Evidence map›Paper›PMID 30228301›Full record

ReviewNature reviews. Cancer2018

Stem cell fate in cancer growth, progression and therapy resistance.

Nikki K Lytle, Alison G Barber, Tannishtha Reya

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 396 papers.

0numbers the graph read from it
0cells of the map it votes in
396citing papers in PubMed
27.0field-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

396 citing papers in PubMed, 661 citations in OpenAlex.

  1. Article
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  8. TheCells · 2026
    Article
  9. Lgr6Genes & diseases · 2026
    Review
  10. Review
  11. Review
  12. Article
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  15. Article
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  18. Balkan medical journal · 2026
    Article
  19. Article
  20. Review

336 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Nikki K LytleDepartments of Pharmacology and Medicine, San Diego School of Medicine, University of California, La Jolla, CA, USA.
Alison G BarberDepartments of Pharmacology and Medicine, San Diego School of Medicine, University of California, La Jolla, CA, USA.
Tannishtha ReyaDepartments of Pharmacology and Medicine, San Diego School of Medicine, University of California, La Jolla, CA, USA. treya@ucsd.edu.
Sanford Consortium for Regenerative Medicine · US

Funding

GRADUATE TRAINING IN CELLULAR &MOLECULAR PHARMACOLOGYT32GM007752 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROWN, JOAN HELLER, HANDEL, TRACY M · 1985 to 2023
$13.5M
Molecular strategies for early detection and targeting of cancerR35CA197699 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Tannishtha Reya · 2015 to 2026
$11.2M
UCSD Cancer Center Training Program in Drug DevelopmentT32CA121938 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Michael Bouvet, Dwayne G. Stupack · 2006 to 2026
$10.3M
Molecular Determinants of Asymmetric DivisionR01DK099335 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI REYA, TANNISHTHA · 2014 to 2017
$1.5M
Stem cell signals in pancreatic adenocarcinoma metastasis and therapy resistanceF31CA206416 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LYTLE, NIKKI KATHERINE · 2016 to 2017
$75k
NCI NIH HHS F31 CA206416NCI NIH HHS R35 CA197699NCI NIH HHS T32 CA121938NIDDK NIH HHS R01 DK099335NIGMS NIH HHS T32 GM007752
6 · The paper itself

Abstract

Although we have come a long way in our understanding of the signals that drive cancer growth, and how these signals can be targeted, effective control of this disease remains a key scientific and medical challenge. The therapy resistance and relapse that are commonly seen are driven in large part by the inherent heterogeneity within cancers that allows drugs to effectively eliminate some, but not all, malignant cells. Here, we focus on the fundamental drivers of this heterogeneity by examining emerging evidence that shows that these traits are often controlled by the disruption of normal cell fate and aberrant adoption of stem cell signals. We discuss how undifferentiated cells are preferentially primed for transformation and often serve as the cell of origin for cancers. We also consider evidence showing that activation of stem cell programmes in cancers can lead to progression, therapy resistance and metastatic growth and that targeting these attributes may enable better control over a difficult disease.

Indexed as

Cell DifferentiationCell Transformation, NeoplasticDisease ProgressionDrug Resistance, NeoplasmHumansNeoplasmsNeoplastic Stem CellsSignal Transduction

Identifiers

PMID30228301
PMCPMC8388042
OpenAlexW2891589486

What OpenQuestion holds

Textmetadata
LicenceTDM
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.