Evidence map›Paper›PMID 37608096›Full record

ReviewBritish journal of cancer2023

A cell cycle centric view of tumour dormancy.

William A Weston, Alexis R Barr

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in British journal of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
11.7field-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

43 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  18. Unlocking Lung Cancer Cell Dormancy: An Epigenetic Perspective.International journal of molecular sciences · 2025
    Review
  19. Review
  20. Article
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

2 authors at 1 institution in 1 country.

William A WestonMRC London Institute of Medical Sciences, Du Cane Road, London, W12 0NN, UK.
Alexis R BarrMRC London Institute of Medical Sciences, Du Cane Road, London, W12 0NN, UK. abarr@ic.ac.uk.ORCID 0000-0002-6684-8114
MRC London Institute of Medical Sciences · GB

Funding

Cancer Research UK 25729Medical Research Council MC_UP_1605/8
6 · The paper itself

Abstract

Tumour dormancy and recurrent metastatic cancer remain the greatest clinical challenge for cancer patients. Dormant tumour cells can evade treatment and detection, while retaining proliferative potential, often for years, before relapsing to tumour outgrowth. Cellular quiescence is one mechanism that promotes and maintains tumour dormancy due to its central role in reducing proliferation, elevating cyto-protective mechanisms, and retaining proliferative potential. Quiescence/proliferation decisions are dictated by intrinsic and extrinsic signals, which regulate the activity of cyclin-dependent kinases (CDKs) to modulate cell cycle gene expression. By clarifying the pathways regulating CDK activity and the signals which activate them, we can better understand how cancer cells enter, maintain, and escape from quiescence throughout the progression of dormancy and metastatic disease. Here we review how CDK activity is regulated to modulate cellular quiescence in the context of tumour dormancy and highlight the therapeutic challenges and opportunities it presents.

Indexed as

Neoplasm Recurrence, LocalCell CycleCell Cycle CheckpointsCell DivisionHumans

Identifiers

PMID37608096
PMCPMC10645753
OpenAlexW4386055123

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.