Evidence map›Paper›PMID 28397828›Full record

ReviewNature reviews. Clinical oncology2017

EMT, CSCs, and drug resistance: the mechanistic link and clinical implications.

Tsukasa Shibue, Robert A Weinberg

Abstract readReview
In one paragraph

Review in Nature reviews. Clinical oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,615 papers.

0numbers the graph read from it
0cells of the map it votes in
1,615citing 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

1,615 citing papers in PubMed.

  1. Mechanisms of chemoresistance in gastric cancer: interplay between microRNAs and the tumor microenvironment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  2. Review
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  7. The logarithmic phase as a therapeutic direction: evaluating pharmacological strategies against cancer progression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
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  17. Epithelial-mesenchymal transition and cancer-associated fibroblasts in tumor progression and therapy resistance: mechanistic convergence and therapeutic opportunities.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  18. Article
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1,555 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

2 authors.

Tsukasa ShibueWhitehead Institute for Biomedical Research, 455 Main Street, Cambridge, Massachusetts 02142, USA.
Robert A WeinbergWhitehead Institute for Biomedical Research, 455 Main Street, Cambridge, Massachusetts 02142, USA.

Funding

Use of Organotypic and Mammary Gland Models to Investigate the Outcomes of ClonalP01CA080111 · NCI · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI WEINBERG, ROBERT A · 1999 to 2018
$36.0M
NCI NIH HHS P01 CA080111
6 · The paper itself

Abstract

The success of anticancer therapy is usually limited by the development of drug resistance. Such acquired resistance is driven, in part, by intratumoural heterogeneity - that is, the phenotypic diversity of cancer cells co-inhabiting a single tumour mass. The introduction of the cancer stem cell (CSC) concept, which posits the presence of minor subpopulations of CSCs that are uniquely capable of seeding new tumours, has provided a framework for understanding one dimension of intratumoural heterogeneity. This concept, taken together with the identification of the epithelial-to-mesenchymal transition (EMT) programme as a critical regulator of the CSC phenotype, offers an opportunity to investigate the nature of intratumoural heterogeneity and a possible mechanistic basis for anticancer drug resistance. In fact, accumulating evidence indicates that conventional therapies often fail to eradicate carcinoma cells that have entered the CSC state via activation of the EMT programme, thereby permitting CSC-mediated clinical relapse. In this Review, we summarize our current understanding of the link between the EMT programme and the CSC state, and also discuss how this knowledge can contribute to improvements in clinical practice.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic AgentsEpithelial-Mesenchymal TransitionHumansNeoplasmsNeoplastic Stem CellsSignal TransductionAntineoplastic Agents

Identifiers

PMID28397828
PMCPMC5720366

What OpenQuestion holds

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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.