Evidence map›Paper›PMID 39706988›Full record

ArticleBritish journal of cancer2025

Pro-survival roles for p21(Cip1/Waf1) in non-small cell lung cancer.

S J Cutty, F A Hughes, P Ortega-Prieto, S Desai, P Thomas, L V Fets, M Secrier, A R Barr

Abstract read
In one paragraph

Article in British journal of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
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

8 authors.

S J CuttyInstitute of Clinical Sciences, Imperial College London, London, UK.
F A HughesDepartment of Mathematics, Imperial College London, London, UK.
P Ortega-PrietoMRC Laboratory of Medical Sciences, London, UK.
S DesaiCharing Cross Hospital, Imperial College London, London, UK.
P ThomasDepartment of Mathematics, Imperial College London, London, UK.
L V FetsMRC Laboratory of Medical Sciences, London, UK.
M SecrierUCL Genetics Institute, Department of Genetics, Evolution and Environment, University College London, London, UK.ORCID http://orcid.org/0000-0003-2758-1741
A R BarrInstitute of Clinical Sciences, Imperial College London, London, UK. a.barr@ic.ac.uk.ORCID http://orcid.org/0000-0002-6684-8114

Funding

Cancer Research UK (CRUK) C63833/A25729Cancer Research UK (CRUK) RCCCEA-Nov21\100001Medical Research Council MR/T018429/1RCUK | Biotechnology and Biological Sciences Research Council (BBSRC) BB/R01356X/1RCUK | Engineering and Physical Sciences Research Council (EPSRC) EP/N014529/1RCUK | Medical Research Council (MRC) MC-A654-5QC70RCUK | Medical Research Council (MRC) MC-A658-5TY60Research Councils UK (RCUK) MR/T018429/1Research Councils UK (RCUK) MR/T042184/1Wellcome TrustWellcome Trust (Wellcome) 204841/Z/16/Z
6 · The paper itself

Abstract

backgroundQuiescence is reversible proliferative arrest. Multiple mechanisms regulate quiescence that are not fully understood. High expression of the CDK inhibitor p21

methodsThrough analysis of patient data and quantitative, single-cell, timelapse imaging of genetically-engineered NSCLC reporter cell lines we investigated the role of p21 in NSCLC during normal proliferation and after chemotherapy.

resultsHigh p21 expression correlates with a poor prognosis in TP53 wild-type, but not TP53 mutant, NSCLC patients and TP53 wild-type NSCLC cells can enter p21-dependent quiescence, downstream of replication stress. Without p21, unrepaired DNA damage propagates into S-phase and cells display increased genomic instability. p21 expression confers survival advantages to TP53 wild-type NSCLC cells, during proliferation and after chemotherapy. p21 can promote tumour relapse by allowing recovery from both G1 and G2 arrests after chemotherapy.

conclusionsp21-dependent quiescence exists in TP53 wild-type NSCLC cells and provides survival advantages to these cells. Targeting p21 function in TP53 wild-type tumours could lead to better outcomes for chemotherapy treatment in NSCLC patients.

Indexed as

Carcinoma, Non-Small-Cell LungCyclin-Dependent Kinase Inhibitor p21Lung NeoplasmsCell Line, TumorCell ProliferationDNA DamageGene Expression Regulation, NeoplasticHumansPrognosisTumor Suppressor Protein p53CDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID39706988
PMCPMC11876327

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.