Evidence map›Paper›PMID 26861406›Full record

ReviewJournal of clinical medicine2016

Hypoxia, Epithelial-Mesenchymal Transition, and TET-Mediated Epigenetic Changes.

Shih-Han Kao, Kou-Juey Wu, Wen-Hwa Lee

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Epithelial-Mesenchymal Transition in Chronic Rhinosinusitis.Journal of rhinology : official journal of the Korean Rhinologic Society · 2024
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Epigenetic crosstalk between hypoxia and tumor driven by HIF regulation.Journal of experimental & clinical cancer research : CR · 2020
    Review
  11. Article
  12. Targeting cancer stem cell pathways for cancer therapy.Signal transduction and targeted therapy · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Pan-Cancer Molecular Classes Transcending Tumor Lineage Across 32 Cancer Types, Multiple Data Platforms, and over 10,000 Cases.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article
  17. Review
  18. Pan-cancer survey of epithelial-mesenchymal transition markers across the Cancer Genome Atlas.Developmental dynamics : an official publication of the American Association of Anatomists · 2018
    Article
  19. Article
  20. Article
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.

Shih-Han KaoResearch Center for Tumor Medical Science and Graduate Institute of Cancer Biology, China Medical University, Taichung 40402, Taiwan. shkao@mail.cmu.edu.tw.
Kou-Juey WuResearch Center for Tumor Medical Science and Graduate Institute of Cancer Biology, China Medical University, Taichung 40402, Taiwan. wukj@mail.cmu.edu.tw.
Wen-Hwa LeeInstitute of Clinical Medicine, China Medical University, Taichung 40402, Taiwan. whlee@uci.edu.
China Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor hypoxia is a pathophysiologic outcome of disrupted microcirculation with inadequate supply of oxygen, leading to enhanced proliferation, epithelial-mesenchymal transition (EMT), metastasis, and chemo-resistance. Epigenetic changes induced by hypoxia are well documented, and they lead to tumor progression. Recent advances show that DNA demethylation mediated by the Ten-eleven translocation (TET) proteins induces major epigenetic changes and controls key steps of cancer development. TET enzymes serve as 5mC (5-methylcytosine)-specific dioxygenases and cause DNA demethylation. Hypoxia activates the expression of TET1, which also serves as a co-activator of HIF-1α transcriptional regulation to modulate HIF-1α downstream target genes and promote epithelial-mesenchymal transition. As HIF is a negative prognostic factor for tumor progression, hypoxia-activated prodrugs (HAPs) may provide a favorable therapeutic approach to lessen hypoxia-induced malignancy.

Indexed as

5hmCDNA demethylationHAPhypoxiaTET

Identifiers

PMID26861406
PMCPMC4773780
OpenAlexW2256234263

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.