Evidence map›Paper›PMID 26560033›Full record

ArticleNature2015

Epithelial-to-mesenchymal transition is not required for lung metastasis but contributes to chemoresistance.

Kari R Fischer, Anna Durrans, Sharrell Lee, Jianting Sheng, Fuhai Li, Stephen T C Wong, Hyejin Choi, Tina El Rayes, Seongho Ryu, Juliane Troeger and 5 more

Abstract read
In one paragraph

Article in Nature, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,138 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,138citing papers in PubMed, 1 pooled it
92.8field-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

1,138 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,780 citations in OpenAlex.

  1. Changes in Tissue Fluidity Predict Tumor Aggressiveness In Vivo.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Pooled it
  2. Article
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  6. Review
  7. Malic enzyme 1 senses L-lactate to determine tumor heterogeneity.Signal transduction and targeted therapy · 2026
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  20. Article

1,078 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 2 countries.

Kari R FischerDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, 1300 York Avenue, New York, New York 10065, USA.
Anna DurransDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, 1300 York Avenue, New York, New York 10065, USA.
Sharrell LeeDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, 1300 York Avenue, New York, New York 10065, USA.
Jianting ShengDepartment of Systems Medicine and Bioengineering, Houston Methodist Research Institute, Houston Methodist Hospital, Houston, Texas 77030, USA.
Fuhai LiDepartment of Systems Medicine and Bioengineering, Houston Methodist Research Institute, Houston Methodist Hospital, Houston, Texas 77030, USA.
Stephen T C WongDepartment of Systems Medicine and Bioengineering, Houston Methodist Research Institute, Houston Methodist Hospital, Houston, Texas 77030, USA.
Hyejin ChoiDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, 1300 York Avenue, New York, New York 10065, USA.
Tina El RayesDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, 1300 York Avenue, New York, New York 10065, USA.
Seongho RyuDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, 1300 York Avenue, New York, New York 10065, USA.
Juliane TroegerDepartment of Medicine, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA.
Robert F SchwabeDepartment of Medicine, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA.
Linda T VahdatDepartment of Medicine, Weill Cornell Medical College of Cornell University, 1300 York Avenue, New York, New York 10065, USA.
Nasser K AltorkiDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, 1300 York Avenue, New York, New York 10065, USA.
Vivek MittalDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, 1300 York Avenue, New York, New York 10065, USA.
Dingcheng GaoDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, 1300 York Avenue, New York, New York 10065, USA.
Cornell University · USColumbia University · USHouston Methodist · USMethodist Hospital · US

Funding

The Core of the Computational BiologyU54CA149196 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI WONG, STEPHEN TC · 2010 to 2015
$10.6M
TRAINING PROGRAM IN MOLECULAR AND CELLULAR BIOLOGYT32GM008539 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI BROWN, ANTHONY M.C. · 1995 to 2020
$5.0M
Molecular mechanisms of tumor-initiated premetastatic niche formation in lung strR01CA135417 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MITTAL, VIVEK, WATNICK, RANDOLPH S · 2010 to 2014
$2.6M
Modeling tumor-stroma crosstalk in lung cancer to identify targets for therapyU01CA188388 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI MITTAL, VIVEK, WONG, STEPHEN TC · 2015 to 2019
$2.5M
Spatiotemporal analysis of Osteopontin in lung cancerF31CA186510 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI FISCHER, KARI · 2014 to 2015
$75k
NCI NIH HHS 1 F31 CA186510-01NCI NIH HHS F31 CA186510NCI NIH HHS R01 CA135417NCI NIH HHS U01 CA188388NCI NIH HHS U54 CA149196NCI NIH HHS U54 CA149196-05NIGMS NIH HHS T32 GM008539
6 · The paper itself

Abstract

The role of epithelial-to-mesenchymal transition (EMT) in metastasis is a longstanding source of debate, largely owing to an inability to monitor transient and reversible EMT phenotypes in vivo. Here we establish an EMT lineage-tracing system to monitor this process in mice, using a mesenchymal-specific Cre-mediated fluorescent marker switch system in spontaneous breast-to-lung metastasis models. We show that within a predominantly epithelial primary tumour, a small proportion of tumour cells undergo EMT. Notably, lung metastases mainly consist of non-EMT tumour cells that maintain their epithelial phenotype. Inhibiting EMT by overexpressing the microRNA miR-200 does not affect lung metastasis development. However, EMT cells significantly contribute to recurrent lung metastasis formation after chemotherapy. These cells survived cyclophosphamide treatment owing to reduced proliferation, apoptotic tolerance and increased expression of chemoresistance-related genes. Overexpression of miR-200 abrogated this resistance. This study suggests the potential of an EMT-targeting strategy, in conjunction with conventional chemotherapies, for breast cancer treatment.

Indexed as

Drug Resistance, NeoplasmEpithelial-Mesenchymal TransitionAnimalsAntineoplastic Agents, AlkylatingApoptosisCell LineageCell ProliferationCell TrackingCyclophosphamideDisease Models, AnimalDisease ProgressionFemaleLung NeoplasmsMaleMammary Neoplasms, ExperimentalMiceAntineoplastic Agents, AlkylatingCyclophosphamideMicroRNAsMirn200 microRNA, mouse

Identifiers

PMID26560033
PMCPMC4662610
OpenAlexW2150322923

What OpenQuestion holds

Textmetadata
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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.