Evidence map›Paper›PMID 34063254›Full record

ReviewCancers2021

Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial-Mesenchymal Plasticity.

Barbora Kvokačková, Ján Remšík, Mohit Kumar Jolly, Karel Souček

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 57 citations in OpenAlex.

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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

4 authors at 3 institutions in 3 countries.

Barbora KvokačkováDepartment of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, 612 65 Brno, Czech Republic.
Ján RemšíkHuman Oncology & Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Mohit Kumar JollyCentre for BioSystems Science and Engineering, Indian Institute of Science, Bangalore 560012, India.ORCID 0000-0002-6631-2109
Karel SoučekDepartment of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, 612 65 Brno, Czech Republic.ORCID 0000-0001-7283-8150
Masaryk University · CZIndian Institute of Science Bangalore · INMemorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Agentura Pro Zdravotnický Výzkum České Republiky 18-08-00245American Brain Tumor Association Basic Research Fellowship JREDepartment of Science and Technology DSTDruckenmiller Center for Lung Cancer Research JREGovernment of India SB/S2/RJN-049/2018Grantová Agentura České Republiky 20-22984SMinisterstvo Školství, Mládeže a Tělovýchovy CZ.02.1.01/0.0/0.0/16_025/0007381NCI NIH HHS P30 CA008748Ramanujan Fellowship awarded by Science and Engineering Research Board SERBTerri Brodeur Breast Cancer Foundation Fellowship JRE
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is a subtype of breast carcinoma known for its unusually aggressive behavior and poor clinical outcome. Besides the lack of molecular targets for therapy and profound intratumoral heterogeneity, the relatively quick overt metastatic spread remains a major obstacle in effective clinical management. The metastatic colonization of distant sites by primary tumor cells is affected by the microenvironment, epigenetic state of particular subclones, and numerous other factors. One of the most prominent processes contributing to the intratumoral heterogeneity is an epithelial-mesenchymal transition (EMT), an evolutionarily conserved developmental program frequently hijacked by tumor cells, strengthening their motile and invasive features. In response to various intrinsic and extrinsic stimuli, malignant cells can revert the EMT state through the mesenchymal-epithelial transition (MET), a process that is believed to be critical for the establishment of macrometastasis at secondary sites. Notably, cancer cells rarely undergo complete EMT and rather exist in a continuum of E/M intermediate states, preserving high levels of plasticity, as demonstrated in primary tumors and, ultimately, in circulating tumor cells, representing a simplified element of the metastatic cascade. In this review, we focus on cellular drivers underlying EMT/MET phenotypic plasticity and its detrimental consequences in the context of TNBC cancer.

Indexed as

epithelial–mesenchymal transitionmesenchymal–epithelial transitionmetastasisplasticitytriple-negative breast cancer

Identifiers

PMID34063254
PMCPMC8125677
OpenAlexW3159103920

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.