Evidence map›Paper›PMID 20176653›Full record

SynthesisCarcinogenesis2010

CASP8 polymorphisms contribute to cancer susceptibility: evidence from a meta-analysis of 23 publications with 55 individual studies.

Ming Yin, Jingrong Yan, Sheng Wei, Qingyi Wei

Open access · bronzeAbstract readMeta-Analysis
In one paragraph

Synthesis in Carcinogenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 4 pooled it
2.6field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 4 syntheses or guidelines pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Fine-mapping CASP8 risk variants in breast cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2012
    Pooled it
  5. Potential advantage of clinical exome sequencing inJournal of medical genetics · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Oncotarget · 2017
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Caspase functions in cell death and disease.Cold Spring Harbor perspectives in biology · 2013
    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

4 authors at 3 institutions in 1 country.

Ming YinDepartment of Epidemiology, The University of Texas, M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
Jingrong Yan
Sheng Wei
Qingyi Wei
The University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · USThe University of Texas Health Science Center at Houston · US

Funding

Molecular Epidemiology of Head and Neck CancerR01ES011740 · NIEHS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WEI, QINGYI · 2001 to 2012
$6.3M
Genotypes and Phenotypes of Apoptosis and Risk of Head and Neck CancerR01CA131274 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WEI, QINGYI · 2009 to 2013
$3.0M
NCI NIH HHS R01 CA131274NIEHS NIH HHS R01 ES011740
6 · The paper itself

Abstract

Several potentially functional polymorphisms of CASP8 encoding an apoptotic enzyme, caspase 8, have been implicated in cancer risk, but individually published studies showed inconclusive results. We performed a meta-analysis of 23 publications with a total of 55 174 cancer cases and 59 336 controls from 55 individual studies. We summarized the data on the associations between three studied CASP8 polymorphisms (G>C D302H, -652 6N del and Ex14-271A>T) and cancer risk and performed subgroup analysis by ethnicity, cancer type, study design and etiology. We found that D302H CC and CG variant genotypes were associated with significantly reduced overall risk of cancers using conservative random genetic models [homozygote comparison: odds ratios (OR) = 0.79; 95% confidence interval (CI): 0.69-0.92; dominant comparison: OR = 0.93, 95% CI: 0.89-0.98; recessive comparison: OR = 0.81, 95% CI: 0.71-0.93). In further stratified analyses, the reduced cancer risk remained for subgroups of Caucasians, breast or estrogen-related cancers, and hospital- or population-based studies, except for an elevated risk for brain tumors. Similarly, the -652 6N del polymorphism was also associated with significantly reduced overall risk of cancers (homozygote comparison: OR = 0.84, 95% CI: 0.75-0.94; dominant comparison: OR = 0.88, 95% CI: 0.81-0.96; recessive comparison: OR = 0.90, 95% CI: 0.82-0.99) and all subgroups analyzed. However, the Ex14-271A>T polymorphism did not appear to have an effect on cancer risk. These results suggest that CASP8 D302H and -652 6N del polymorphisms are potential biomarkers for cancer risk.

Indexed as

Genetic Predisposition to DiseasePolymorphism, GeneticCaspase 8Gene DeletionGenotypeHumansNeoplasmsCASP8 protein, humanCaspase 8

Identifiers

PMID20176653
PMCPMC2864415
OpenAlexW2166400823

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.