Evidence map›Paper›PMID 36598661›Full record

ReviewCancer metastasis reviews2023

Dormant cancer cells: programmed quiescence, senescence, or both?

Kevin Truskowski, Sarah R Amend, Kenneth J Pienta

Full text readReview
In one paragraph

Review in Cancer metastasis reviews, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing 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

56 citing papers in PubMed.

  1. Review
  2. Article
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  5. Review
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  7. Article
  8. Review
  9. Review
  10. Chemotherapy Supports Cancer Cell Dissemination in a Melanoma Preclinical Model.Asian Pacific journal of cancer prevention : APJCP · 2026
    Article
  11. Article
  12. Article
  13. Review
  14. Article
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  16. Article
  17. Review
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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

3 authors.

Kevin TruskowskiBrady Urological Institute, Johns Hopkins School of Medicine, 600 North Wolfe St, Baltimore, MD, USA. ktrusko1@jhmi.edu.ORCID http://orcid.org/0000-0001-8064-3230
Sarah R AmendBrady Urological Institute, Johns Hopkins School of Medicine, 600 North Wolfe St, Baltimore, MD, USA.
Kenneth J PientaBrady Urological Institute, Johns Hopkins School of Medicine, 600 North Wolfe St, Baltimore, MD, USA.

Funding

Tumor microvesicle-mediated modulation of the bone microenvironmentP01CA093900 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KELLER, EVAN T · 2004 to 2024
$29.6M
TRANS_NETWORK PROJECTSU54CA143803 · NCI · PRINCETON UNIVERSITY · PI AUSTIN, ROBERT H. · 2009 to 2013
$14.2M
Mechanisms That Regulate Dormancy of Disseminated Tumor Cells in the Bone MarrowU54CA163124 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHIOZAWA, YUSUKE · 2011 to 2015
$3.0M
Reactive Stroma and Tumor Associated Macrophages in Prostate Cancer ProgressionU01CA143055 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PIENTA, KENNETH J., ROWLEY, DAVID R · 2010 to 2014
$2.7M
NCI NIH HHS P01 CA093900NCI NIH HHS U01 CA143055NCI NIH HHS U54 CA143803NCI NIH HHS U54 CA163124US National Cancer Institute CA093900US National Cancer Institute CA143055US National Cancer Institute CA163124US National Cancer Institute U54CA143803
6 · The paper itself

Abstract

Metastasis is the overwhelming driver of cancer mortality, accounting for the majority of cancer deaths. Many patients present with metastatic relapse years after eradication of the primary lesion. Disseminated cancer cells can undergo a durable proliferative arrest and lie dormant in secondary tissues before reentering the cell cycle to seed these lethal relapses. This process of cancer cell dormancy remains poorly understood, largely due to difficulties in studying these dormant cells. In the face of these challenges, the application of knowledge from the cellular senescence and quiescence fields may help to guide future thinking on the study of dormant cancer cells. Both senescence and quiescence are common programs of proliferative arrest that are integral to tissue development and homeostasis. Despite phenotypic differences, these two states also share common characteristics, and both likely play a role in cancer dormancy and delayed metastatic relapse. Understanding the cell biology behind these states, their overlaps and unique characteristics is critical to our future understanding of dormant cancer cells, as these cells likely employ some of the same molecular programs to promote survival and dissemination. In this review, we highlight the biology underlying these non-proliferative states, relate this knowledge to what we currently know about dormant cancer cells, and discuss implications for future work toward targeting these elusive metastatic seeds.

Indexed as

NeoplasmsCell CycleHumansRecurrenceCancerCell cycleDormancyMetastasisQuiescenceSenescence

Identifiers

PMID36598661
PMCPMC10014758

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read2
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.