Evidence map›Paper›PMID 32535731›Full record

ReviewMedical oncology (Northwood, London, England)2020

The issues with tissues: the wide range of cell fate separation enables the evolution of multicellularity and cancer.

Emma U Hammarlund, Sarah R Amend, Kenneth J Pienta

Open access · hybridAbstract readReview
In one paragraph

Review in Medical oncology (Northwood, London, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 41% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Cancer, collapse, and the politics of somatic evolution.Evolution, medicine, and public health · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Modeling cancer's ecological and evolutionary dynamics.Medical oncology (Northwood, London, England) · 2023
    Article
  8. Review
  9. Cancer recurrence and lethality are enabled by enhanced survival and reversible cell cycle arrest of polyaneuploid cells.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. 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

3 authors at 2 institutions in 3 countries.

Emma U HammarlundTranslational Cancer Research, Department of Laboratory Medicine, Lund University, Lund, Sweden. emma.hammarlund@med.lu.se.ORCID http://orcid.org/0000-0001-7625-4793
Sarah R AmendThe Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, MD, 21287, USA.ORCID http://orcid.org/0000-0002-5606-1262
Kenneth J PientaThe Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, MD, 21287, USA.ORCID http://orcid.org/0000-0002-4138-2186
Johns Hopkins University · USUniversity of Southern Denmark · DK

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 CA093900NCI NIH HHS CA143055NCI NIH HHS CA163124NCI NIH HHS U01 CA143055NCI NIH HHS U54CA143803
6 · The paper itself

Abstract

Our understanding of the rises of animal and cancer multicellularity face the same conceptual hurdles: what makes the clade originate and what makes it diversify. Between the events of origination and diversification lies complex tissue organization that gave rise to novel functionality for organisms and, unfortunately, for malignant transformation in cells. Tissue specialization with distinctly separated cell fates allowed novel functionality at organism level, such as for vertebrate animals, but also involved trade-offs at the cellular level that are potentially disruptive. These trade-offs are under-appreciated and here we discuss how the wide separation of cell phenotypes may contribute to cancer evolution by (a) how factors can reverse differentiated cells into a window of phenotypic plasticity, (b) the reversal to phenotypic plasticity coupled with asexual reproduction occurs in a way that the host cannot adapt, and (c) the power of the transformation factor correlates to the power needed to reverse tissue specialization. The role of reversed cell fate separation for cancer evolution is strengthened by how some tissues and organisms maintain high cell proliferation and plasticity without developing tumours at a corresponding rate. This demonstrates a potential proliferation paradox that requires further explanation. These insights from the cancer field, which observes tissue evolution in real time and closer than any other field, allow inferences to be made on evolutionary events in animal history. If a sweet spot of phenotypic and reproductive versatility is key to transformation, factors stimulating cell fate separation may have promoted also animal diversification on Earth.

Indexed as

AnimalsBiological EvolutionCell DifferentiationCell PlasticityCell SurvivalEcosystemHumansNeoplasmsSelection, GeneticAnimalsCambrian explosionCancerEvolutionMulticellularityPhenotypic separation

Identifiers

PMID32535731
PMCPMC7293661
OpenAlexW3034857773

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.