Evidence map›Paper›PMID 34058338›Full record

ReviewSeminars in cancer biology2021

Epithelial-mesenchymal transition: Insights into nickel-induced lung diseases.

Hyun-Wook Lee, Cynthia C Jose, Suresh Cuddapah

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

43 citing papers in PubMed, 92 citations in OpenAlex.

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  8. The role and mechanisms of the HIF-1 signaling pathway in LC-COPD.Journal of cancer research and clinical oncology · 2025
    Review
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  14. The Role of WDR77 in Cancer: More than a PRMT5 Interactor.Molecular cancer research : MCR · 2025
    Review
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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

3 authors at 1 institution in 1 country.

Hyun-Wook LeeDepartment of Environmental Medicine, New York University School of Medicine, New York, NY, 10010, USA.
Cynthia C JoseDepartment of Environmental Medicine, New York University School of Medicine, New York, NY, 10010, USA.
Suresh CuddapahDepartment of Environmental Medicine, New York University School of Medicine, New York, NY, 10010, USA. Electronic address: suresh.cuddapah@nyulangone.org.
New York University · US

Funding

RESEARCH IN ENVIRONMENTAL HEALTH SCIENCES (CENTER GRANT)P30ES000260 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ZELIKOFF, JUDITH TERRY · 1985 to 2020
$26.1M
Persistent transcriptional changes induced by nickel through epigenetic alterationsR01ES031402 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX, CUDDAPAH, SURESH · 2020 to 2024
$2.1M
Epigenetic reprogramming by nickel through chromatin domain disruptionR01ES024727 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CUDDAPAH, SURESH · 2015 to 2019
$1.9M
NIEHS NIH HHS P30 ES000260NIEHS NIH HHS R01 ES024727NIEHS NIH HHS R01 ES031402
6 · The paper itself

Abstract

Nickel compounds are environmental toxicants, prevalent in the atmosphere due to their widespread use in several industrial processes, extensive consumption of nickel containing products, as well as burning of fossil fuels. Exposure to nickel is associated with a multitude of chronic inflammatory lung diseases including asthma, chronic obstructive pulmonary disease (COPD) and pulmonary fibrosis. In addition, nickel exposure is implicated in the development of nasal and lung cancers. Interestingly, a common pathogenic mechanism underlying the development of diseases associated with nickel exposure is epithelial-mesenchymal transition (EMT). EMT is a process by which the epithelial cells lose their junctions and polarity and acquire mesenchymal traits, including increased ability to migrate and invade. EMT is a normal and essential physiological process involved in differentiation, development and wound healing. However, EMT also contributes to a number of pathological conditions, including fibrosis, cancer and metastasis. Growing evidence suggest that EMT induction could be an important outcome of nickel exposure. In this review, we discuss the role of EMT in nickel-induced lung diseases and the mechanisms associated with EMT induction by nickel exposure.

Indexed as

AnimalsEpithelial-Mesenchymal TransitionHumansLung DiseasesNickelNickelEpigeneticsEpithelial-mesenchymal transitionHIF-1NickelTGF-β

Identifiers

PMID34058338
PMCPMC8627926
OpenAlexW3165288008

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.