Evidence map›Paper›PMID 30992279›Full record

ReviewCancer discovery2019

Cellular Plasticity in Cancer.

Salina Yuan, Robert J Norgard, Ben Z Stanger

Abstract readReview
In one paragraph

Review in Cancer discovery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 306 papers.

0numbers the graph read from it
0cells of the map it votes in
306citing 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

306 citing papers in PubMed.

  1. Cell plasticity in cancer and therapy resistance.Experimental & molecular medicine · 2026
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  18. Squamous-state excursions activate APOBEC3A in cancer.bioRxiv : the preprint server for biology · 2026
    Article
  19. Article
  20. Article

246 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.

Salina Yuan *Abramson Family Cancer Research Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania.
Robert J Norgard *Abramson Family Cancer Research Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania.
Ben Z StangerAbramson Family Cancer Research Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania. bstanger@upenn.edu.

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Robert H. Vonderheide · 1985 to 2026
$222.3M
Molecular Determinants and Therapeutic Consequences of Immune Heterogeneity in CancerR01CA229803 · NCI · UNIVERSITY OF PENNSYLVANIA · PI STANGER, BEN Z · 2018 to 2022
$3.7M
Investigating the role of C1-INH in pancreatic ductal adenocarcinoma progressionF30CA224970 · NCI · UNIVERSITY OF PENNSYLVANIA · PI YUAN, SALINA · 2018 to 2020
$114k
NCI NIH HHS F30 CA224970NCI NIH HHS P30 CA016520NCI NIH HHS R01 CA229803
6 · The paper itself

Abstract

During cancer progression, tumor cells undergo molecular and phenotypic changes collectively referred to as cellular plasticity. Such changes result from microenvironmental cues, stochastic genetic and epigenetic alterations, and/or treatment-imposed selective pressures, thereby contributing to tumor heterogeneity and therapy resistance. Epithelial-mesenchymal plasticity is the best-known case of tumor cell plasticity, but recent work has uncovered other examples, often with functional consequences. In this review, we explore the nature and role(s) of these diverse cellular plasticity programs in premalignant progression, tumor evolution, and adaptation to therapy and consider ways in which targeting plasticity could lead to novel anticancer treatments. SIGNIFICANCE: Changes in cell identity, or cellular plasticity, are common at different stages of tumor progression, and it has become clear that cellular plasticity can be a potent mediator of tumor progression and chemoresistance. Understanding the mechanisms underlying the various forms of cell plasticity may deliver new strategies for targeting the most lethal aspects of cancer: metastasis and resistance to therapy.

Indexed as

AnimalsCell PlasticityDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionHumansMetaplasiaNeoplasmsNeoplastic Stem CellsSignal Transduction

Identifiers

PMID30992279
PMCPMC6606363

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.