandan Xu, Tianliang Zhang, Wenwei Hu, Zhaohui Feng

Open access · goldAbstract readReview
In one paragraph

Review in Journal of molecular cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 215 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
215citing papers in PubMed, 1 pooled it
13.3field-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

215 citing papers in PubMed, 1 synthesis or guideline pooled it, 340 citations in OpenAlex.

  1. Pooled it
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  4. Revisiting tumor immunogenicity through the lens of mutant p53: Implications for cancer immunotherapy.Apoptosis : an international journal on programmed cell death · 2026
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155 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

6 authors at 2 institutions in 1 country.

Cen ZhangDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers-State University of New Jersey, New Brunswick, NJ 08903, USA.
Juan LiuDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers-State University of New Jersey, New Brunswick, NJ 08903, USA.
Dandan XuDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers-State University of New Jersey, New Brunswick, NJ 08903, USA.
Tianliang ZhangDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers-State University of New Jersey, New Brunswick, NJ 08903, USA.
Wenwei HuDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers-State University of New Jersey, New Brunswick, NJ 08903, USA.
Zhaohui FengDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers-State University of New Jersey, New Brunswick, NJ 08903, USA.
Rutgers Cancer Institute of New JerseyRutgers, The State University of New Jersey · US

Funding

The role of chronic stress in regulation of mutant p53 and tumorigenesisR01CA203965 · NCI · RBHS -CANCER INSTITUTE OF NEW JERSEY · PI HU, WENWEI · 2017 to 2021
$1.8M
SENP6, a novel p53 negative regulator, is an important new player in cancerR01CA214746 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI FENG, ZHAOHUI · 2018 to 2022
$1.8M
Metabolic reprogramming in breast cancerR01CA227912 · NCI · RBHS -CANCER INSTITUTE OF NEW JERSEY · PI FENG, ZHAOHUI, HU, WENWEI · 2018 to 2022
$1.8M
NCI NIH HHS R01 CA203965NCI NIH HHS R01 CA214746NCI NIH HHS R01 CA227912
6 · The paper itself

Abstract

p53 is a key tumor suppressor, and loss of p53 function is frequently a prerequisite for cancer development. The p53 gene is the most frequently mutated gene in human cancers; p53 mutations occur in >50% of all human cancers and in almost every type of human cancers. Most of p53 mutations in cancers are missense mutations, which produce the full-length mutant p53 (mutp53) protein with only one amino acid difference from wild-type p53 protein. In addition to loss of the tumor-suppressive function of wild-type p53, many mutp53 proteins acquire new oncogenic activities independently of wild-type p53 to promote cancer progression, termed gain-of-function (GOF). Mutp53 protein often accumulates to very high levels in cancer cells, which is critical for its GOF. Given the high mutation frequency of the p53 gene and the GOF activities of mutp53 in cancer, therapies targeting mutp53 have attracted great interest. Further understanding the mechanisms underlying mutp53 protein accumulation and GOF will help develop effective therapies treating human cancers containing mutp53. In this review, we summarize the recent advances in the studies on mutp53 regulation and GOF as well as therapies targeting mutp53 in human cancers.

Indexed as

Disease ProgressionAnimalsGain of Function MutationGenomic InstabilityHumansNeoplasmsTumor MicroenvironmentTumor Suppressor Protein p53Tumor Suppressor Protein p53cancer therapygain-of-functionmutationp53tumorigenesistumor suppressor

Identifiers

PMID32722796
PMCPMC7749743
OpenAlexW3045935025

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.