Evidence map›Paper›PMID 36207426›Full record

ReviewExperimental & molecular medicine2022

DNA damage response revisited: the p53 family and its regulators provide endless cancer therapy opportunities.

Yasser Abuetabh, H Helena Wu, Chengsen Chai, Habib Al Yousef, Sujata Persad, Consolato M Sergi, Roger Leng

Open access · goldAbstract readReview
In one paragraph

Review in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed, 1 pooled it
21.2field-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

157 citing papers in PubMed, 1 synthesis or guideline pooled it, 225 citations in OpenAlex.

  1. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
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  10. Veterinary sciences · 2026
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97 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

7 authors at 2 institutions in 2 countries.

Yasser Abuetabh370 Heritage Medical Research Center, Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, Alberta, T6G 2S2, Canada.
H Helena Wu370 Heritage Medical Research Center, Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, Alberta, T6G 2S2, Canada.
Chengsen Chai370 Heritage Medical Research Center, Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, Alberta, T6G 2S2, Canada.
Habib Al Yousef370 Heritage Medical Research Center, Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, Alberta, T6G 2S2, Canada.
Sujata PersadDepartment of Pediatrics, University of Alberta, Edmonton, AB, T6G 2E1, Canada.
Consolato M SergiDivision of Anatomical Pathology, Children's Hospital of Eastern Ontario (CHEO), University of Ottawa, Ottawa, ON, K1H 8L1, Canada.
Roger Leng370 Heritage Medical Research Center, Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, Alberta, T6G 2S2, Canada. rleng@ualberta.ca.
University of Alberta · CAUniversity of Ottawa · CA

Funding

CIHR
6 · The paper itself

Abstract

Antitumor therapeutic strategies that fundamentally rely on the induction of DNA damage to eradicate and inhibit the growth of cancer cells are integral approaches to cancer therapy. Although DNA-damaging therapies advance the battle with cancer, resistance, and recurrence following treatment are common. Thus, searching for vulnerabilities that facilitate the action of DNA-damaging agents by sensitizing cancer cells is an active research area. Therefore, it is crucial to decipher the detailed molecular events involved in DNA damage responses (DDRs) to DNA-damaging agents in cancer. The tumor suppressor p53 is active at the hub of the DDR. Researchers have identified an increasing number of genes regulated by p53 transcriptional functions that have been shown to be critical direct or indirect mediators of cell fate, cell cycle regulation, and DNA repair. Posttranslational modifications (PTMs) primarily orchestrate and direct the activity of p53 in response to DNA damage. Many molecules mediating PTMs on p53 have been identified. The anticancer potential realized by targeting these molecules has been shown through experiments and clinical trials to sensitize cancer cells to DNA-damaging agents. This review briefly acknowledges the complexity of DDR pathways/networks. We specifically focus on p53 regulators, protein kinases, and E3/E4 ubiquitin ligases and their anticancer potential.

Indexed as

NeoplasmsTumor Suppressor Protein p53DNA DamageDNA RepairHumansProtein KinasesUbiquitin-Protein LigasesProtein KinasesTumor Suppressor Protein p53Ubiquitin-Protein Ligases

Identifiers

PMID36207426
PMCPMC9636249
OpenAlexW4303423653

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.