Evidence map›Paper›PMID 26579821›Full record

Observational studyMedicine2015

Polymorphisms and Plasma Levels of Tissue Inhibitor of Metalloproteinase-3: Impact on Genetic Susceptibility and Clinical Outcome of Oral Cancer.

Chun-Wen Su, Yi-Wen Huang, Mu-Kuan Chen, Shih-Chi Su, Shun-Fa Yang, Chiao-Wen Lin

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Long-Term Effect of TIMP3 Gene Expression on Thyroid Cancer: A Cure Model Analysis.Asian Pacific journal of cancer prevention : APJCP · 2024
    Article
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  12. Associations ofInternational journal of molecular sciences · 2020
    Article
  13. Article
  14. The genetic basis of Turner syndrome aortopathy.American journal of medical genetics. Part C, Seminars in medical genetics · 2019
    Article
  15. TIMP-3 as a therapeutic target for cancer.Therapeutic advances in medical oncology · 2019
    Review
  16. Article
  17. Article
  18. Review
  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

6 authors at 1 institution in 1 country.

Chun-Wen SuFrom the Institute of Medicine, Chung Shan Medical University, Taichung (C-WS, Y-WH, M-KC, S-FY); Department of Health, Pulmonary and Critical Care Unit, Chang Hua Hospital (Y-WH); Department of Otorhinolaryngology-Head and Neck Surgery, Changhua Christian Hospital, Changhua (M-KC); Whole-Genome Research Core Laboratory of Human Diseases, Chang Gung Memorial Hospital, Keelung, Taiwan (S-CS), Department of Medical Research, Chung Shan Medical University Hospital (S-FY), Department of Dentistry, Chung Shan Medical University Hospital (C-WL), and Institute of Oral Sciences, Chung Shan Medical University, Taichung, Taiwan (C-WL).
Yi-Wen Huang
Mu-Kuan Chen
Shih-Chi Su
Shun-Fa Yang
Chiao-Wen Lin
Chung Shan Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oral cancer, the fourth most common cancer among men in Taiwan, is associated with environmental carcinogens. Tissue inhibitor of metalloproteinase-3 (TIMP3), a member of the TIMP family, is the only protein that binds to the extracellular matrix for suppressing cancer cell growth, angiogenesis, migration, and invasion. The association of TIMP3 polymorphism with oral cancer susceptibility, however, has not yet been reported. In this study, 1947 participants-1200 healthy male controls and 747 male patients with oral cancer-were recruited. Allelic discrimination of TIMP3 -1296 T > C (rs9619311), TIMP3 C > T (rs9862), and TIMP3 C > T (rs11547635) polymorphisms were assessed through real-time polymerase chain reaction. The authors discovered that individuals carrying the polymorphic rs9862 allele are more susceptible to oral cancer [odds ratio (OR), 1.5; 95% confidence interval (CI), 1.2-1.9; adjusted OR (AOR), 1.6; 95% CI, 1.2-2.1] after adjustment for betel quid chewing, alcohol, and tobacco consumption. Among 601 betel quid chewers, the TIMP3 polymorphism rs9862 T/T carriers had a 32.2-fold (95% CI, 20.2-51.3) increased oral cancer risk compared with those carrying C/C and not chewing betel quid. In addition, the authors observed a significant association between rs9862 variants and large tumors (OR, 1.5; 95% CI, 1.0-2.3) development. Moreover, TIMP3 plasma levels significantly increased in oral cancer patients who have large tumor or carry T allele rs9862 polymorphism. In conclusion, these results suggest that gene-environment interactions between the TIMP3 rs9862 polymorphisms and betel quid may alter oral cancer susceptibility and tumor growth in Taiwanese men.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAdultAgedBiomarkers, TumorCarcinoma, Squamous CellCase-Control StudiesGene-Environment InteractionHumansMaleMiddle AgedMouth NeoplasmsReal-Time Polymerase Chain ReactionRisk FactorsTaiwanTissue Inhibitor of Metalloproteinase-3Biomarkers, TumorTIMP3 protein, humanTissue Inhibitor of Metalloproteinase-3

Identifiers

PMID26579821
PMCPMC4652830
OpenAlexW2312736449

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.