Evidence map›Paper›PMID 32467609›Full record

ReviewExperimental & molecular medicine2020

Endothelial-to-mesenchymal transition in anticancer therapy and normal tissue damage.

Kyu Jin Choi, Jae-Kyung Nam, Ji-Hee Kim, Seo-Hyun Choi, Yoon-Jin Lee

Open access · goldAbstract readReview
In one paragraph

Review in Experimental & molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 7% 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

73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 104 citations in OpenAlex.

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  11. Nitration in cancer signaling.Redox biology · 2026
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13 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

5 authors at 2 institutions in 2 countries.

Kyu Jin Choi *Division of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul, 139-706, Korea.
Jae-Kyung Nam *Division of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul, 139-706, Korea.
Ji-Hee KimDivision of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul, 139-706, Korea.
Seo-Hyun ChoiDepartment of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA.
Yoon-Jin LeeDivision of Radiation Biomedical Research, Korea Institute of Radiological & Medical Sciences, Seoul, 139-706, Korea. yjlee8@kirams.re.kr.
Korea Institute of Radiological and Medical Sciences · KRMemorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Endothelial-to-mesenchymal transition (EndMT) involves the phenotypic conversion of endothelial-to-mesenchymal cells, and was first discovered in association with embryonic heart development. EndMT can regulate various processes, such as tissue fibrosis and cancer. Recent findings have shown that EndMT is related to resistance to cancer therapy, such as chemotherapy, antiangiogenic therapy, and radiation therapy. Based on the known effects of EndMT on the cardiac toxicity of anticancer therapy and tissue damage of radiation therapy, we propose that EndMT can be targeted as a strategy for overcoming tumor resistance while reducing complications, such as tissue damage. In this review, we discuss EndMT and its roles in damaging cardiac and lung tissues, as well as EndMT-related effects on tumor vasculature and resistance in anticancer therapy. Modulating EndMT in radioresistant tumors and radiation-induced tissue fibrosis can especially increase the efficacy of radiation therapy. In addition, we review the role of hypoxia and reactive oxygen species as the main stimulating factors of tissue damage due to vascular damage and EndMT. We consider drugs that may be clinically useful for regulating EndMT in various diseases. Finally, we argue the importance of EndMT as a therapeutic target in anticancer therapy for reducing tissue damage.

Indexed as

Epithelial-Mesenchymal TransitionTumor MicroenvironmentAnimalsCombined Modality TherapyDisease ManagementDisease SusceptibilityHumansNeoplasmsNeovascularization, PathologicOrgan SpecificityTreatment Outcome

Identifiers

PMID32467609
PMCPMC7272420
OpenAlexW3031489764

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.