Evidence map›Paper›PMID 24744584›Full record

ReviewWorld journal of gastroenterology2014

Somatic alterations in mitochondrial DNA and mitochondrial dysfunction in gastric cancer progression.

Hsin-Chen Lee, Kuo-Hung Huang, Tien-Shun Yeh, Chin-Wen Chi

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. The Key Role of Mitochondrial Function in Health and Disease.Antioxidants (Basel, Switzerland) · 2023
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Mitochondrial dysfunction, UPRCell & bioscience · 2021
    Review
  19. Article
  20. The Significance of Mitochondrial Dysfunction in Cancer.International journal of molecular sciences · 2020
    Review
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 1 institution in 1 country.

Hsin-Chen LeeHsin-Chen Lee, Chin-Wen Chi, Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan.
Kuo-Hung HuangHsin-Chen Lee, Chin-Wen Chi, Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan.
Tien-Shun YehHsin-Chen Lee, Chin-Wen Chi, Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan.
Chin-Wen ChiHsin-Chen Lee, Chin-Wen Chi, Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan.
National Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Energy metabolism reprogramming was recently identified as one of the cancer hallmarks. One of the underlying mechanisms of energy metabolism reprogramming is mitochondrial dysfunction caused by mutations in nuclear genes or mitochondrial DNA (mtDNA). In the past decades, several types of somatic mtDNA alterations have been identified in gastric cancer. However, the role of these mtDNA alterations in gastric cancer progression remains unclear. In this review, we summarize recently identified somatic mtDNA alterations in gastric cancers as well as the relationship between these alterations and the clinicopathological features of gastric cancer. The causative factors and potential roles of the somatic mtDNA alterations in cancer progression are also discussed. We suggest that point mutations and mtDNA copy number decreases are the two most common mtDNA alterations that result in mitochondrial dysfunction in gastric cancers. The two primary mutation types (transition mutations and mononucleotide or dinucleotide repeat instability) imply potential causative factors. Mitochondrial dysfunction-generated reactive oxygen species may be involved in the malignant changes of gastric cancer. The search for strategies to prevent mtDNA alterations and inhibit the mitochondrial retrograde signaling will benefit the development of novel treatments for gastric cancer and other malignancies.

Indexed as

Disease ProgressionDNA DamageDNA, MitochondrialHumansMitochondriaMutationPoint MutationReactive Oxygen SpeciesSignal TransductionStomachStomach NeoplasmsDNA, MitochondrialReactive Oxygen SpeciesGastric cancerMitochondrial dysfunctionSomatic mitochondrial DNA mutations

Identifiers

PMID24744584
PMCPMC3983450
OpenAlexW2067456259

What OpenQuestion holds

Textmetadata
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.