Evidence map›Paper›PMID 27187358›Full record

ReviewInternational journal of molecular sciences2016

The Growing Complexity of Cancer Cell Response to DNA-Damaging Agents: Caspase 3 Mediates Cell Death or Survival?

Razmik Mirzayans, Bonnie Andrais, Piyush Kumar, David Murray

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
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  6. Discovery of Potent IsoquinolinequinoneJournal of medicinal chemistry · 2024
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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

4 authors at 1 institution in 1 country.

Razmik MirzayansDepartment of Oncology, University of Alberta, Cross Cancer Institute, Edmonton, AB T6G 1Z2, Canada. razmik.mirzayans@ahs.ca.
Bonnie AndraisDepartment of Oncology, University of Alberta, Cross Cancer Institute, Edmonton, AB T6G 1Z2, Canada. bonnie.andrais@ahs.ca.
Piyush KumarDepartment of Oncology, University of Alberta, Cross Cancer Institute, Edmonton, AB T6G 1Z2, Canada. pkumar@ualberta.ca.
David MurrayDepartment of Oncology, University of Alberta, Cross Cancer Institute, Edmonton, AB T6G 1Z2, Canada. david.murray5@ahs.ca.
University of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is widely stated that wild-type p53 either mediates the activation of cell cycle checkpoints to facilitate DNA repair and promote cell survival, or orchestrates apoptotic cell death following exposure to cancer therapeutic agents. This reigning paradigm has been challenged by numerous discoveries with different human cell types, including solid tumor-derived cell lines. Thus, activation of the p53 signaling pathway by ionizing radiation and other DNA-damaging agents hinders apoptosis and triggers growth arrest (e.g., through premature senescence) in some genetic backgrounds; such growth arrested cells remain viable, secrete growth-promoting factors, and give rise to progeny with stem cell-like properties. In addition, caspase 3, which is best known for its role in the execution phase of apoptosis, has been recently reported to facilitate (rather than suppress) DNA damage-induced genomic instability and carcinogenesis. This observation is consistent with an earlier report demonstrating that caspase 3 mediates secretion of the pro-survival factor prostaglandin E₂, which in turn promotes enrichment of tumor repopulating cells. In this article, we review these and related discoveries and point out novel cancer therapeutic strategies. One of our objectives is to demonstrate the growing complexity of the DNA damage response beyond the conventional "repair and survive, or die" hypothesis.

Indexed as

ApoptosisAnimalsCarcinogenesisCaspase 3Cell SurvivalDinoprostoneHumansMutagensCaspase 3DinoprostoneMutagensapoptosisCaspase 3DNA damage responseDNA double-strand breaksionizing radiationmultinucleationp21WAF1 (CDKN1A)premature senescenceprostaglandin E2γH2AX foci

Identifiers

PMID27187358
PMCPMC4881530
OpenAlexW2356569879

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.